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Here, we utilized a two-brain perspective to examine the codependence of maternal and paternal caregiving. Dual-EEG hyperscanning measured child-mother and child-father interbrain synchrony in high- versus low-stress ecologies. Participants were 77 families comprising mothers, fathers, and children (N=231): 49 had children with anxiety disorders, and 28 healthy controls. In low-stress families, mother-child interbrain synchrony exceeded father-child, but higher father-child neural synchrony was found in high-stress families. For both mother and father, quality of caregiving moderated the degree of neural synchrony with the second parent; when one parent's behavioral sensitivity decreased, neural synchrony with the other parent increased. Results demonstrate interbrain mechanisms of complementarity within families and indicate that human parenting operates within highly responsive family-level dynamics. Our findings have important implications for whole-family interventions. Biological sciences/Psychology/Human behaviour Biological sciences/Neuroscience/Cognitive neuroscience Biological sciences/Biological techniques/Electrophysiology/Electroencephalography – EEG Figures Figure 1 Figure 2 Figure 3 1. Introduction Throughout mammalian evolution, the care of infants has been, in the main, a maternal enterprise. Of approximately 5,400 mammalian species, only about 5% exhibit biparental care where fathers contribute substantively to the rearing of offspring beyond conception 1,2 . This leads to a fundamental asymmetry, where maternal care is obligate and phylogenetically ancient, shaped by hormonal cascade resulting from pregnancy, parturition, and lactation, while paternal care is facultative, emerging only under specific ecological and social conditions that favor male parental caregiving 3,4 . When paternal investment does occur, it invariably operates within the context of maternal care and family units, creating a system in which paternal behavior complements maternal caregiving and is sensitive to maternal provisions, offspring needs, and the ecological challenges of the family 5,6 . Human Fatherhood as Complementary Coordination Humans represent a remarkable exception among primates in the extent of their paternal investment. The evolution of cooperative breeding, prolonged offspring dependency, and complex social structures and norms created selective pressures for paternal engagement in childrearing 6,7 . Unlike most mammals, contemporary human fathers routinely provide direct care, protection, provisioning, and social learning opportunities 8 that complement maternal contributions and are sensitive to ecological conditions 9–11 . Such facultative fathering carries profound implications for family organization, when the family system reorganizes into a dynamic balance where each parent’s neural and behavioral engagement is sensitive to that of the partner's. The father's brain is especially sensitive to maternal contributions and caregiving 12–14 . We term these mutual influences ‘complementary coordination system’, representing how the quality of one parent’s caregiving influences the expression of the other's parenting while both continuously recalibrate to the family's needs and contextual demands. The biobehavioral synchrony model provides a framework for understanding how the coordinated social behaviors of caregivers and children create enduring neural templates for social response 15,16 . From birth, parent–infant dyads coordinate their gaze, vocalizations, affect, and autonomic arousal to establish multi-level coordination spanning behavioral, physiological, and endocrine systems, forming the basis for later affiliative bonds 17,18 . Through iterative cycles of contingent exchanges, early synchrony scaffolds the infant’s emerging neural and behavioral architecture for social participation and predicts long‑term outcomes in terms of self‑regulation, symbol use, empathy, and social competencies across childhood, adolescence, and up until adulthood 19–23 . Inter-Brain Synchrony with Mother and Father Among the consistent findings to emerge from the biobehavioral synchrony framework is that mothers and fathers tend to engage in different types of affective coordination 9 . Mother–infant interactions are characterized by low-to-medium arousal and gentle rhythmic coordination reflecting what we term as the ‘rhythms of safety’, which promotes emotional comfort, social skills, and secure base 24 . Father–infant interactions, by contrast, involve high-arousal play, social exploration, involving sudden bursts of emotional intensity, creating what we refer to as the ‘rhythms of exploration’ that support mastery in the outside world, curiosity, and self-regulation 9,25–27 . Recent advances in hyperscanning, the simultaneous recording of neural activity from two or more individuals, have made it possible to examine whether these distinct behavioral styles are mirrored in inter-brain coupling during naturalistic interactions. A growing body of work has demonstrated robust mother–child neural synchrony, particularly in frontal, temporal, and parietal regions implicated in social cognition, joint attention, and emotion regulation 28–37 . Individual differences in maternal caregiving quality have been shown to predict the magnitude of their neural synchrony: higher sensitivity correlates with enhanced frontotemporal coupling, while intrusive behavior is associated with diminished neural coordination 28 . Notably, maternal sensitivity and intrusiveness in infancy were found to predict the degree of mother–child frontotemporal neural synchrony more than a decade later, suggesting that early caregiving shapes the long-term architecture of interpersonal neural coordination 38 . Very few studies to date explored father–child interbrain synchrony, but the existing research similarly shows that it recruits prefrontal and temporo-parietal circuits. During cooperative problem solving, father–child dyads exhibited increased synchrony in the dorsolateral prefrontal cortex and in temporo-parietal regions relative to individual task performance 39 . Moreover, variations in frontal and fronto-temporal coupling were associated with fathers' role attitudes and self-reported engagement quality, linking neural alignment to paternal involvement 39 . Father–child prefrontal synchrony was also confirmed during co-viewing of emotionally arousing stimuli 40 . When comparing mother–child and father–child neural synchrony during shared co-viewing of videos and free-play, in dyads that were not part of the same family, revealed that mothers exhibited greater frontal cortex synchrony with their children than fathers during passive co-viewing. Mothers also showed greater left frontal neural synchrony during free-play, correlating with child involvement, while fathers exhibited stronger right frontal synchrony linked to child-initiated behaviors and play agency 41 . A separate fNIRS study found that interbrain synchrony in the left temporo-parietal junction was associated with parental warmth, autonomy support, and shared positive affect, though only in mother–child, but not father–child dyads 33 . Critically, however, these studies drew mother–child and father–child dyads from different families, which precluded direct within-family comparisons of how the two parent–child subsystems jointly organize and whether the neural synchrony between one parent and the child depends in some way on the synchrony formed with the other parent. Still, these findings implicate the fronto-temporal network as a shared substrate of parent–child neural coordination and suggest that paternal engagement modulates interbrain prefrontal and temporo-parietal alignment, though its behavioral correlates may differ from those of mothers. Family Systems and Complementary Processes between Mothering and Fathering in High- and Low-Stress Ecologies Family systems facing stress can provide a critical window into processes of complementarity between parents and how they are impacted by alterations in family functioning. Evidence indicates that in families with a child diagnosed with anxiety disorder, family life is marked by elevated stress, problems in family functioning, and disrupted regulation, including outbursts, overcontrolling, and less warm parenting 42,43 . Maternal psychopathology, particularly anxiety, frequently co‑occurs with child anxiety and studies of clinical samples consistently show that substantial proportions of mothers whose children meet criteria for an anxiety disorder are themselves diagnosed with an anxiety disorder or suffer elevated anxiety symptoms 44,45 . This creates bidirectional amplification of distress within the family system. Under such conditions, the balance of mother-child and father-child behavioral and neural synchrony may fundamentally reorganize to compensate for these alterations and allow children a better chance at adaptation and mental health. Evidence from families in which mothers suffer depression supports this hypothesis. Greater father involvement and more sensitive and engaged paternal behavior attenuate the effects of maternal depression on child social-emotional outcomes, increasing positivity and harmony during observed family interactions and reducing child externalizing and internalizing problems as compared to families comprised of depressed mothers and uninvolved fathers 46–49 . These findings suggest that family systems may be underpinned by compensatory inter-parental mechanisms: when one parent’s capacity for optimal caregiving is compromised, the other parent intensifies his or her engagement to partly buffer the effects on the child. In the current study, we explore, for the first time, the existence of complementary processes in the parents' neural coordination with their children. Stress and Family Ecology Impact Neural Synchrony and the Parental Brain Hyperscanning studies have only begun to link parental psychopathology and stress to alterations in parent–child inter-brain synchrony. Parenting stress has been found to correlate with reduced mother–child prefrontal synchrony during joint activities in early childhood 50 , and a systematic review of the hyperscanning literature confirmed that anxiety, stress, or depressive symptoms in at least one interacting partner are broadly associated with diminished interpersonal neural coupling 51 . In contrast, sensitive and supportive parenting and better parent–child relationship quality are related to greater neural synchrony 28,30–33,38,41 . This suggests that anxious or depressed parenting may disrupt neural attunement, while warm, responsive caregiving enhances it. The paternal brain exhibits remarkable adaptability to the family context. Unlike the maternal brain, which undergoes substantial structural and functional reorganization during pregnancy and the postpartum period 52,53 , the paternal brain exhibits experience-dependent plasticity that is especially sensitive to caregiving involvement and family circumstances 14,54,55 . Neuroimaging studies show that fathers' amygdala connectivity with superior temporal sulcus circuits scales with caregiving involvement, with primary-caregiving fathers developing amygdala activation patterns resembling those of mothers 14 . Compared to non-fathers, fathers show enhanced activation in mentalizing and reward-related regions when viewing child stimuli, and testosterone is negatively correlated with these responses 56 . Paternal prefrontal and caudate responses to own-infant cues are further linked to parental sensitivity 57 , the paternal brain's responsiveness to infant cues is shaped by caregiving context and family circumstances (for review, see 58 ), and corticostriatal connectivity in parents' brains when viewing coparental stimuli predicts collaborative coparenting and child well-being 59 . Such sensitivity to context suggests that paternal neural engagement, including interbrain synchrony between fathers and children, may be particularly responsive to family needs, maternal functioning, and child developmental challenges. The Current Study Despite the aforementioned theoretical foundation and research evidence on inter-parental complementarity, mother–child and father–child neural coupling have not yet been systematically compared within the same family dynamic, with prior studies on parent-child interbrain synchrony examining children with either mother or father, not with both. Direct observation on processes of interbrain synchrony between the child and each parent can shed light on how families reorganize to various ecological demands and how one parent's neural attunement complements that of the other's. This gap is critical. If parent–child neural synchrony reflects family-level adaptations, the child's neural engagement with one parent cannot be fully understood without the other parent. The present study provides this assessment of interbrain synchrony within families during naturalistic parent–child play. We investigated how mother–child and father–child neural coordination patterns emerge, interact, and complement one another, and how these family-level dynamics vary between families living in high-stress contexts with a child diagnosed with an anxiety disorder, as compared to typically developing children. Our pre-registered investigation addressed five main hypotheses consistent with the biobehavioral synchrony framework. First, we predicted robust neural synchrony across both parent–child interactions compared to surrogate control data, validating a genuine inter-brain coupling during social interactions. Second, we expected mother–child and father–child neural synchrony to show distinct and complementary patterns reflecting different interaction styles. Third, we hypothesized that children with anxiety disorders would exhibit altered balance in neural coordination across parents with potential enhancement of father–child synchrony when mother–child synchrony is disrupted, thereby reflecting compensatory family dynamics. Fourth, we predicted that parental caregiving quality would predict parent–child neural synchrony through complementary mechanisms. As such, the quality of parenting provided by one parent would moderate the association between the other parent’s behavior and his or her neural coordination with the child. Fifth, we expected that child anxiety would systematically reorganize neural synchrony patterns, with differential effects on synchrony with mothers versus fathers that illuminate how family-level stress shapes neural coordination across pathways of safety (maternal) and exploration (paternal). 2. Results 2.1. Validation of Inter-Brain Synchrony To confirm that the observed neural coupling reflects genuine inter-brain synchrony rather than shared sensory input or environmental noise, we compared wPLI values from real parent–child dyads against surrogate control data (see Methods). Difference scores (real minus surrogate) were computed for each parent–child configuration (mother–child, father–child) and frequency band (alpha, beta), yielding four comparisons. As these difference scores deviated significantly from normality (Shapiro–Wilk tests, all p < 0.03), we employed non-parametric Wilcoxon signed-rank tests with rank-biserial correlations ( r rb ) as effect sizes. False Discovery Rate (FDR) correction was applied across the four tests; all corrected p -values remained below 0.001. 2.1.1. Alpha Rhythm Synchrony Mother–child dyads ( N = 71) exhibited significantly higher alpha synchrony ( M = 0.083, SD = 0.013) than surrogate data ( M = 0.069, SD = 0.005; W = 2488, z = 6.93, p (FDR) < 0.001, r rb = 0.95, 95% CI [0.87, 0.99]). Father–child dyads ( N = 73) similarly showed significantly higher alpha synchrony (M = 0.088, SD = 0.017) than surrogate data ( M = 0.074, SD = 0.010; W = 2502, z = 6.33, p (FDR) < 0.001, r rb = 0.85, 95% CI [0.72, 0.95]). See Figure 2A. 2.1.2. Beta Rhythm Synchrony Mother–child dyads ( N = 71) exhibited significantly higher beta synchrony ( M = 0.088, SD = 0.010) than surrogate data ( M = 0.071, SD = 0.004; W = 2556, z = 7.32, p (FDR) < 0.001, r rb = 1.00, 95% CI [1.00, 1.00], all 74 real values exceeded their paired surrogate values, yielding a ceiling effect on this measure). Father–child dyads ( N = 73) similarly showed significantly higher beta synchrony ( M = 0.092, SD = 0.014) than surrogate data ( M = 0.076, SD = 0.010; W = 2623, z = 7.00, p (FDR) < 0.001, r rb = 0.94, 95% CI [0.87, 0.98]). These findings and effect sizes indicate robust inter-brain neural synchrony in both parent–child configurations (Figure 2B). Detailed distributions of real versus surrogate synchrony values for each parent–child dyad and frequency band are presented in Supplementary Figures S1–S4. 2.2. Differential Balance of Mother–Child versus Father–Child Neural Synchrony 2.2.1. Alpha Band To examine whether the balance of parent–child neural synchrony differed between child anxiety and control families, we computed the Δ synchrony scores (real - surrogate) and conducted a 2×2 mixed ANOVA with Parent (mother-child, father-child) as a within-subjects factor and Child Anxiety (clinical, control) as a between-subjects factor ( N = 68 families with complete data for both dyads). For alpha synchrony, neither the main effect of Parent (F(1,66) = 0.57, p = 0.452, η² p = 0.009, 90% CI [0.000, 0.017]) nor of Child Anxiety (F(1,66) = 0.10, p = 0.751, η² p = 0.002, 90% CI [0.000, 0.003]) reached significance. The Parent × Child Anxiety interaction showed a trend in the same direction as the beta-band results reported below, but did not reach significance (F(1,66) = 3.06, p = 0.085, η² p = 0.044, 90% CI [0.000, 0.089]). 2.2.2. Beta Band Consistent with this trend, neural beta synchrony yielded a significant Parent × Child Anxiety interaction (F(1,66) = 12.68, p < 0.001, η² p = 0.161, 90% CI [0.05, 0.29]). Similar to the alpha band synchrony findings, neither the main effects of Parent (F(1,66) = 1.55, p = 0.217, η² p = 0.023, 90% CI [0.000, 0.046]) nor of Child Anxiety (F(1,66) = 0.72, p = 0.401, η² p = 0.011, 90% CI [0.000, 0.022]) reached significance. Notably, the significant interaction indicates that the relative balance of mother–child versus father–child beta synchrony differs between clinical and typically developing children. We decomposed this interaction in two complementary ways. First, we compared the mother-minus-father Δ synchrony difference score between samples. Clinical families showed a significantly more negative difference ( M = −0.004, SD = 0.009) than control families ( M = 0.009, SD = 0.021), indicating a reversal in the relative dominance of each parent's neural coupling with the child (Welch's t (29.87) = 2.98, p = 0.006, d = 0.81, 95% CI [−1.34, −0.27]). Second, within each sample, we compared mother–child and father–child neural beta synchrony using Wilcoxon signed-rank tests (FDR-corrected across the two comparisons; see Figure 2C–D). In control families, mother–child dyads showed significantly greater beta synchrony enhancement ( M = 0.020, SD = 0.012) than father–child dyads ( M = 0.011, SD = 0.017; W = 249, z = 2.33, p (FDR) = .019, r rb = 0.53, 95% CI [0.13, 0.88]), indicating that mothers serve as the primary neural regulatory agent in typically developing families. Critically, this pattern reversed in clinical child anxiety families: father–child dyads showed significantly greater beta synchrony enhancement ( M = 0.019, SD = 0.008) than mother–child dyads ( M = 0.015, SD = 0.005; W = 707, z = −2.83, p (FDR) = .008, r rb = −0.49, 95% CI [−0.76, −0.18]). Together, these results show a double dissociation pattern: the between-group comparison confirms that the mother–child and father-child synchrony balance reverses between samples, and both within-group comparisons independently reach significance. This pattern indicates that childhood anxiety reorganizes the distribution of neural coupling across parent–child subsystems, with fathers emerging as the primary source of inter-brain synchrony when families contend with child anxiety. Table 1. Mixed ANOVA results for alpha and beta Δ synchrony (real − surrogate) Alpha Δ (8–12 Hz) Beta Δ (13–30 Hz) Effect F p η²p F p η²p Parent (P) 0.57 .452 .009 1.55 .217 .023 Child Anxiety (S) 0.10 .751 .002 0.72 .401 .011 Parent × Child Anxiety 3.06 .085 .044 12.68 <.001*** .161 Table 1. 2×2 mixed ANOVAs on neural synchrony (real − surrogate) with Parent (mother-child, father-child) as within-subjects factor and Child Anxiety (clinical, control) as between-subjects factor. df = (1, 66). ***P < .001. 2.3. Parental Quality Predicts Neural Synchrony Through Complementary Mechanisms Following, to examine how parenting quality predicts parent–child neural synchrony, we conducted hierarchical regression analyses separately for mother–child and father–child neural beta synchrony ( N = 65 families with complete behavioral and neural data). Parenting quality has been assessed using two composite scores derived from the CIB system 60 . For maternal behavior, the Maternal Sensitive Support (maternal parenting) construct has been used, while for the father, the Paternal Exploratory Encouragement construct has been used (paternal parenting, see 4.7. Behavioral Coding). Each model included three steps: Child Anxiety status (clinical / control) (Step 1), maternal and paternal parenting quality (Step 2), and all two-way interactions among these predictors (Step 3). 2.3.1. Mother–Child Neural Synchrony At the first step of the model, Child Anxiety significantly predicted mother–child neural synchrony ( R² = 0.084, F(1,63) = 5.74, p = 0.020), with clinical families showing lower synchrony ( β = −0.0051, 95% CI [−0.0093, −0.0008], t (63) = −2.40, p = 0.020). Adding parenting quality marginally improved the model’s fit ( ΔR² = 0.071, F(2,61) = 2.55, p = 0.086; total R² = 0.154), but neither maternal ( β = 0.0022, p = 0.239) nor paternal parenting ( β = −0.0059, p = 0.150) showed significant main effects. Critically, adding interactions (step 3) significantly improved the model fit ( ΔR² = 0.152, F(3,58) = 4.24, p = 0.009; final R² = 0.306, F(6,58) = 4.27, p = 0.001). In the final model, maternal parenting emerged as a significant positive predictor ( β = 0.0622, 95% CI [0.011, 0.114], t (58) = 2.43, p = 0.018), while neither paternal parenting ( β = 0.0464, p = 0.113) nor Child Anxiety were significant ( β = −0.0491, p = 0.129). Among interactions, the Maternal × Paternal Parenting interaction was significant ( β = −0.0206, 95% CI [−0.038, −0.003], t (58) = −2.40, p = 0.019) and the Child Anxiety × Paternal Parenting interaction approached significance ( β = 0.0167, p = 0.054), while the Child Anxiety × Maternal Parenting interaction was not significant ( β = −0.0012, p = 0.753). Decomposition of the Maternal × Paternal Parenting interaction revealed that maternal parenting quality most strongly predicted mother–child synchrony when paternal parenting was low (simple slope = 0.006), whereas this association was no longer evident when paternal parenting was high (simple slope = −0.005), indicating that the neural co-regulatory contribution of maternal behavior is most pronounced when paternal engagement is least optimal. This demonstrates a compensatory mechanism: high-quality maternal parenting buffers against less optimal paternal engagement in predicting mother–child neural synchrony (Figure 3C. For full model, see Table 2). 2.3.2. Father–Child Neural Synchrony In contrast to mother–child neural synchrony pattern, Child Anxiety status predicted higher father–child neural synchrony (R² = 0.103, F(1,63) = 7.25, p = 0.009; β = 0.0084, 95% CI [0.0022, 0.0146], t (63) = 2.69, p = 0.009). Adding parenting quality significantly improved fit (ΔR² = 0.106, F(2,61) = 4.10, p = 0.021; total R² = 0.209), with paternal parenting showing a significant positive effect ( β = 0.0130, 95% CI [0.0015, 0.0245], t (61) = 2.26, p = 0.027) but maternal parenting showing no effect ( p = 0.340). Adding interactions (step 3) significantly improved the model (ΔR² = 0.143, F(3,58) = 4.29, p = 0.008; final R² = 0.353, F(6,58) = 5.27, p < 0.001). In the final model, paternal parenting was the strongest predictor ( β = 0.1528, 95% CI [0.070, 0.235], t (58) = 3.71, p < 0.001), followed by maternal parenting ( β = 0.1135, 95% CI [0.040, 0.187], t (58) = 3.10, p = 0.003) and Child Anxiety ( β = 0.1086, 95% CI [0.018, 0.200], t (58) = 2.39, p = 0.020). The Maternal × Paternal interaction was also significant ( β = −0.0384, 95% CI [−0.063, −0.014], t (58) = −3.14, p = 0.003), as was the Child Anxiety × Paternal Parenting interaction ( β = −0.0280, 95% CI [−0.052, −0.004], t (58) = −2.32, p = 0.024), w hile the Child Anxiety × Maternal interaction was not significant ( β = −0.0048, p = 0.362). Simple slope analysis of the Maternal × Paternal interaction revealed that when maternal parenting was low, paternal parenting strongly predicted father–child synchrony (simple slope = 0.050); when maternal parenting was high, this paternal effect was substantially reduced (simple slope = 0.007). This mirrors the compensatory pattern observed for mother–child synchrony (Figure 3D). Table 2. Hierarchical regression predicting parent–child neural synchrony: full model coefficients ( N = 65) Predictor β 95% CI t p R² ΔR² ΔF Step Mother–Child Synchrony Child Anxiety −0.049 [−.113, .015] −1.54 .129 .084 .084 5.74* 1 Maternal Sensitive Support 0.062 [.011, .114] 2.43 .018* 2 Paternal Exploratory Encouragement 0.046 [−.011, .104] 1.61 .113 .154 .071 2.55 Child Anxiety × Maternal Sensitive Support −0.001 [−.009, .006] −0.32 .753 3 Child Anxiety × Paternal Exploratory Encouragement 0.017 [<.001, .034] 1.97 .054 Maternal Sensitive Support × Paternal Exploratory Encouragement −0.021 [−.038,−.003] −2.40 .019* .306 .152 4.24** Father–Child Synchrony Child Anxiety 0.109 [.018, .200] 2.39 .020* .103 .103 7.25** 1 Maternal Sensitive Support 0.114 [.040, .187] 3.10 .003** 2 Paternal Exploratory Encouragement 0.153 [.070, .235] 3.71 <.001*** .209 .106 4.10* Child Anxiety × Maternal Sensitive Support −0.005 [−.015, .006] −0.92 .362 3 Child Anxiety × Paternal Exploratory Encouragement −0.028 [−.052,−.004] −2.32 .024* Maternal Sensitive Support × Paternal Exploratory Encouragement −0.038 [−.063,−.014] −3.14 .003** .353 .143 4.29** Table 2. All β, t, and p values reported in the results reflect the full model (Step 3). Synchrony is measured as neural synchrony in the beta rhythm Δ (real – surrogate wPLI). *P < .05, **P < .01, ***P < .001. 3. Discussion The current study addressed mechanisms of neural complementarity within families. We examined whether the neural coupling that one parent creates with the child during naturalistic interactions is shaped by the family context and the neural coupling and caregiving quality of the other parent. Our key findings indicate that parent–child interbrain synchrony operates as a family-level coordination system rather than a set of independent dyadic neural coupling processes. The findings support and extend each of our preregistered hypotheses. We found that mothers and fathers create complementary neural coordination patterns with their children, and that the child's anxiety fundamentally reorganizes the balance between the two parent-child sub-units of the family, so that one parent's caregiving quality modulates the neural synchrony between the other parent and the child, even when that parent is not physically present during the interaction. Our first findings confirm that neural synchrony is evident in all social interactions tested, across parents and clinical groups. Both mother–child and father–child dyads exhibited significantly higher inter-brain synchrony than surrogate controls across both alpha and beta frequency bands. These findings contribute to the expanding hyperscanning literature, which demonstrates that inter-brain synchrony is not merely an epiphenomenon of shared sensory input, but rather reflects genuine neural coordination, resulting from social interaction 61–63 . Our results also expand previous hyperscanning studies on neural coupling during parent–child social interaction 28–33,36–41,50,64–66 . Our results strengthen and extend the biobehavioral synchrony framework 15,17,18,67 by showing that both maternal and paternal neural synchrony with their children are robust phenomena, detectable even during a brief naturalistic free-play interaction. The magnitude of the effects found in our validation analysis likely reflects the ecological validity of the paradigm, which triggers a repertoire of social exchanges that drive inter-brain synchrony in real-world interactions. Context-Dependent Complementarity in Neural Coordination Our second hypothesis predicted that mothers and fathers would show distinct patterns of neural synchrony with their children. The absence of a significant main effect for parent in either alpha or beta frequency bands indicates that both parents achieve comparable overall levels of synchrony enhancement during interaction. This finding is corroborated by the validation analysis, which confirmed robust mother–child and father–child neural synchrony during free-play. Such equivalence is in itself noteworthy: while prior hyperscanning work has focused predominantly on mother–child dyads, with only isolated studies of father–child synchrony, the present study is, to our knowledge, the first to assess both parents within the same family context. The parent × group interaction, which was significant in the beta rhythm, with a parallel trend in alpha rhythm, indicates that the balance between mother–child and father–child neural coupling shifts as a function of family context and regulatory demands, rather than being fixed. The primacy of the beta-band effect is theoretically meaningful given the established role of beta in social regulation and caregiving. Beta oscillations are implicated in top-down regulatory processes, prediction, and the active maintenance of cognitive states 68 , and have been specifically linked to parent–child attachment processes in mothers 69,70 . Beta rhythms also underpin a range of complex social functions, including empathy 32,71 , mentalization 72 , prediction of others' actions 73 , and the continuous updating of predictive models 74 , that collectively enable the rapid mutual adaptation required for inter-brain coordination during social interaction 61 . The selective reorganization of beta synchrony in clinical families, therefore, points to a context-sensitive redistribution of neural regulatory coupling across parent–child pathways that operates at the frequency band underpinning the social-cognitive infrastructure of caregiving. The same trend of greater mother–child synchrony in control families and greater father–child synchrony in clinical families also emerged in the alpha band, although it did not reach the statistical significance threshold. This tentative extension to alpha is noteworthy given alpha's established role in the affective and attentional dimensions of parent–child interaction. Alpha-band synchrony is enhanced during naturalistic parent–child interactions and is modulated by emotional quality and dyadic engagement 65 . Alpha synchrony is particularly pronounced during early development, where increased alpha coupling between infants and adults occurs during direct gaze and infant-directed speech 75 , and correlates with independent measures of emotional connection 76 . Such convergence across frequency bands raises the possibility that the functional reorganization of parental neural coupling in clinical families is not beta-specific, but reflects a broader cross-frequency shift in the relative dominance of maternal versus paternal neural coordination. That said, the alpha effect did not reach significance and must be interpreted with caution. Whether this reorganization generalizes across frequency bands remains an open question requiring replication in larger, adequately powered samples. Taken together, these findings are consistent with the biobehavioral synchrony framework, which distinguishes the types of behavioral synchrony infants create with mother and father. The "rhythms of safety” with mother are characterized by low-arousal and promote regulation and security, and the “rhythms of exploration” with father are characterized by high-arousal play fostering resilience and environmental exploration 9,24,25,77 . Our results suggest that while these dyadic styles differ in specific behaviors, they are similar in promoting a sense of synchrony, coordination, and attunement and translate into complementary neural coordination systems that are flexibly deployed according to family need. The absence of a parent main effect, coupled with a context-dependent interaction, points to functional specialization rather than hierarchical organization: maternal and paternal neural coupling with the child are not universally different in magnitude, but are calibrated to family circumstances, with their relative contributions shifting precisely when regulatory demands are highest. Our third hypothesis predicted that when the family ecology is one of heightened stress, such as in the case of a child with anxiety disorder, there is a reorganization of the balance between parents, in this case, in parents' neural coordination. This hypothesis received strong support. We found that in low-stress families of typically-developing children, mother–child dyads exhibited significantly greater neural synchrony than father–child dyads, consistent with the primacy of the maternal co-regulatory function in most families 24 . In clinical families, this pattern was reversed, and father–child dyads showed significantly greater neural synchrony. This double dissociation, which was significant in both directions for beta rhythm, provides the first neural evidence for mechanisms of complementarity within families. Such complementary dynamics have long been hypothesized by family systems' theories 78,79 , and indicate that, under stress the family system not only deteriorates but actively reorganizes its regulatory architecture. Notably, high-stress family ecologies, such as those with a child diagnosed with anxiety disorder, are frequently marked by co-occurring maternal psychopathology. This pattern, which occurred in over 60% of our clinical families (see Supplementary Analysis 1: Maternal Psychopathology as Grouping Variable – ANOVA) is consistent with findings from large epidemiological studies. A meta-analysis of 34 studies and over 295,000 participants found that maternal anxiety is significantly associated with preschool children’s internalizing problem behaviors, externalizing problem behaviors, and overall problem behaviors 80 . Consistently, a meta-analysis of 191 studies on maternal perinatal depression and anxiety documented consistent associations with offspring socio-emotional, cognitive, and behavioral difficulties across development, from infancy through adolescence 81 . Family-based studies further report elevated rates of co-occurring maternal anxiety or depression in families where children exhibited anxiety disorders 82,83 . Taken together, these findings underscore that maternal internalizing psychopathology is common in families in which children suffer from anxiety, amplifying the functional significance of the complementary paternal regulatory role identified in our study. In this context, our findings indicate that fathers appear to rise to a complementary role, exhibiting active neural upregulation that sustained the child's access to inter-brain regulatory input when the mother–child synchrony pathway is compromised. The neurobiological plausibility of such reorganization rests on evidence that the paternal brain exhibits remarkable experience-dependent plasticity. Unlike the maternal brain, which undergoes obligatory neurodevelopmental changes during pregnancy and postpartum 52 , the paternal brain's caregiving networks are shaped by involvement and family context 14 . Research on paternal caregiving has shown that fathers who serve as primary caregivers develop amygdala–STS connectivity patterns resembling those of mothers, suggesting substantial neural plasticity in parental brain networks ( 14 . Paternal neural responses, including oxytocin release, amygdala activation, and social brain network engagement, were found to be dynamically modulated by co-parenting quality, maternal functioning (and psychopathologies, including maternal postpartum depression), and family coordination 14,84,85 . Neuroimaging studies show that fathers' amygdala connectivity with temporal-limbic circuits increases proportionally with caregiving time 57 , default mode network activity associated with mentalizing and empathy shows experience-dependent enhancement 14,56 , and co-parenting quality modulates parental brain responses to infant cues 59 and that, overall, responsiveness of the paternal brain to infant cues is shaped by the caregiving context and the family ecology 58 . Our findings extend these single-brain findings to inter-brain coordination and indicate that when child and maternal psychopathology disrupt the typical development of mother-child neural synchrony, fathers' brain engages in complementary neural reorganization that enhances its coupling with the child. This interpretation aligns with behavioral evidence indicating that fathers increase their caregiving involvement when mothers present psychopathology or depression 46,86 , and with findings that link such paternal involvement to the buffering role of the father and show their moderating effects under conditions of family stress 46,87,88 . For instance, reducing the negative impact of maternal depression on child psychopathology by 50% 48,49 . Our findings extend this behavioral literature to the neural level and demonstrate that paternal complementarity is accompanied by measurable reorganization of inter-brain synchrony across the two parent–child subsystems. Notably, a substantial proportion of over 60% of the mothers in the clinical sample also met criteria for anxiety disorders or depressive disorders (Supplementary Analyses S1), raising the possibility that maternal internalizing psychopathology contributes to the attenuation of mother–child synchrony and the compensatory upregulation of father–child neural coupling. This interpretation is further supported by the finding in Supplementary Analyses S1 and S2, in which the families are grouped by maternal diagnosis, rather than child anxiety disorder, and produces an identical crossover pattern, suggesting that it is the family-level stress, irrespective of which member is the identified patient, that drives the reorganization of the parental neural coordination system, as suggested by the family systems' perspective. Brain–Behavior Coupling and Cross-Parental Modulation Prior parent-child hyperscanning studies have shown that caregiving behavior predicts the magnitude of neural synchrony. Maternal behavior affects synchrony both during and beyond the immediate interactions 28–32,38 and sensitive and intrusive behaviors are linked with fronto-temporal coordination 28,38 . Brain-to-brain synchrony mediates the associations between parents' and children's emotion regulation, linking neural coupling to regulatory capacities 35 . These findings position inter-brain synchrony as a neural marker of relationship quality and call to examine whether parenting effects may operate, at least partly, through family-level mechanisms. The fourth hypothesis, which suggested that parental behavior quality predict neural synchrony through cross-parental modulation, was confirmed. Of note, the hierarchical regression analyses demonstrated that the neural mechanism of inter-brain synchrony is sensitive not only to the behavior of the parent currently interacting with the child, but also to the behavior of the co-parent who is absent during the interaction. This strong interaction effect was found for both mother and father, above and beyond the nature of the family ecology. Two observational constructs capturing the positive behavioral quality of parental interaction, Maternal Sensitive Support for mothers and Paternal Exploratory Encouragement for fathers, yielded significant interaction effects for both mother–child and father–child dyads, revealing a consistent compensatory pattern: when the child receives lower-quality caregiving from one parent, the other parent's behavioral quality more strongly predicted neural synchrony with the child. Specifically, Paternal Exploratory Encouragement quality had its strongest effect on father–child synchrony when maternal parenting was low, and maternal parenting quality had its strongest effect on mother–child synchrony when paternal parenting was low. When the co-parent provided high-quality care, the predictive relationship between one parent’s caregiving quality and neural synchrony was attenuated, suggesting that the family system has sufficient regulatory capacity and the incremental benefit of each parent's individual quality diminishes. The interaction between family ecology, indexed by child anxiety, and Paternal Exploratory Encouragement that emerged for father–child interbrain synchrony provides additional evidence for context-sensitive neural coupling. In clinical families, the positive association between Paternal Exploratory Encouragement quality and father–child neural synchrony was amplified, suggesting that paternal behavior becomes a more powerful determinant of neural coordination when the family faces increased regulatory demands. This is consistent with the broader observation that father involvement becomes particularly important for child outcomes under conditions of family stress 46,87,88 . These findings align with previous hyperscanning studies indicating that fathers' self-reported attitudes toward their caregiving role prospectively predict father–child neural synchrony during cooperative problem solving 39 , and that supportive parenting behaviors and higher-quality parent–child relationships are associated with greater inter-brain synchrony across both mothers and fathers 33 . Our findings extend previous work by showing that father–child synchrony is not only sensitive to trait-like paternal characteristics but is dynamically modulated by the amount of stress in the family's ecology, increasing when child anxiety is present. Family-Level Neural Coordination This cross-parental modulation adds a novel dimension to the growing literature on indirect effects in family systems. Research on marital quality and co-parenting has established that the spousal relationship profoundly shapes each parent's interaction with the child 89,90 , and neuroimaging studies have shown that co-parenting quality modulates parental brain responses to infant cues 59 . As early as four months of age, infants are attentive to the relational messages exchanged between their parents, adjusting their own regulatory behavior in response to inter-parental dynamics 91 . The child's brain, therefore, is not only attuned to the immediate process with a single caregiver but is already calibrated to the relational ecology of the broader family system. Our results extend this principle to preschool-age children, suggesting that the brain's sensitivity to the family's regulatory landscape persists well beyond infancy and is reflected in the real-time neural coupling that occurs during parent–child interaction. Our finding that paternal parenting quality predicts mother–child neural synchrony, and vice versa, suggests a neural mechanism through which these indirect family effects may operate, with co-parenting behaviors shaping the neurobiological substrate of each parent–child relationship. Taken together, our findings reveal two distinct but converging pieces of evidence for family-level neural coordination. First, in the context of childhood anxiety, the father can become the primary regulatory agent at the neural level. The family system reorganizes and the father's neural engagement increases to complement the reduction in the mother’s neural coupling. This finding resonates with the broader literature showing that both maternal and paternal depression predict adverse child outcomes 47,86 , and extends work on paternal buffering of maternal depression effects to neural mechanisms of regulation 48,49 . Second, the neural mechanism of inter-brain synchrony is sensitive to the behavior of the co-parent who is absent during the interaction; each parent's caregiving quality shaped, to some extent, the neural synchrony with the other parent. Such complementary modulation extends the biobehavioral synchrony framework, which posits that parent–child synchrony emerges through repeated co-regulatory exchanges and serves as the primary mechanism through which caregivers scaffold children's developing neural networks toward the outside world 15,16,18 . Notably, we also show (Supplementary Analyses 1) that these results are robust to alternative operationalizations of family risk: when the families were grouped by maternal psychopathological diagnosis rather than child anxiety, the same crossover interaction pattern emerged in the beta band (Supplementary Analysis 1; Supplementary Table S1; Supplementary Figure S6), and hierarchical regressions again revealed significant cross-parental modulation of neural synchrony (Supplementary Analysis 2; Supplementary Table S2; Supplementary Figure S7). These converging results strengthen the interpretation that family-level clinical risk, whether indexed by child anxiety diagnosis or maternal psychopathology, is the factor which reorganizes the balance of neural synchrony across parental subsystems. Clinical Implications, Limitations, and Future Directions Our findings have important clinical implications. Current evidence-based interventions for childhood anxiety disorders predominantly target the mother–child relationship 92,93 , reflecting both the historical emphasis on maternal caregiving and the practical challenge of engaging fathers in treatment. Our findings suggest that fathers may serve as an important yet underutilized therapeutic resource. Interventions that strategically leverage the complementarity of the paternal synchrony pathway, or that target the co-parenting relationship to optimize the neural coordination system across both parents, may prove more effective than those addressing either parent in isolation. The brain–behavior coupling results further suggest that improving one parent's caregiving quality may have cascading effects on the other parent's neural synchrony with the child, pointing toward family-level intervention approaches grounded in neuroscience. Several limitations should be acknowledged. First, the cross-sectional design cannot establish causal directionality and it is not possible to ascertain whether the enhanced father–child synchrony in clinical families represents an adaptive compensatory response, a pre-existing difference, or a correlate of different interaction styles remains to be determined through longitudinal research. Second, the sample included only heterosexual two-parent families, and the generalizability to other family configurations, including single-parent families, same-sex parents, and families with non-parental caregivers, requires further investigation. Finally, although power analyses indicated adequate statistical sensitivity for the primary analyses, the trend-level alpha band interaction ( p = .085) suggests that replication in larger samples is warranted to evaluate whether the compensatory reorganization extends across frequency bands. In conclusion, the present study demonstrates that parent–child neural synchrony operates as a family-level coordination system characterized by mechanisms of complementarity between the maternal and paternal pathways. When childhood anxiety disrupts the normative balance, the family system actively reorganizes, and fathers assume an enhanced neural regulatory role that complements the attenuated mother–child coupling. Such complementarity is not merely reactive to the immediate interaction context but is sensitive to the broader caregiving familial dynamics, including the behavior of the co-parent who is not present during the interaction. These findings extend the biobehavioral synchrony framework from a dyadic to whole-family level analysis and provide neural evidence that human parenting operates as an integrated system where the contributions of each parent are continuously calibrated to the needs of the child and the coparental dynamics. 4. Methods The project has been pre-registered: https://osf.io/fzxs4/files/92spu 4.1. Participants and Study Design The study included a total of 83 two-parent family triads stratified into two groups: 53 families with children aged 3–7 years diagnosed with an anxiety disorder and 30 families with typically developing children of the same age range. After applying EEG quality criteria, the final analytic sample comprised 77 families (49 clinical, 28 control). The mean age of the mothers was 39.05 years (SD = 4.16) in the control group and 39.87 years (SD = 4.20) in the clinical group (total: M = 39.50, SD = 4.15). For the fathers, mean age was 42.16 years (SD = 4.55) in the control group and 41.14 years (SD = 3.73) in the clinical group. Among children in the final analytic sample, mean age was 5.52 years (SD = 1.20) in the control group and 5.41 years (SD = 1.14) in the clinical group (total: M = 5.45, SD = 1.16; range: 3.0–7.6 years), with no significant group difference ( t (72) = 0.40, P = .689; age data available for 74 of 77 children). Across the sample, 53.2% were boys ( n = 41) and 46.8% were girls ( n = 36); sex distributions were comparable across groups (control: 64.3% boys; clinical: 46.9% boys; χ²(1) = 1.51, P = .219). All participating families consisted of children living with two heterosexual parents in the same household, with all family members fluent in the local language. Children in the anxiety group met DSM-5 criteria for an anxiety disorder as confirmed through comprehensive clinical assessment, with anxiety symptoms of sufficient severity to warrant therapeutic intervention and no concurrent participation in other psychological treatments. Control group children were screened to ensure absence of clinically significant behavioural or emotional difficulties, no history of psychiatric diagnosis, and no current psychological interventions. Exclusion criteria for all participants included neurological disorders or head injuries in any family member, uncorrected vision or hearing impairments, and inability to tolerate EEG equipment. Anxiety group participants were recruited through clinical referral sources, with all children undergoing comprehensive psychological assessment including structured clinical interviews and standardized questionnaires administered by licensed clinicians. Control group families were recruited through community sources and screened via detailed intake interviews with parents to confirm absence of psychological concerns and ensure demographic matching with the anxiety group. The study was approved by the institutional ethics committee and all participants provided written informed consent (parents) and age-appropriate assent (children). Of the total 83 family triads that were enrolled, the data of 6 families were excluded due to EEG signal quality, yielding a total of 77 families (49 clinical, 28 control). Within these families, mother–child EEG data were unavailable for three dyads (in which the mother did not participate in the EEG recording), and father–child data were unavailable for two dyads (in which the fathers were not present or did not participate in the recording), resulting in 74 and 75 usable mother–child and father–child dyads, respectively. 4.2. Experimental Design and Procedure Laboratory sessions were scheduled during afternoon hours (14:00–16:00) to optimize child cooperation and minimize fatigue effects, conducted in a standardized laboratory environment equipped with synchronized four-camera recording systems. Upon arrival, families completed informed consent procedures while children acclimated to the laboratory environment for approximately 45 minutes. The preparation phase included detailed protocol explanation and systematic EEG cap application following a standardized protocol, beginning with parents to model the procedure for children, followed by child cap placement only after demonstrated comfort with the environment. Electrode impedances were verified and adjusted to maintain signal quality throughout the session. Following successful EEG preparation, experimenters exited the observation room to minimize interference with naturalistic family interactions. The experimental session comprised several sequential phases designed to assess neural synchrony across different interaction contexts (Figure 1). Phase 1 began with a 3-minute free-play interaction between the child and the same parent, during which the parent received standardized instructions to engage in naturalistic play using a pre-selected set of age-appropriate toys placed on a designated table. Phase 2 involved parents switching, with the first parent exiting to the waiting area and the second parent entering to engage in a sequential free-play interaction with the child. The order of parent participation was counterbalanced across families to control for potential order effects. EEG data were continuously recorded throughout all phases, with behavioral interactions simultaneously captured via the four-camera system with synchronized timestamps. Real-time monitoring of EEG signal quality ensured data integrity, with sessions discontinued and rescheduled if signal quality could not be maintained or if child distress occurred. 4.3. EEG Data Acquisition Simultaneous EEG recording was conducted using three Acticap helmets, each equipped with 32 active electrodes arranged according to the international 10/20 system and integrated chin stabilization to minimize movement artifacts. Within the scope of the study, only two interactors were present at any given interaction. Signal acquisition parameters included analog bandpass filtering between 0.1 and 500 Hz with continuous sampling at 1000 Hz. Electrode impedances were maintained below 10 kΩ throughout recording sessions, with the common ground electrode positioned at AFz. To ensure temporal precision essential for cross-brain measurements, the two EEG caps used in each interaction were connected to a single amplifier unit, enabling millisecond-level synchronization accuracy between participant recordings. 4.4. Data Preprocessing EEG data preprocessing was conducted using Python 3.8 with the MNE software package (v0.17.0). Initial preprocessing involved separation of dual-participant data files to two separate files to enable individual artifact detection and signal optimization. All EEG recordings underwent digital bandpass filtering between 1 and 50 Hz using finite impulse response filter to eliminate low-frequency drift and high-frequency noise while preserving neural oscillations of interest. Data were segmented into 1000 ms epochs with 500 ms sliding windows to maximize data utilization while maintaining temporal resolution for connectivity analyses. Artifact removal proceeded in two sequential stages: first, an unsupervised Bayesian optimization algorithm (AutoReject) eliminated trials containing transient jumps in isolated channels and artifacts affecting channel groups; second, Independent Component Analysis (ICA) using MNE’s implementations of FastICA and CORRMAP 94 removed systematic physiological artifacts. ICA-based artifact removal targeted ocular artifacts, muscular activity components and non-physiological artifacts. Independent components corresponding to these artifact sources were manually identified by trained analysts and served as templates for automated detection and removal of similar components across all participants, ensuring consistent artifact removal criteria throughout the dataset. 4.5. Inter-Brain Synchrony Quantification Inter-brain neural synchrony was quantified using the weighted Phase Lag Index (wPLI; 95 ), a measure that indexes the consistency of phase relationships between neural oscillations while minimizing the influence of volume conduction and shared environmental noise through a weighting scheme that attenuates phase differences near zero. wPLI has been shown to outperform traditional coherence-based measures in naturalistic recording conditions 95,96 and has been validated extensively for hyperscanning applications across different samples and developmental stages 28–32,37,38,97,98 . Analysis focused on two rhythms of interest: the alpha rhythm (8–12 Hz) and beta rhythm (13–30 Hz). Our focus on alpha and beta frequency bands was motivated by converging evidence: in mother-child and adult-child dyads, inter-brain synchrony is often observed in the alpha band, linked to empathy, shared attention and joint engagement 32,65,75,99 . Beta rhythms were additionally evaluated based on evidence of beta-band activation in mother–child dyads with older children 30–32,37,38 and the arousal characteristics of father–child interactions 9 . Analytic signal computation employed finite impulse response (FIR) filtering with Hamming window application to minimize spectral leakage and edge artifacts, followed by Hilbert transform to extract instantaneous phase information. Spatial analysis was restricted to theoretically motivated regions of interest based on established literature regarding social cognition and interpersonal neural coupling. The analysis incorporated four bilateral ROIs encompassing frontal regions (Fp1, F3, F7 for the left hemisphere; Fp2, F4, F8 for the right hemisphere), associated with executive control and social cognition 100–103 , and temporo-parietal regions (P7, T7, P3 for left hemisphere; P8, T8, P4 for right hemisphere), implicated in theory of mind, attention, and sensorimotor integration 104,105 . The wPLI for each inter-brain link was calculated as the mean connectivity of each of the 3 electrodes in one target ROI with each of the 3 electrodes in the second target ROI, resulting in 9 connectivity values averaged for each ROI combination into one inter-brain link. Inter-brain connectivity was examined across all possible ROI pairings between the two interactors’ neural networks, including ipsilateral and contralateral connections across frontal and temporo-parietal regions. Individual wPLI values were computed for each inter-brain link, followed by network-level aggregation through averaging of all linkages to generate a composite whole-network inter-brain synchrony measure in the fronto-temporo-parietal network. 4.6. Surrogate Data Generation To validate the specificity of neural synchrony during real parent–child interactions, surrogate data were generated by computing wPLI values between one member of a dyad and the second member from a different dyad within the same sample. This process was repeated for all possible cross-dyad combinations. A stringent quality control criterion required surrogate dyads to share at least 50% clean epochs from the entire interaction period, with dyads did not meet the minimum epoch-sharing threshold removed from analyses. For each original dyad, surrogate values were averaged across all valid permutations to create a single representative surrogate value matched to the real connectivity value of the dyad. 4.7. Behavioral Coding Parent–child interactions were coded using the Coding Interactive Behavior system (CIB; 60 ), a well-validated global rating system for social interactions across the lifespan with over 300 published applications across diverse populations and contexts 18,67 and has been successfully implemented in hyperscanning research 28–32,38,97,98,106 . The CIB employs 52 codes rated on 5-point scales that were averaged into theoretically-based constructs. This study utilized the Maternal Sensitive Support and Paternal Exploratory Encouragement constructs, adapted for each sample’s relational context. Based on the theoretical framework of Feldman 9 , maternal and paternal behaviors differ in arousal, regulation and intensity, with mother–child interaction framed as “rhythms of safety”, versus the father’s more engaging and stimulating “rhythms of exploration”. In accordance with this framework, the Maternal Sensitive Support construct comprised the following codes: mother positive affect, maternal lead, vocal appropriateness, and elaboration. The Paternal Exploratory Encouragement construct, in line, included positive social exploration of environment and father’s adaptability (reverse coded from over-consistency), as well as the reverse codes of constriction, tension, over-regulation, and structure limit. Both constructs were coded such that higher scores reflected more positive parental behaviors, in line with the theoretical literature. Coding was performed by trained raters blind to study hypotheses. Inter-rater reliability was established on 20% of interactions, with all codes achieving >90% agreement (mean ICC = 0.93, range = 0.89–0.99). 4.8. Statistical Analysis Analysis proceeded in three stages. In the first stage, inter-brain synchrony was validated by comparing real versus surrogate wPLI values. Shapiro-Wilk tests indicated significant deviations from normality for difference scores across all comparisons (all P < 0.03), justifying the use of Wilcoxon signed-rank tests with rank-biserial correlations ( r rb ) as effect sizes, applying False Discovery Rate (FDR) correction across four comparisons (two parents × two frequency bands). In the second stage, differential synchrony patterns were examined using 2×2 mixed ANOVAs on Δ synchrony scores (real minus surrogate) with Parent (mother–child, father–child) as a within-subjects factor and Child Anxiety (clinical, control) as a between-subjects factor, separately for alpha and beta bands. Partial eta-squared (η²p) effect sizes are reported with 90% confidence intervals, consistent with the convention for ANOVA effect sizes. The significant beta interaction was decomposed through: (a) an independent-samples comparison of the mother-minus-father difference score between groups (Welch’s t-test with 95% CI for Cohen’s d derived from the non-central t-distribution, justified by Shapiro-Wilk confirmation of normality in both groups, P > .13), and (b) within-sample paired Wilcoxon signed-rank tests comparing mother–child versus father–child synchrony (FDR-corrected). Prior to analysis, univariate outliers were identified separately for each parent–child dyad type (mother–child, father–child) and sample (control, clinical) on the beta Δ synchrony scores, and the same exclusions were applied uniformly across both frequency bands. This dyad-level approach was adopted on the grounds that extreme synchrony values likely reflect session-level characteristics — such as atypical interaction dynamics or residual signal artifacts — that are not specific to a single frequency band; applying consistent exclusions also ensures a comparable analytic sample across the alpha and beta analyses reported in Table 1. Participants with values exceeding 2.5 standard deviations above the group mean were excluded from the relevant dyad-specific analyses (3 families from mother–child analyses, 2 from father–child analyses), resulting in analytic samples of N = 71 for mother–child and N = 73 for father–child comparisons, with N = 68 families providing complete data for both dyads. A supplementary sensitivity analysis retaining the full sample without any exclusions confirmed that the beta-band interaction remained significant and that the same crossover direction greater mother–child synchrony in control families and greater father–child synchrony in clinical families was preserved in the alpha band (Supplementary Sensitivity Analysis, Tables S-SA1–S-SA2, Figures S-SA1–S-SA3). This analysis was evaluated again as an omnibus 2×2×2 mixed ANOVA incorporating both the validation (real vs. surrogate) and differential balance including parent (mother-child, father-child) and sample (clinical, control) components (Supplementary Analysis 3; Supplementary Table S3; Supplementary Figure S8). This analysis yielded a highly significant three-way Parent × Data Type × Child Anxiety interaction for beta synchrony, confirming that the crossover pattern of our results reflects genuine differential neural coupling rather than non-specific group differences. Finally, in the third stage of analysis, hierarchical regression models examined brain–behavior coupling, predicting parent–child beta Δ synchrony from Child Anxiety (Step 1), Maternal and paternal parenting quality (Step 2), and all two-way interactions (Step 3). Analyses were conducted using Python 3.8 (scipy v1.7, 107 ; statsmodels v0.13, 108 and JASP v0.18 (JASP Team, 2024). 4.9. Power Analysis Post-hoc power analyses were conducted to evaluate the statistical sensitivity of the study given the final analytic sample. For the primary analysis, in which the Parent × Child Anxiety interaction on beta Δ synchrony (F(1,66) = 12.68, η² p = 0.161), observed power exceeded 0.93, well above the conventional 0.8 threshold. A sensitivity analysis indicated that the study was powered at 80% to detect interaction effects as small as η² p = 0.108 (F ≥ 8.08) for the 2×2 mixed ANOVA design. The between-group comparison of the Δ mother-child minus father-child neural synchrony balance score ( d = 0.81) yielded power of 0.87 with the observed sample sizes ( n = 25 control, n = 43 clinical). For the within-sample Wilcoxon signed-rank tests comparing mother–child versus father–child beta synchrony (r_rb = 0.53 and −0.49 for control and clinical samples, respectively), post-hoc power was computed using the equivalent paired effect sizes (d_z = 0.43 and 0.45), as standard power analysis frameworks require parametric effect size input. This yielded power of 0.53 for the control comparison ( n = 25) and 0.82 for the clinical comparison ( n = 43). Although power for the smaller control subsample was moderate, both tests achieved statistical significance, and these decomposition tests serve to characterize a significant omnibus interaction rather than standing as independent primary hypotheses. All four validation analyses (real vs. surrogate) achieved power exceeding 0.999, reflecting large effect sizes ( r rb = 0.85–1.00). For the hierarchical regression models, the full models predicting mother–child synchrony (R² = 0.306, f² = 0.44) and father–child synchrony (R² = 0.353, f² = 0.55) yielded power of 0.97 and 0.99, respectively ( N = 65, 6 predictors). The Step 3 interaction increments (ΔR² = 0.152 and 0.143, f²change = 0.22) both achieved power of 0.84. Collectively, these analyses confirm that the study was adequately powered for the primary and secondary analyses, with the exception of the alpha interaction trend (F = 3.06, power = 0.41), which has been interpreted cautiously and warrants replication in larger samples. A supplementary sensitivity analysis confirmed that all key findings were robust when retaining the full sample without outlier exclusions (see Supplementary Sensitivity Analysis). Declarations Data Availability The data generated in this study cannot be made publicly available due to participant privacy protections under our ethical approval (IRB) protocol. Requests for access to anonymized, aggregated data may be directed to the corresponding author and will be evaluated on a case-by-case basis. Data sharing requests must include: (1) a research proposal outlining intended use, (2) confirmation of institutional ethics approval, and (3) a data use agreement. Requests will be fulfilled within 30 days where feasible and compliant with privacy regulations. Code Availability All analysis code is publicly available at https://github.com/Yoavshapira1/FelmanLabEEGpipeline. The repository includes preprocessing scripts, neural synchrony analysis pipelines, statistical analysis code, and visualization functions. Acknowledgements The study was supported by the Simms/Mann Foundation Chair to Ruth Feldman and by the Bezos Family Foundation. The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript. Author Contributions Conceptualization: L.S. and R.F.; methodology: L.S. and R.F.; investigation and data curation: L.S., C.S., O.S-R., Y.A.; formal analysis: L.S., C.S., O.H., I.P.; writing: L.S. and R.F.; writing – review and editing: R.F., C.S., O.H., O.S-R, Y.A. Competing Interests The authors declare no competing interests. Resource Availability Any requests for further information and resources that would not compromise the participants’ privacy should be directed to and will be fulfilled by the corresponding author. Declaration of Generative AI and AI-Assisted Technologies During the preparation of this work we employed AI tools only to improve the language and readability of the paper. After using this tool, humans reviewed and edited the content as needed, and take full responsibility for the content of the publication. 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Neuroscience & Biobehavioral Reviews, 157, 105523. Additional Declarations There is NO Competing Interest. Supplementary Files SupplementaryMaterialsNC.docx Supplementary Materials Cite Share Download PDF Status: Under Review Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-9335839","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Article","associatedPublications":[],"authors":[{"id":619919298,"identity":"81f19ecf-ba12-41fd-8b8b-6479c6f34327","order_by":0,"name":"Ruth Feldman","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA6ElEQVRIie3PsQrCMBCA4QsHyRKdIxV9BhEUUfFZStcWX8ChUoiLOuvkWzhbCj6DGBcRnOsiIiJqqTrZ4CaYf7jccN8QAJPpB2M++iLdKcSPyTSEL8iTICWTB8FvCPLk1RHW769XvQ3UJ93lrnWel/MIJD64GYSHQdNd7qG4cljVG6uKRMDCdP6ZdIQtLZdGIIRDLW+oyJ1QzGUQXt7eyTUljaHq6Ikg0vJkSuCkbD3hdtD0xhEXfFcrjHzlSCRB5l84i0LlHqOSYPZenC6qPRsEYXzIIC+aTCKT6evv312+OTaZTKZ/6QZY2kivUdRmiQAAAABJRU5ErkJggg==","orcid":"https://orcid.org/0000-0001-5048-1381","institution":"Reichman University","correspondingAuthor":true,"prefix":"","firstName":"Ruth","middleName":"","lastName":"Feldman","suffix":""},{"id":619919299,"identity":"90d8298f-4f50-4387-8ba5-48244cd60fbb","order_by":1,"name":"Linoy Schwartz","email":"","orcid":"https://orcid.org/0000-0002-7628-6960","institution":"Reichman University","correspondingAuthor":false,"prefix":"","firstName":"Linoy","middleName":"","lastName":"Schwartz","suffix":""},{"id":619919300,"identity":"d049f46d-5833-4e5c-97f9-34a1cc35403f","order_by":2,"name":"Carmel Shilo","email":"","orcid":"","institution":"Reichman University","correspondingAuthor":false,"prefix":"","firstName":"Carmel","middleName":"","lastName":"Shilo","suffix":""},{"id":619919301,"identity":"61c14e37-abf7-4d59-aa66-9ab58a21dfd5","order_by":3,"name":"Olga Hayut","email":"","orcid":"","institution":"Reichman University","correspondingAuthor":false,"prefix":"","firstName":"Olga","middleName":"","lastName":"Hayut","suffix":""},{"id":619919302,"identity":"668a9a5b-2bd5-4c83-acf1-48357f907793","order_by":4,"name":"Yael Apter","email":"","orcid":"","institution":"Reichman University","correspondingAuthor":false,"prefix":"","firstName":"Yael","middleName":"","lastName":"Apter","suffix":""},{"id":619919303,"identity":"7a157749-6f41-4f05-a7b1-474e36e3f793","order_by":5,"name":"Ortal Shimon-Raz","email":"","orcid":"https://orcid.org/0000-0002-6464-8370","institution":"Icahn School of Medicine at Mount Sinai","correspondingAuthor":false,"prefix":"","firstName":"Ortal","middleName":"","lastName":"Shimon-Raz","suffix":""},{"id":619919304,"identity":"b6e7cac7-0233-4cb0-8a62-dcfb917f3581","order_by":6,"name":"Itai Peleg","email":"","orcid":"","institution":"Reichman University","correspondingAuthor":false,"prefix":"","firstName":"Itai","middleName":"","lastName":"Peleg","suffix":""}],"badges":[],"createdAt":"2026-04-06 16:26:05","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-9335839/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-9335839/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":108097592,"identity":"e11d33e2-acb6-48f7-9733-1b9dde68cc1c","added_by":"auto","created_at":"2026-04-29 10:15:00","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":8035173,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cem\u003e\u003cstrong\u003eStudy paradigm.\u003c/strong\u003e\u003c/em\u003e\u003cem\u003e \u003c/em\u003e\u003cem\u003e\u003cstrong\u003e(A)\u003c/strong\u003e\u003c/em\u003e\u003cem\u003e Experimental design. Seventy-seven family triads (28 control, 49 clinical; children aged 3–7 years with anxiety disorders) participated in two separate hyperscanning EEG sessions: a mother–child and a father–child free-play interaction (3 minutes each, counterbalanced order), with simultaneous dual-cap recording. Inter-brain synchrony was quantified using the weighted Phase Lag Index (wPLI) in the alpha (8–12 Hz) and beta (13–30 Hz) frequency bands. Parental quality interaction was coded using the Coding Interactive Behavior system. \u003c/em\u003e\u003cem\u003e\u003cstrong\u003e(B)\u003c/strong\u003e\u003c/em\u003e\u003cem\u003e Illustration of the parent–child free-play paradigm, depicting mother–child (left) and father–child (right) interactions with age-appropriate toys during simultaneous EEG hyperscanning. \u003c/em\u003e\u003cem\u003e\u003cstrong\u003e(C)\u003c/strong\u003e\u003c/em\u003e\u003cem\u003e Schematic representation of the inter-brain network. Fronto-temporal regions of interest were used to compute inter-brain connectivity across all ipsilateral and contralateral ROI pairings between parent and child, yielding a composite whole-network synchrony measure.\u003c/em\u003e\u003c/p\u003e","description":"","filename":"Figure1.png","url":"https://assets-eu.researchsquare.com/files/rs-9335839/v1/932c877e696f5b82fa09a040.png"},{"id":108182218,"identity":"60803f95-3f5a-4ba5-b220-9842d2cd6500","added_by":"auto","created_at":"2026-04-30 08:59:15","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":708854,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cem\u003e\u003cstrong\u003eValidation of inter-brain synchrony. (A)\u003c/strong\u003e\u003c/em\u003e\u003cem\u003e Alpha band real vs. surrogate synchrony by parent. \u003c/em\u003e\u003cem\u003e\u003cstrong\u003e(B)\u003c/strong\u003e\u003c/em\u003e\u003cem\u003e Beta band real vs. surrogate synchrony by parent. \u003c/em\u003e\u003cem\u003e\u003cstrong\u003e(C)\u003c/strong\u003e\u003c/em\u003e\u003cem\u003e Beta Δ synchrony (real – surrogate) showing the crossover double dissociation: in control families, mothers show higher synchrony than fathers (p\u003c/em\u003e\u003csub\u003e\u003cem\u003e(FDR)\u003c/em\u003e\u003c/sub\u003e\u003cem\u003e) = .019); in clinical families, fathers show higher synchrony than mothers (p\u003c/em\u003e\u003csub\u003e\u003cem\u003e(FDR)\u003c/em\u003e\u003c/sub\u003e\u003csub\u003e \u003c/sub\u003e\u003cem\u003e= .008). Significance brackets denote within-sample Wilcoxon signed-rank tests, FDR-corrected. \u003c/em\u003e\u003cem\u003e\u003cstrong\u003e(D)\u003c/strong\u003e\u003c/em\u003e\u003cem\u003e Interaction plot illustrating the crossover. Diamonds = means ± 95% CI; individual points = participants.\u003c/em\u003e\u003c/p\u003e","description":"","filename":"Figure2.png","url":"https://assets-eu.researchsquare.com/files/rs-9335839/v1/1415cef0f3a8e8fa20d09943.png"},{"id":108181790,"identity":"95ab56fa-dde2-4ba1-bd5b-8cb08461f24a","added_by":"auto","created_at":"2026-04-30 08:58:55","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":530472,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cem\u003e\u003cstrong\u003eBrain–behavior coupling in family neural synchrony. (A) \u003c/strong\u003e\u003c/em\u003e\u003cem\u003eMother–child and \u003c/em\u003e\u003cem\u003e\u003cstrong\u003e(B)\u003c/strong\u003e\u003c/em\u003e\u003cem\u003e father–child beta Δ synchrony (real minus surrogate wPLI) by Child Anxiety group (N = 65; n = 24 control, n= 41 clinical). Violins show the full distribution; individual data points are jittered. Diamonds = mean ± 95% CI \u003c/em\u003e\u003cem\u003e\u003cstrong\u003e(C) \u003c/strong\u003e\u003c/em\u003e\u003cem\u003eInteraction between maternal and paternal parenting quality predicting mother–child beta Δ synchrony; simple slopes plotted at ±1 SD of paternal parenting. Blue shades: light = low paternal (−1 SD), dark = high paternal (+1 SD).\u003c/em\u003e\u003cem\u003e\u003cstrong\u003e (D) \u003c/strong\u003e\u003c/em\u003e\u003cem\u003eInteraction between maternal and paternal parenting quality predicting father–child beta Δ synchrony; simple slopes plotted at ±1 SD of maternal parenting. Red/coral shades: light = low maternal (−1 SD), dark = high maternal (+1 SD), *P \u0026lt; .05, **P \u0026lt; .01.\u003c/em\u003e\u003c/p\u003e","description":"","filename":"Figure3.png","url":"https://assets-eu.researchsquare.com/files/rs-9335839/v1/63984dba3aa8596c1c7bce06.png"},{"id":108183848,"identity":"946faffa-f4ee-43de-a9d9-572be3f5a507","added_by":"auto","created_at":"2026-04-30 09:02:58","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":10545612,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-9335839/v1/83afc99c-f4bc-4076-8508-c9f7da234853.pdf"},{"id":108097595,"identity":"7ec12392-7f7f-46da-b652-f9e167c051ec","added_by":"auto","created_at":"2026-04-29 10:15:01","extension":"docx","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":4835188,"visible":true,"origin":"","legend":"Supplementary Materials","description":"","filename":"SupplementaryMaterialsNC.docx","url":"https://assets-eu.researchsquare.com/files/rs-9335839/v1/67dffe2eecbde99c04becaf6.docx"}],"financialInterests":"There is \u003cb\u003eNO\u003c/b\u003e Competing Interest.","formattedTitle":"Two-brain perspective on family dynamics; Complementarity in mother-child and father-child interbrain synchrony","fulltext":[{"header":"1. Introduction","content":"\u003cp\u003eThroughout mammalian evolution, the care of infants has been, in the main, a maternal enterprise. Of approximately 5,400 mammalian species, only about 5% exhibit biparental care where fathers contribute substantively to the rearing of offspring beyond conception\u003csup\u003e1,2\u003c/sup\u003e. This leads to a fundamental asymmetry, where maternal care is obligate and phylogenetically ancient, shaped by hormonal cascade resulting from pregnancy, parturition, and lactation, while paternal care is facultative, emerging only under specific ecological and social conditions that favor male parental caregiving \u003csup\u003e3,4\u003c/sup\u003e. When paternal investment does occur, it invariably operates within the context of maternal care and family units, creating a system in which paternal behavior complements maternal caregiving and is sensitive to maternal provisions, offspring needs, and the ecological challenges of the family \u003csup\u003e5,6\u003c/sup\u003e.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eHuman Fatherhood as Complementary Coordination\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eHumans represent a remarkable exception among primates in the extent of their paternal investment. The evolution of cooperative breeding, prolonged offspring dependency, and complex social structures and norms created selective pressures for paternal engagement in childrearing \u003csup\u003e6,7\u003c/sup\u003e. Unlike most mammals, contemporary human fathers routinely provide direct care, protection, provisioning, and social learning opportunities \u003csup\u003e8\u003c/sup\u003e that complement maternal contributions and are sensitive to ecological conditions \u003csup\u003e9–11\u003c/sup\u003e. Such facultative fathering carries profound implications for family organization, when the family system reorganizes into a dynamic balance where each parent’s neural and behavioral engagement is sensitive to that of the partner's. The father's brain is especially sensitive to maternal contributions and caregiving \u003csup\u003e12–14\u003c/sup\u003e. We term these mutual influences ‘complementary coordination system’, representing how the quality of one parent’s caregiving influences the expression of the other's parenting while both continuously recalibrate to the family's needs and contextual demands.\u003c/p\u003e\n\u003cp\u003eThe \u003cem\u003ebiobehavioral synchrony\u003c/em\u003e model provides a framework for understanding how the coordinated social behaviors of caregivers and children create enduring neural templates for social response \u003csup\u003e15,16\u003c/sup\u003e. From birth, parent–infant dyads coordinate their gaze, vocalizations, affect, and autonomic arousal to establish multi-level coordination spanning behavioral, physiological, and endocrine systems, forming the basis for later affiliative bonds \u003csup\u003e17,18\u003c/sup\u003e. Through iterative cycles of contingent exchanges, early synchrony scaffolds the infant’s emerging neural and behavioral architecture for social participation and predicts long‑term outcomes in terms of self‑regulation, symbol use, empathy, and social competencies across childhood, adolescence, and up until adulthood \u003csup\u003e19–23\u003c/sup\u003e.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eInter-Brain Synchrony with Mother and Father\u0026nbsp;\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAmong the consistent findings to emerge from the \u003cem\u003ebiobehavioral synchrony\u003c/em\u003e framework is that mothers and fathers tend to engage in different types of affective coordination \u003csup\u003e9\u003c/sup\u003e. Mother–infant interactions are characterized by low-to-medium arousal and gentle rhythmic coordination reflecting what we term as the ‘rhythms of safety’, which promotes emotional comfort, social skills, and secure base \u003csup\u003e24\u003c/sup\u003e. Father–infant interactions, by contrast, involve high-arousal play, social exploration, involving sudden bursts of emotional intensity, creating what we refer to as the ‘rhythms of exploration’ that support mastery in the outside world, curiosity, and self-regulation \u003csup\u003e9,25–27\u003c/sup\u003e.\u003c/p\u003e\n\u003cp\u003eRecent advances in hyperscanning, the simultaneous recording of neural activity from two or more individuals, have made it possible to examine whether these distinct behavioral styles are mirrored in inter-brain coupling during naturalistic interactions. A growing body of work has demonstrated robust mother–child neural synchrony, particularly in frontal, temporal, and parietal regions implicated in social cognition, joint attention, and emotion regulation \u003csup\u003e28–37\u003c/sup\u003e. Individual differences in maternal caregiving quality have been shown to predict the magnitude of their neural synchrony: higher sensitivity correlates with enhanced frontotemporal coupling, while intrusive behavior is associated with diminished neural coordination \u003csup\u003e28\u003c/sup\u003e. Notably, maternal sensitivity and intrusiveness in infancy were found to predict the degree of mother–child frontotemporal neural synchrony more than a decade later, suggesting that early caregiving shapes the long-term architecture of interpersonal neural coordination \u003csup\u003e38\u003c/sup\u003e.\u003c/p\u003e\n\u003cp\u003eVery few studies to date explored father–child interbrain synchrony, but the existing research similarly shows that it recruits prefrontal and temporo-parietal circuits. During cooperative problem solving, father–child dyads exhibited increased synchrony in the dorsolateral prefrontal cortex and in temporo-parietal regions relative to individual task performance \u003csup\u003e39\u003c/sup\u003e. Moreover, variations in frontal and fronto-temporal coupling were associated with fathers' role attitudes and self-reported engagement quality, linking neural alignment to paternal involvement \u003csup\u003e39\u003c/sup\u003e. Father–child prefrontal synchrony was also confirmed during co-viewing of emotionally arousing stimuli \u003csup\u003e40\u003c/sup\u003e. When comparing mother–child and father–child neural synchrony during shared co-viewing of videos and free-play, in dyads that were not part of the same family, revealed that mothers exhibited greater frontal cortex synchrony with their children than fathers during passive co-viewing. Mothers also showed greater left frontal neural synchrony during free-play, correlating with child involvement, while fathers exhibited stronger right frontal synchrony linked to child-initiated behaviors and play agency \u003csup\u003e41\u003c/sup\u003e. A separate fNIRS study found that interbrain synchrony in the left temporo-parietal junction was associated with parental warmth, autonomy support, and shared positive affect, though only in mother–child, but not father–child dyads \u003csup\u003e33\u003c/sup\u003e. Critically, however, these studies drew mother–child and father–child dyads from different families, which precluded direct within-family comparisons of how the two parent–child subsystems jointly organize and whether the neural synchrony between one parent and the child depends in some way on the synchrony formed with the other parent. Still, these findings implicate the fronto-temporal network as a shared substrate of parent–child neural coordination and suggest that paternal engagement modulates interbrain prefrontal and temporo-parietal alignment, though its behavioral correlates may differ from those of mothers.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eFamily Systems and Complementary Processes between Mothering and Fathering in High- and Low-Stress Ecologies\u0026nbsp;\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eFamily systems facing stress can provide a critical window into processes of complementarity between parents and how they are impacted by alterations in family functioning. Evidence indicates that in families with a child diagnosed with anxiety disorder, family life is marked by elevated stress, problems in family functioning, and disrupted regulation, including outbursts, overcontrolling, and less warm parenting \u003csup\u003e42,43\u003c/sup\u003e. Maternal psychopathology, particularly anxiety, frequently co‑occurs with child anxiety and studies of clinical samples consistently show that substantial proportions of mothers whose children meet criteria for an anxiety disorder are themselves diagnosed with an anxiety disorder or suffer elevated anxiety symptoms \u003csup\u003e44,45\u003c/sup\u003e. This creates bidirectional amplification of distress within the family system. Under such conditions, the balance of mother-child and father-child behavioral and neural synchrony may fundamentally reorganize to compensate for these alterations and allow children a better chance at adaptation and mental health.\u003c/p\u003e\n\u003cp\u003eEvidence from families in which mothers suffer depression supports this hypothesis. Greater father involvement and more sensitive and engaged paternal behavior attenuate the effects of maternal depression on child social-emotional outcomes, increasing positivity and harmony during observed family interactions and reducing child externalizing and internalizing problems as compared to families comprised of depressed mothers and uninvolved fathers \u003csup\u003e46–49\u003c/sup\u003e. These findings suggest that family systems may be underpinned by compensatory inter-parental mechanisms: when one parent’s capacity for optimal caregiving is compromised, the other parent intensifies his or her engagement to partly buffer the effects on the child. In the current study, we explore, for the first time, the existence of complementary processes in the parents' neural coordination with their children.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eStress and Family Ecology Impact Neural Synchrony and the Parental Brain\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eHyperscanning studies have only begun to link parental psychopathology and stress to alterations in parent–child inter-brain synchrony. Parenting stress has been found to correlate with reduced mother–child prefrontal synchrony during joint activities in early childhood \u003csup\u003e50\u003c/sup\u003e, and a systematic review of the hyperscanning literature confirmed that anxiety, stress, or depressive symptoms in at least one interacting partner are broadly associated with diminished interpersonal neural coupling \u003csup\u003e51\u003c/sup\u003e. In contrast, sensitive and supportive parenting and better parent–child relationship quality are related to greater neural synchrony \u003csup\u003e28,30–33,38,41\u003c/sup\u003e. This suggests that anxious or depressed parenting may disrupt neural attunement, while warm, responsive caregiving enhances it.\u003c/p\u003e\n\u003cp\u003eThe paternal brain exhibits remarkable adaptability to the family context. Unlike the maternal brain, which undergoes substantial structural and functional reorganization during pregnancy and the postpartum period \u003csup\u003e52,53\u003c/sup\u003e, the paternal brain exhibits experience-dependent plasticity that is especially sensitive to caregiving involvement and family circumstances \u003csup\u003e14,54,55\u003c/sup\u003e. Neuroimaging studies show that fathers' amygdala connectivity with superior temporal sulcus circuits scales with caregiving involvement, with primary-caregiving fathers developing amygdala activation patterns resembling those of mothers \u003csup\u003e14\u003c/sup\u003e. Compared to non-fathers, fathers show enhanced activation in mentalizing and reward-related regions when viewing child stimuli, and testosterone is negatively correlated with these responses \u003csup\u003e56\u003c/sup\u003e. Paternal prefrontal and caudate responses to own-infant cues are further linked to parental sensitivity \u003csup\u003e57\u003c/sup\u003e, the paternal brain's responsiveness to infant cues is shaped by caregiving context and family circumstances (for review, see \u003csup\u003e58\u003c/sup\u003e), and corticostriatal connectivity in parents' brains when viewing coparental stimuli predicts collaborative coparenting and child well-being \u003csup\u003e59\u003c/sup\u003e. Such sensitivity to context suggests that paternal neural engagement, including interbrain synchrony between fathers and children, may be particularly responsive to family needs, maternal functioning, and child developmental challenges.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eThe Current Study\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eDespite the aforementioned theoretical foundation and research evidence on inter-parental complementarity, mother–child and father–child neural coupling have not yet been systematically compared within the same family dynamic, with prior studies on parent-child interbrain synchrony examining children with either mother or father, not with both. Direct observation on processes of interbrain synchrony between the child and each parent can shed light on how families reorganize to various ecological demands and how one parent's neural attunement complements that of the other's. This gap is critical. If parent–child neural synchrony reflects family-level adaptations, the child's neural engagement with one parent cannot be fully understood without the other parent. The present study provides this assessment of interbrain synchrony within families during naturalistic parent–child play. We investigated how mother–child and father–child neural coordination patterns emerge, interact, and complement one another, and how these family-level dynamics vary between families living in high-stress contexts with a child diagnosed with an anxiety disorder, as compared to typically developing children.\u003c/p\u003e\n\u003cp\u003eOur pre-registered investigation addressed five main hypotheses consistent with the \u003cem\u003ebiobehavioral synchrony\u003c/em\u003e framework. First, we predicted robust neural synchrony across both parent–child interactions compared to surrogate control data, validating a genuine inter-brain coupling during social interactions. Second, we expected mother–child and father–child neural synchrony to show distinct and complementary patterns reflecting different interaction styles. Third, we hypothesized that children with anxiety disorders would exhibit altered balance in neural coordination across parents with potential enhancement of father–child synchrony when mother–child synchrony is disrupted, thereby reflecting compensatory family dynamics. Fourth, we predicted that parental caregiving quality would predict parent–child neural synchrony through complementary mechanisms. As such, the quality of parenting provided by one parent would moderate the association between the other parent’s behavior and his or her neural coordination with the child. Fifth, we expected that child anxiety would systematically reorganize neural synchrony patterns, with differential effects on synchrony with mothers versus fathers that illuminate how family-level stress shapes neural coordination across pathways of safety (maternal) and exploration (paternal).\u003c/p\u003e"},{"header":"2. Results","content":"\u003ch2\u003e2.1. Validation of Inter-Brain Synchrony\u003c/h2\u003e\n\u003cp\u003eTo confirm that the observed neural coupling reflects genuine inter-brain synchrony rather than shared sensory input or environmental noise, we compared wPLI values from real parent\u0026ndash;child dyads against surrogate control data (see Methods). Difference scores (real minus surrogate) were computed for each parent\u0026ndash;child configuration (mother\u0026ndash;child, father\u0026ndash;child) and frequency band (alpha, beta), yielding four comparisons. As these difference scores deviated significantly from normality (Shapiro\u0026ndash;Wilk tests, all \u003cem\u003ep\u003c/em\u003e \u0026lt; 0.03), we employed non-parametric Wilcoxon signed-rank tests with rank-biserial correlations (\u003cem\u003er\u003csub\u003erb\u003c/sub\u003e\u003c/em\u003e) as effect sizes. False Discovery Rate \u003cem\u003e(FDR)\u003c/em\u003e correction was applied across the four tests; all corrected \u003cem\u003ep\u003c/em\u003e-values remained below 0.001.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003e2.1.1. Alpha Rhythm Synchrony\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eMother\u0026ndash;child dyads (\u003cem\u003eN =\u003c/em\u003e 71) exhibited significantly higher alpha synchrony (\u003cem\u003eM\u003c/em\u003e = 0.083, SD = 0.013) than surrogate data (\u003cem\u003eM\u0026nbsp;\u003c/em\u003e= 0.069, SD = 0.005; \u003cem\u003eW\u003c/em\u003e = 2488, \u003cem\u003ez\u003c/em\u003e = 6.93, \u003cem\u003ep\u003csub\u003e(FDR)\u0026nbsp;\u003c/sub\u003e\u003c/em\u003e\u0026lt; 0.001, \u003cem\u003er\u003csub\u003erb\u003c/sub\u003e\u003c/em\u003e = 0.95, 95% CI [0.87, 0.99]). Father\u0026ndash;child dyads (\u003cem\u003eN =\u003c/em\u003e 73) similarly showed significantly higher alpha synchrony (M = 0.088, SD = 0.017) than surrogate data (\u003cem\u003eM\u003c/em\u003e = 0.074, SD = 0.010; \u003cem\u003eW\u003c/em\u003e = 2502, \u003cem\u003ez\u0026nbsp;\u003c/em\u003e= 6.33, \u003cem\u003ep\u003csub\u003e(FDR)\u0026nbsp;\u003c/sub\u003e\u003c/em\u003e\u0026lt; 0.001, \u003cem\u003er\u003csub\u003erb\u003c/sub\u003e\u003c/em\u003e\u003cem\u003e\u0026nbsp;\u003c/em\u003e= 0.85, 95% CI [0.72, 0.95]). See Figure 2A.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003e2.1.2. Beta Rhythm Synchrony\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eMother\u0026ndash;child dyads (\u003cem\u003eN =\u003c/em\u003e 71) exhibited significantly higher beta synchrony (\u003cem\u003eM\u003c/em\u003e = 0.088, SD = 0.010) than surrogate data (\u003cem\u003eM\u003c/em\u003e = 0.071, SD = 0.004; \u003cem\u003eW\u003c/em\u003e = 2556, \u003cem\u003ez\u003c/em\u003e = 7.32, \u003cem\u003ep\u003csub\u003e(FDR)\u0026nbsp;\u003c/sub\u003e\u003c/em\u003e\u0026lt; 0.001, \u003cem\u003er\u003csub\u003erb\u003c/sub\u003e\u003c/em\u003e = 1.00, 95% CI [1.00, 1.00], all 74 real values exceeded their paired surrogate values, yielding a ceiling effect on this measure). Father\u0026ndash;child dyads (\u003cem\u003eN =\u003c/em\u003e 73) similarly showed significantly higher beta synchrony (\u003cem\u003eM\u003c/em\u003e = 0.092, SD = 0.014) than surrogate data (\u003cem\u003eM\u003c/em\u003e = 0.076, SD = 0.010; \u003cem\u003eW\u003c/em\u003e = 2623, \u003cem\u003ez\u003c/em\u003e = 7.00, \u003cem\u003ep\u003csub\u003e(FDR)\u0026nbsp;\u003c/sub\u003e\u003c/em\u003e\u0026lt; 0.001, \u003cem\u003er\u003csub\u003erb\u003c/sub\u003e\u003c/em\u003e = 0.94, 95% CI [0.87, 0.98]). These findings and effect sizes indicate robust inter-brain neural synchrony in both parent\u0026ndash;child configurations (Figure 2B). Detailed distributions of real versus surrogate synchrony values for each parent\u0026ndash;child dyad and frequency band are presented in Supplementary Figures S1\u0026ndash;S4.\u003c/p\u003e\n\u003ch2\u003e2.2. Differential Balance of Mother\u0026ndash;Child versus Father\u0026ndash;Child Neural Synchrony\u003c/h2\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003e2.2.1. Alpha Band\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eTo examine whether the balance of parent\u0026ndash;child neural synchrony differed between child anxiety and control families, we computed the \u0026Delta; synchrony scores (real - surrogate) and conducted a 2\u0026times;2 mixed ANOVA with Parent (mother-child, father-child) as a within-subjects factor and Child Anxiety (clinical, control) as a between-subjects factor (\u003cem\u003eN =\u003c/em\u003e 68 families with complete data for both dyads). For alpha synchrony, neither the main effect of Parent (F(1,66) = 0.57, \u003cem\u003ep =\u003c/em\u003e 0.452, \u0026eta;\u0026sup2;\u003cem\u003ep =\u003c/em\u003e 0.009, 90% CI [0.000, 0.017]) nor of Child Anxiety (F(1,66) = 0.10, \u003cem\u003ep =\u003c/em\u003e 0.751, \u0026eta;\u0026sup2;\u003cem\u003ep =\u003c/em\u003e 0.002, 90% CI [0.000, 0.003]) reached significance. The Parent \u0026times; Child Anxiety interaction showed a trend in the same direction as the beta-band results reported below, but did not reach significance (F(1,66) = 3.06, \u003cem\u003ep =\u003c/em\u003e 0.085, \u0026eta;\u0026sup2;\u003cem\u003ep =\u003c/em\u003e 0.044, 90% CI [0.000, 0.089]).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003e2.2.2. Beta Band\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eConsistent with this trend, neural beta synchrony yielded a significant Parent \u0026times; Child Anxiety interaction (F(1,66) = 12.68, \u003cem\u003ep\u0026nbsp;\u003c/em\u003e\u0026lt; 0.001, \u0026eta;\u0026sup2;\u003cem\u003ep =\u003c/em\u003e 0.161, 90% CI [0.05, 0.29]). Similar to the alpha band synchrony findings, neither the main effects of Parent (F(1,66) = 1.55, \u003cem\u003ep =\u003c/em\u003e 0.217, \u0026eta;\u0026sup2;\u003cem\u003ep =\u003c/em\u003e 0.023, 90% CI [0.000, 0.046]) nor of Child Anxiety (F(1,66) = 0.72, \u003cem\u003ep =\u003c/em\u003e 0.401, \u0026eta;\u0026sup2;\u003cem\u003ep =\u003c/em\u003e 0.011, 90% CI [0.000, 0.022]) reached significance. Notably, the significant interaction indicates that the relative balance of mother\u0026ndash;child versus father\u0026ndash;child beta synchrony differs between clinical and typically developing children.\u003c/p\u003e\n\u003cp\u003eWe decomposed this interaction in two complementary ways. First, we compared the mother-minus-father \u0026Delta; synchrony difference score between samples. Clinical families showed a significantly more negative difference (\u003cem\u003eM\u003c/em\u003e = \u0026minus;0.004, SD = 0.009) than control families (\u003cem\u003eM\u0026nbsp;\u003c/em\u003e= 0.009, SD = 0.021), indicating a reversal in the relative dominance of each parent\u0026apos;s neural coupling with the child (Welch\u0026apos;s \u003cem\u003et\u003c/em\u003e(29.87) = 2.98, \u003cem\u003ep =\u003c/em\u003e 0.006, \u003cem\u003ed\u003c/em\u003e = 0.81, 95% CI [\u0026minus;1.34, \u0026minus;0.27]). Second, within each sample, we compared mother\u0026ndash;child and father\u0026ndash;child neural beta synchrony using Wilcoxon signed-rank tests (FDR-corrected across the two comparisons; see Figure 2C\u0026ndash;D). In control families, mother\u0026ndash;child dyads showed significantly greater beta synchrony enhancement (\u003cem\u003eM\u003c/em\u003e = 0.020, SD = 0.012) than father\u0026ndash;child dyads (\u003cem\u003eM\u003c/em\u003e = 0.011, SD = 0.017; \u003cem\u003eW\u003c/em\u003e = 249, \u003cem\u003ez\u003c/em\u003e = 2.33, \u003cem\u003ep\u003csub\u003e(FDR)\u003c/sub\u003e\u003c/em\u003e = .019, \u003cem\u003er\u003csub\u003erb\u003c/sub\u003e\u003c/em\u003e = 0.53, 95% CI [0.13, 0.88]), indicating that mothers serve as the primary neural regulatory agent in typically developing families. Critically, this pattern reversed in clinical child anxiety families: father\u0026ndash;child dyads showed significantly greater beta synchrony enhancement (\u003cem\u003eM\u003c/em\u003e = 0.019, SD = 0.008) than mother\u0026ndash;child dyads (\u003cem\u003eM\u003c/em\u003e = 0.015, SD = 0.005; \u003cem\u003eW\u003c/em\u003e = 707, \u003cem\u003ez\u003c/em\u003e = \u0026minus;2.83, \u003cem\u003ep\u003csub\u003e(FDR)\u003c/sub\u003e\u003c/em\u003e = .008, \u003cem\u003er\u003csub\u003erb\u003c/sub\u003e\u003c/em\u003e\u003cem\u003e\u0026nbsp;\u003c/em\u003e= \u0026minus;0.49, 95% CI [\u0026minus;0.76, \u0026minus;0.18]). Together, these results show a double dissociation pattern: the between-group comparison confirms that the mother\u0026ndash;child and father-child synchrony balance reverses between samples, and both within-group comparisons independently reach significance. This pattern indicates that childhood anxiety reorganizes the distribution of neural coupling across parent\u0026ndash;child subsystems, with fathers emerging as the primary source of inter-brain synchrony when families contend with child anxiety.\u003c/p\u003e\n\u003cp\u003e\u003cbr\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 1.\u0026nbsp;\u003c/strong\u003eMixed ANOVA results for alpha and beta \u0026Delta; synchrony (real \u0026minus; surrogate)\u003c/p\u003e\n\u003ctable width=\"100%\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eAlpha \u0026Delta; (8\u0026ndash;12 Hz)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003e\u0026nbsp;\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003e\u0026nbsp;\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eBeta \u0026Delta; (13\u0026ndash;30 Hz)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003e\u0026nbsp;\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003e\u0026nbsp;\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eEffect\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003eF\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003ep\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003e\u0026eta;\u0026sup2;p\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003eF\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003ep\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003e\u0026eta;\u0026sup2;p\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eParent (P)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.57\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.452\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.009\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1.55\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.217\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.023\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eChild Anxiety (S)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.751\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.002\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.72\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.401\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.011\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eParent \u0026times; Child Anxiety\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e3.06\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.085\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.044\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e12.68\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026lt;.001***\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.161\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eTable 1.\u003c/em\u003e\u003c/strong\u003e\u003cem\u003e\u0026nbsp;2\u0026times;2 mixed ANOVAs on neural synchrony (real \u0026minus; surrogate) with Parent (mother-child, father-child) as within-subjects factor and Child Anxiety (clinical, control) as between-subjects factor. df = (1, 66). ***P \u0026lt; .001.\u003c/em\u003e\u003c/p\u003e\n\u003ch2\u003e2.3. Parental Quality Predicts Neural Synchrony Through Complementary Mechanisms\u003c/h2\u003e\n\u003cp\u003eFollowing, to examine how parenting quality predicts parent\u0026ndash;child neural synchrony, we conducted hierarchical regression analyses separately for mother\u0026ndash;child and father\u0026ndash;child neural beta synchrony (\u003cem\u003eN =\u003c/em\u003e 65 families with complete behavioral and neural data). Parenting quality has been assessed using two composite scores derived from the CIB system \u003csup\u003e60\u003c/sup\u003e. For maternal behavior, the \u003cem\u003eMaternal Sensitive Support\u003c/em\u003e (maternal parenting) construct has been used, while for the father, the \u003cem\u003ePaternal Exploratory Encouragement\u003c/em\u003e construct has been used (paternal parenting, see 4.7. Behavioral Coding). Each model included three steps: Child Anxiety status (clinical / control) (Step 1), maternal and paternal parenting quality (Step 2), and all two-way interactions among these predictors (Step 3).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003e2.3.1. Mother\u0026ndash;Child Neural Synchrony\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAt the first step of the model, Child Anxiety significantly predicted mother\u0026ndash;child neural synchrony (\u003cem\u003eR\u0026sup2;\u003c/em\u003e = 0.084, F(1,63) = 5.74, \u003cem\u003ep =\u003c/em\u003e 0.020), with clinical families showing lower synchrony (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= \u0026minus;0.0051, 95% CI [\u0026minus;0.0093, \u0026minus;0.0008], \u003cem\u003et\u003c/em\u003e(63) = \u0026minus;2.40, \u003cem\u003ep =\u003c/em\u003e 0.020). Adding parenting quality marginally improved the model\u0026rsquo;s fit (\u003cem\u003e\u0026Delta;R\u0026sup2;\u003c/em\u003e = 0.071, F(2,61) = 2.55, \u003cem\u003ep =\u003c/em\u003e 0.086; total \u003cem\u003eR\u0026sup2;\u003c/em\u003e = 0.154), but neither maternal (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= 0.0022, \u003cem\u003ep =\u003c/em\u003e 0.239) nor paternal parenting (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= \u0026minus;0.0059, \u003cem\u003ep =\u003c/em\u003e 0.150) showed significant main effects.\u003c/p\u003e\n\u003cp\u003eCritically, adding interactions (step 3) significantly improved the model fit (\u003cem\u003e\u0026Delta;R\u0026sup2;\u003c/em\u003e = 0.152, F(3,58) = 4.24, \u003cem\u003ep =\u003c/em\u003e 0.009; final R\u0026sup2; = 0.306, F(6,58) = 4.27, \u003cem\u003ep =\u003c/em\u003e 0.001). In the final model, maternal parenting emerged as a significant positive predictor (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= 0.0622, 95% CI [0.011, 0.114], \u003cem\u003et\u003c/em\u003e(58) = 2.43, \u003cem\u003ep =\u003c/em\u003e 0.018), while neither paternal parenting (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= 0.0464, \u003cem\u003ep =\u003c/em\u003e 0.113) nor Child Anxiety were significant (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= \u0026minus;0.0491, \u003cem\u003ep =\u003c/em\u003e 0.129). Among interactions, the Maternal \u0026times; Paternal Parenting interaction was significant (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= \u0026minus;0.0206, 95% CI [\u0026minus;0.038, \u0026minus;0.003], \u003cem\u003et\u003c/em\u003e(58) = \u0026minus;2.40, \u003cem\u003ep =\u003c/em\u003e 0.019) and the Child Anxiety \u0026times; Paternal Parenting interaction approached significance (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= 0.0167, \u003cem\u003ep =\u003c/em\u003e 0.054), while the Child Anxiety \u0026times; Maternal Parenting interaction was not significant (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= \u0026minus;0.0012, \u003cem\u003ep =\u003c/em\u003e 0.753).\u003c/p\u003e\n\u003cp\u003eDecomposition of the Maternal \u0026times; Paternal Parenting interaction revealed that maternal parenting quality most strongly predicted mother\u0026ndash;child synchrony when paternal parenting was low (simple slope = 0.006), whereas this association was no longer evident when paternal parenting was high (simple slope = \u0026minus;0.005), indicating that the neural co-regulatory contribution of maternal behavior is most pronounced when paternal engagement is least optimal. This demonstrates a compensatory mechanism: high-quality maternal parenting buffers against less optimal paternal engagement in predicting mother\u0026ndash;child neural synchrony (Figure 3C. For full model, see Table 2).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003e2.3.2. Father\u0026ndash;Child Neural Synchrony\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eIn contrast to mother\u0026ndash;child neural synchrony pattern, Child Anxiety status predicted higher father\u0026ndash;child neural synchrony (R\u0026sup2; = 0.103, F(1,63) = 7.25, \u003cem\u003ep =\u003c/em\u003e 0.009; \u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= 0.0084, 95% CI [0.0022, 0.0146], \u003cem\u003et\u003c/em\u003e(63) = 2.69, \u003cem\u003ep =\u003c/em\u003e 0.009). Adding parenting quality significantly improved fit (\u0026Delta;R\u0026sup2; = 0.106, F(2,61) = 4.10, \u003cem\u003ep =\u003c/em\u003e 0.021; total R\u0026sup2; = 0.209), with paternal parenting showing a significant positive effect (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= 0.0130, 95% CI [0.0015, 0.0245], \u003cem\u003et\u003c/em\u003e(61) = 2.26, \u003cem\u003ep =\u003c/em\u003e 0.027) but maternal parenting showing no effect (\u003cem\u003ep \u0026nbsp;\u003c/em\u003e= 0.340).\u003c/p\u003e\n\u003cp\u003eAdding interactions (step 3) significantly improved the model (\u0026Delta;R\u0026sup2; = 0.143, F(3,58) = 4.29, \u003cem\u003ep =\u003c/em\u003e 0.008; final R\u0026sup2; = 0.353, F(6,58) = 5.27, \u003cem\u003ep\u0026nbsp;\u003c/em\u003e\u0026lt; 0.001). In the final model, paternal parenting was the strongest predictor (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= 0.1528, 95% CI [0.070, 0.235], \u003cem\u003et\u003c/em\u003e(58) = 3.71, \u003cem\u003ep\u0026nbsp;\u003c/em\u003e\u0026lt; 0.001), followed by maternal parenting (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= 0.1135, 95% CI [0.040, 0.187], \u003cem\u003et\u003c/em\u003e(58) = 3.10, \u003cem\u003ep =\u003c/em\u003e 0.003) and Child Anxiety (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= 0.1086, 95% CI [0.018, 0.200], \u003cem\u003et\u003c/em\u003e(58) = 2.39, \u003cem\u003ep =\u003c/em\u003e 0.020). The Maternal \u0026times; Paternal interaction was also significant (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= \u0026minus;0.0384, 95% CI [\u0026minus;0.063, \u0026minus;0.014], \u003cem\u003et\u003c/em\u003e(58) = \u0026minus;3.14, \u003cem\u003ep =\u003c/em\u003e 0.003), as was the Child Anxiety \u0026times; Paternal Parenting interaction (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= \u0026minus;0.0280, 95% CI [\u0026minus;0.052, \u0026minus;0.004], \u003cem\u003et\u003c/em\u003e(58) = \u0026minus;2.32, \u003cem\u003ep =\u003c/em\u003e 0.024), w\thile the Child Anxiety \u0026times; Maternal interaction was not significant (\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e= \u0026minus;0.0048, \u003cem\u003ep =\u003c/em\u003e 0.362). Simple slope analysis of the Maternal \u0026times; Paternal interaction revealed that when maternal parenting was low, paternal parenting strongly predicted father\u0026ndash;child synchrony (simple slope = 0.050); when maternal parenting was high, this paternal effect was substantially reduced (simple slope = 0.007). This mirrors the compensatory pattern observed for mother\u0026ndash;child synchrony (Figure 3D).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 2.\u0026nbsp;\u003c/strong\u003eHierarchical regression predicting parent\u0026ndash;child neural synchrony: full model coefficients (\u003cem\u003eN =\u003c/em\u003e 65)\u003c/p\u003e\n\u003ctable style=\"width: 100%;\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003ePredictor\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003e\u0026beta;\u0026nbsp;\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e95% CI\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003et\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003ep\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003eR\u0026sup2;\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003e\u0026Delta;R\u0026sup2;\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u0026Delta;F\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eStep\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003eMother\u0026ndash;Child Synchrony\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eChild Anxiety\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026minus;0.049\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e[\u0026minus;.113, .015]\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026minus;1.54\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.129\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.084\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.084\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e5.74*\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eMaternal Sensitive Support\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.062\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e[.011, .114]\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e2.43\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.018*\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003ePaternal Exploratory Encouragement\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.046\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e[\u0026minus;.011, .104]\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1.61\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.113\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.154\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.071\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e2.55\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eChild Anxiety \u0026times; Maternal Sensitive Support\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026minus;0.001\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e[\u0026minus;.009, .006]\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026minus;0.32\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.753\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eChild Anxiety \u0026times; Paternal Exploratory Encouragement\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.017\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e[\u0026lt;.001, .034]\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1.97\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.054\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eMaternal Sensitive Support \u0026times; Paternal Exploratory Encouragement\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026minus;0.021\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e[\u0026minus;.038,\u0026minus;.003]\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026minus;2.40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.019*\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.306\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.152\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e4.24**\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003eFather\u0026ndash;Child Synchrony\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eChild Anxiety\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.109\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e[.018, .200]\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e2.39\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.020*\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.103\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.103\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e7.25**\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eMaternal Sensitive Support\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.114\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e[.040, .187]\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e3.10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.003**\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003ePaternal Exploratory Encouragement\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.153\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e[.070, .235]\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e3.71\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026lt;.001***\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.209\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.106\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e4.10*\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eChild Anxiety \u0026times; Maternal Sensitive Support\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026minus;0.005\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e[\u0026minus;.015, .006]\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026minus;0.92\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.362\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eChild Anxiety \u0026times; Paternal Exploratory Encouragement\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026minus;0.028\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e[\u0026minus;.052,\u0026minus;.004]\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026minus;2.32\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.024*\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eMaternal Sensitive Support \u0026times; Paternal Exploratory Encouragement\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026minus;0.038\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e[\u0026minus;.063,\u0026minus;.014]\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026minus;3.14\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.003**\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.353\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.143\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e4.29**\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eTable 2.\u003c/em\u003e\u003c/strong\u003e\u003cem\u003e\u0026nbsp;All \u0026beta;, t, and p values reported in the results reflect the full model (Step 3). Synchrony is measured as neural synchrony in the beta rhythm \u0026Delta; (real \u0026ndash; surrogate wPLI). *P \u0026lt; .05, **P \u0026lt; .01, ***P \u0026lt; .001.\u003c/em\u003e\u003c/p\u003e"},{"header":"3. Discussion","content":"\u003cp\u003eThe current study addressed mechanisms of neural complementarity within families. We examined whether the neural coupling that one parent creates with the child during naturalistic interactions is shaped by the family context and the neural coupling and caregiving quality of the other parent. Our key findings indicate that parent–child interbrain synchrony operates as a family-level coordination system rather than a set of independent dyadic neural coupling processes. The findings support and extend each of our preregistered hypotheses. We found that mothers and fathers create complementary neural coordination patterns with their children, and that the child's \u0026nbsp;anxiety fundamentally reorganizes the balance between the two parent-child sub-units of the family, so that one parent's caregiving quality modulates the neural synchrony between the other parent and the child, even when that parent is not physically present during the interaction.\u003c/p\u003e\n\u003cp\u003eOur first findings confirm that neural synchrony is evident in all social interactions tested, across parents and clinical groups. Both mother–child and father–child dyads exhibited significantly higher inter-brain synchrony than surrogate controls across both alpha and beta frequency bands. These findings contribute to the expanding hyperscanning literature, which demonstrates that inter-brain synchrony is not merely an epiphenomenon of shared sensory input, but rather reflects genuine neural coordination, resulting from social interaction \u003csup\u003e61–63\u003c/sup\u003e. Our results also expand previous hyperscanning studies on neural coupling during parent–child social interaction \u003csup\u003e28–33,36–41,50,64–66\u003c/sup\u003e. Our results strengthen and extend the \u003cem\u003ebiobehavioral synchrony\u0026nbsp;\u003c/em\u003eframework \u003csup\u003e15,17,18,67\u0026nbsp;\u003c/sup\u003eby showing that both maternal and paternal neural synchrony with their children are robust phenomena, detectable even during a brief naturalistic free-play interaction. The magnitude of the effects found in our validation analysis likely reflects the ecological validity of the paradigm, which triggers a repertoire of social exchanges that drive inter-brain synchrony in real-world interactions.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eContext-Dependent Complementarity in Neural Coordination\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eOur second hypothesis predicted that mothers and fathers would show distinct patterns of neural synchrony with their children. The absence of a significant main effect for parent in either alpha or beta frequency bands indicates that both parents achieve comparable overall levels of synchrony enhancement during interaction. This finding is corroborated by the validation analysis, which confirmed robust mother–child and father–child neural synchrony during free-play. Such equivalence is in itself noteworthy: while prior hyperscanning work has focused predominantly on mother–child dyads, with only isolated studies of father–child synchrony, the present study is, to our knowledge, the first to assess both parents within the same family context.\u003c/p\u003e\n\u003cp\u003eThe parent × group interaction, which was significant in the beta rhythm, with a parallel trend in alpha rhythm, indicates that the balance between mother–child and father–child neural coupling shifts as a function of family context and regulatory demands, rather than being fixed. The primacy of the beta-band effect is theoretically meaningful given the established role of beta in social regulation and caregiving. Beta oscillations are implicated in top-down regulatory processes, prediction, and the active maintenance of cognitive states \u003csup\u003e68\u003c/sup\u003e, and have been specifically linked to parent–child attachment processes in mothers \u003csup\u003e69,70\u003c/sup\u003e.\u0026nbsp;Beta rhythms also underpin a range of complex social functions, including empathy \u003csup\u003e32,71\u003c/sup\u003e, mentalization \u003csup\u003e72\u003c/sup\u003e, prediction of others' actions \u003csup\u003e73\u003c/sup\u003e, and the continuous updating of predictive models \u003csup\u003e74\u003c/sup\u003e, that collectively enable the rapid mutual adaptation required for inter-brain coordination during social interaction \u003csup\u003e61\u003c/sup\u003e. The selective reorganization of beta synchrony in clinical families, therefore, points to a context-sensitive redistribution of neural regulatory coupling across parent–child pathways that operates at the frequency band underpinning the social-cognitive infrastructure of caregiving.\u003c/p\u003e\n\u003cp\u003eThe same trend of greater mother–child synchrony in control families and greater father–child synchrony in clinical families also emerged in the alpha band, although it did not reach the statistical significance threshold. This tentative extension to alpha is noteworthy given alpha's established role in the affective and attentional dimensions of parent–child interaction. Alpha-band synchrony is enhanced during naturalistic parent–child interactions and is modulated by emotional quality and dyadic engagement \u003csup\u003e65\u003c/sup\u003e. Alpha synchrony is particularly pronounced during early development, where increased alpha coupling between infants and adults occurs during direct gaze and infant-directed speech \u003csup\u003e75\u003c/sup\u003e, and correlates with independent measures of emotional connection \u003csup\u003e76\u003c/sup\u003e. Such convergence across frequency bands raises the possibility that the functional reorganization of parental neural coupling in clinical families is not beta-specific, but reflects a broader cross-frequency shift in the relative dominance of maternal versus paternal neural coordination. That said, the alpha effect did not reach significance and must be interpreted with caution. Whether this reorganization generalizes across frequency bands remains an open question requiring replication in larger, adequately powered samples.\u003c/p\u003e\n\u003cp\u003eTaken together, these findings are consistent with the \u003cem\u003ebiobehavioral synchrony\u003c/em\u003e framework, which distinguishes the types of behavioral synchrony infants create with mother and father. The \u0026nbsp;\"rhythms of safety” with mother are characterized by low-arousal and promote regulation and security, and the “rhythms of exploration” with father are characterized by high-arousal play fostering resilience and environmental exploration \u003csup\u003e9,24,25,77\u003c/sup\u003e. Our results suggest that while these dyadic styles differ in specific behaviors, \u0026nbsp;they are similar in promoting a sense of synchrony, coordination, and attunement and translate into complementary neural coordination systems that are flexibly deployed according to family need. The absence of a parent main effect, coupled with a context-dependent interaction, points to functional specialization rather than hierarchical organization: maternal and paternal neural coupling with the child are not universally different in magnitude, but are calibrated to family circumstances, with their relative contributions shifting precisely when regulatory demands are highest.\u003c/p\u003e\n\u003cp\u003eOur third hypothesis predicted that when the family ecology is one of heightened stress, such as in the case of a child with anxiety disorder, there is a reorganization of the balance between parents, in this case, in parents' neural coordination. This hypothesis received strong support. We found that in low-stress families of typically-developing children, mother–child dyads exhibited significantly greater neural synchrony than father–child dyads, consistent with the primacy of the maternal co-regulatory function in most families \u003csup\u003e24\u003c/sup\u003e. In clinical families, this pattern was reversed, and father–child dyads showed significantly greater neural synchrony.\u003c/p\u003e\n\u003cp\u003eThis double dissociation, which was significant in both directions for beta rhythm, provides the first neural evidence for mechanisms of complementarity within families. Such complementary dynamics have long been hypothesized by family systems' theories \u003csup\u003e78,79\u003c/sup\u003e, and indicate that, under stress the family system not only deteriorates but actively reorganizes its regulatory architecture.\u003c/p\u003e\n\u003cp\u003eNotably, high-stress family ecologies, such as those with a child diagnosed with anxiety disorder, are frequently marked by co-occurring maternal psychopathology. This pattern, which occurred in over 60% of our clinical families (see Supplementary Analysis 1: Maternal Psychopathology as Grouping Variable – ANOVA) is consistent with findings from large epidemiological studies. \u0026nbsp;A meta-analysis of 34 studies and over 295,000 participants found that maternal anxiety is significantly associated with preschool children’s internalizing problem behaviors, externalizing problem behaviors, and overall problem behaviors \u003csup\u003e80\u003c/sup\u003e. Consistently, a meta-analysis of 191 studies on maternal perinatal depression and anxiety documented consistent associations with offspring socio-emotional, cognitive, and behavioral difficulties across development, from infancy through adolescence \u003csup\u003e81\u003c/sup\u003e. Family-based studies further report elevated rates of co-occurring maternal anxiety or depression in families where children exhibited anxiety disorders \u003csup\u003e82,83\u003c/sup\u003e. Taken together, these findings underscore that maternal internalizing psychopathology is common in families in which children suffer from anxiety, amplifying the functional significance of the complementary paternal regulatory role identified in our study. In this context, our findings indicate that fathers appear to rise to a complementary role, exhibiting active neural upregulation that sustained the child's access to inter-brain regulatory input when the mother–child synchrony pathway is compromised.\u003c/p\u003e\n\u003cp\u003eThe neurobiological plausibility of such reorganization rests on evidence that the paternal brain exhibits remarkable experience-dependent plasticity. Unlike the maternal brain, which undergoes obligatory neurodevelopmental changes during pregnancy and postpartum \u003csup\u003e52\u003c/sup\u003e, the paternal brain's caregiving networks are shaped by involvement and family context \u003csup\u003e14\u003c/sup\u003e. Research on paternal caregiving has shown that fathers who serve as primary caregivers develop amygdala–STS connectivity patterns resembling those of mothers, suggesting substantial neural plasticity in parental brain networks (\u003csup\u003e14\u003c/sup\u003e. Paternal neural responses, including oxytocin release, amygdala activation, and social brain network engagement, were found to be dynamically modulated by co-parenting quality, maternal functioning (and psychopathologies, including maternal postpartum depression), and family coordination \u003csup\u003e14,84,85\u003c/sup\u003e. Neuroimaging studies show that fathers' amygdala connectivity with temporal-limbic circuits increases proportionally with caregiving time \u003csup\u003e57\u003c/sup\u003e, default mode network activity associated with mentalizing and empathy shows experience-dependent enhancement \u003csup\u003e14,56\u003c/sup\u003e, and co-parenting quality modulates parental brain responses to infant cues \u003csup\u003e59\u003c/sup\u003e and that, overall, responsiveness of the \u0026nbsp;paternal brain to infant cues is shaped by the caregiving context and the family ecology \u003csup\u003e58\u003c/sup\u003e.\u0026nbsp;Our findings extend these single-brain findings to inter-brain coordination and indicate that when child and maternal psychopathology disrupt the typical development of mother-child neural synchrony, fathers' brain engages in complementary neural reorganization that enhances its coupling with the child.\u003c/p\u003e\n\u003cp\u003eThis interpretation aligns with behavioral evidence indicating that fathers increase their caregiving involvement when mothers present psychopathology or depression \u003csup\u003e46,86\u003c/sup\u003e, and with findings that link such paternal involvement to the buffering role of the father and show their moderating effects under conditions of family stress \u003csup\u003e46,87,88\u003c/sup\u003e.\u0026nbsp;For instance, reducing the negative impact of maternal depression on child psychopathology by 50% \u003csup\u003e48,49\u003c/sup\u003e. Our findings extend this behavioral literature to the neural level and demonstrate that paternal complementarity is accompanied by measurable reorganization of inter-brain synchrony across the two parent–child subsystems. Notably, a substantial proportion of over 60% of the mothers in the clinical sample also met criteria for anxiety disorders or depressive disorders (Supplementary Analyses S1), raising the possibility that maternal internalizing psychopathology contributes to the attenuation of mother–child synchrony and the compensatory upregulation of father–child neural coupling. This interpretation is further supported by the finding in Supplementary Analyses S1 and S2, in which the families are grouped by maternal diagnosis, rather than child anxiety disorder, and produces an identical crossover pattern, suggesting that it is the family-level stress, irrespective of which member is the identified patient, that drives the reorganization of the parental neural coordination system, as suggested by the family systems' perspective.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eBrain–Behavior Coupling and Cross-Parental Modulation\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003ePrior parent-child hyperscanning studies have shown that caregiving behavior predicts the magnitude of neural synchrony. Maternal behavior affects synchrony both during and beyond the immediate interactions \u003csup\u003e28–32,38\u003c/sup\u003e and sensitive and intrusive behaviors are linked with fronto-temporal coordination \u003csup\u003e28,38\u003c/sup\u003e. Brain-to-brain synchrony mediates the associations between parents' and children's emotion regulation, linking neural coupling to regulatory capacities \u003csup\u003e35\u003c/sup\u003e. These findings position inter-brain synchrony as a neural marker of relationship quality and call to examine whether parenting effects may operate, at least partly, through family-level mechanisms.\u003c/p\u003e\n\u003cp\u003eThe fourth hypothesis, which suggested that parental behavior quality predict neural synchrony through cross-parental modulation, was confirmed. Of note, the hierarchical regression analyses demonstrated that the neural mechanism of inter-brain synchrony is sensitive not only to the behavior of the parent currently interacting with the child, but also to the behavior of the co-parent who is absent during the interaction. This strong interaction effect was found for both mother and father, above and beyond the nature of the family ecology. Two observational constructs capturing the positive behavioral quality of parental interaction, \u003cem\u003eMaternal Sensitive Support\u003c/em\u003e for mothers and \u003cem\u003ePaternal Exploratory Encouragement\u003c/em\u003e for fathers, yielded significant interaction effects for both mother–child and father–child dyads, revealing a consistent compensatory pattern: when the child receives lower-quality caregiving from one parent, the other parent's behavioral quality more strongly predicted neural synchrony with the child. Specifically, \u003cem\u003ePaternal Exploratory Encouragement\u003c/em\u003e quality had its strongest effect on father–child synchrony when maternal parenting was low, and maternal parenting quality had its strongest effect on mother–child synchrony when paternal parenting was low. When the co-parent provided high-quality care, the predictive relationship between one parent’s caregiving quality and neural synchrony was attenuated, suggesting that the family system has sufficient regulatory capacity and the incremental benefit of each parent's individual quality diminishes.\u003c/p\u003e\n\u003cp\u003eThe interaction between family ecology, indexed by child anxiety, and \u003cem\u003ePaternal Exploratory Encouragement\u003c/em\u003e that emerged for father–child interbrain synchrony provides additional evidence for context-sensitive neural coupling. In clinical families, the positive association between \u003cem\u003ePaternal Exploratory Encouragement\u003c/em\u003e quality and father–child neural synchrony was amplified, suggesting that paternal behavior becomes a more powerful determinant of neural coordination when the family faces increased regulatory demands. This is consistent with the broader observation that father involvement becomes particularly important for child outcomes under conditions of family stress \u003csup\u003e46,87,88\u003c/sup\u003e.\u003c/p\u003e\n\u003cp\u003eThese findings align with previous hyperscanning studies indicating that fathers' self-reported attitudes toward their caregiving role prospectively predict father–child neural synchrony during cooperative problem solving \u003csup\u003e39\u003c/sup\u003e , and that supportive parenting behaviors and higher-quality parent–child relationships are associated with greater inter-brain synchrony across both mothers and fathers \u003csup\u003e33\u003c/sup\u003e. Our findings extend previous work by showing that father–child synchrony is not only sensitive to trait-like paternal characteristics but is dynamically modulated by the amount of stress in the family's ecology, increasing when child anxiety is present.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eFamily-Level Neural Coordination\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis cross-parental modulation adds a novel dimension to the growing literature on indirect effects in family systems. Research on marital quality and co-parenting has established that the spousal relationship profoundly shapes each parent's interaction with the child \u003csup\u003e89,90\u003c/sup\u003e, and neuroimaging studies have shown that co-parenting quality modulates parental brain responses to infant cues \u003csup\u003e59\u003c/sup\u003e. As early as four months of age, infants are attentive to the relational messages exchanged between their parents, adjusting their own regulatory behavior in response to inter-parental dynamics \u003csup\u003e91\u003c/sup\u003e. The child's brain, therefore, is not only attuned to the immediate process with a single caregiver but is already calibrated to the relational ecology of the broader family system. Our results extend this principle to preschool-age children, suggesting that the brain's sensitivity to the family's regulatory landscape persists well beyond infancy and is reflected in the real-time neural coupling that occurs during parent–child interaction. Our finding that paternal parenting quality predicts mother–child neural synchrony, and vice versa, suggests a neural mechanism through which these indirect family effects may operate, with co-parenting behaviors shaping the neurobiological substrate of each parent–child relationship.\u003c/p\u003e\n\u003cp\u003eTaken together, our findings reveal two distinct but converging pieces of evidence for family-level neural coordination. First, in the context of childhood anxiety, the father can become the primary regulatory agent at the neural level. The family system reorganizes and the father's neural engagement increases to complement the reduction in the mother’s neural coupling. This finding resonates with the broader literature showing that \u003cem\u003eboth\u003c/em\u003e maternal and paternal depression predict adverse child outcomes \u003csup\u003e47,86\u003c/sup\u003e, and extends work on paternal buffering of maternal depression effects to neural mechanisms of regulation \u003csup\u003e48,49\u003c/sup\u003e. Second, the neural mechanism of inter-brain synchrony is sensitive to the behavior of the co-parent who is absent during the interaction; each parent's caregiving quality shaped, to some extent, the neural synchrony with the other parent. Such complementary modulation extends the \u003cem\u003ebiobehavioral synchrony\u003c/em\u003e framework, which posits that parent–child synchrony emerges through repeated co-regulatory exchanges and serves as the primary mechanism through which caregivers scaffold children's developing neural networks toward the outside world \u003csup\u003e15,16,18\u003c/sup\u003e. Notably, we also show (Supplementary Analyses 1) that these results are robust to alternative operationalizations of family risk: when the families were grouped by maternal psychopathological diagnosis rather than child anxiety, the same crossover interaction pattern emerged in the beta band (Supplementary Analysis 1; Supplementary Table S1; Supplementary Figure S6), and hierarchical regressions again revealed significant cross-parental modulation of neural synchrony (Supplementary Analysis 2; Supplementary Table S2; Supplementary Figure S7). These converging results strengthen the interpretation that family-level clinical risk, whether indexed by child anxiety diagnosis or maternal psychopathology, is the factor which reorganizes the balance of neural synchrony across parental subsystems.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eClinical Implications, Limitations, and Future Directions\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eOur findings have important clinical implications. Current evidence-based interventions for childhood anxiety disorders predominantly target the mother–child relationship \u003csup\u003e92,93\u003c/sup\u003e, reflecting both the historical emphasis on maternal caregiving and the practical challenge of engaging fathers in treatment. Our findings suggest that fathers may serve as an important yet underutilized therapeutic resource. Interventions that strategically leverage the complementarity of the paternal synchrony pathway, or that target the co-parenting relationship to optimize the neural coordination system across both parents, may prove more effective than those addressing either parent in isolation. The brain–behavior coupling results further suggest that improving one parent's caregiving quality may have cascading effects on the other parent's neural synchrony with the child, pointing toward family-level intervention approaches grounded in neuroscience.\u003c/p\u003e\n\u003cp\u003eSeveral limitations should be acknowledged. First, the cross-sectional design cannot establish causal directionality and it is not possible to ascertain whether the enhanced father–child synchrony in clinical families represents an adaptive compensatory response, a pre-existing difference, or a correlate of different interaction styles remains to be determined through longitudinal research. Second, the sample included only heterosexual two-parent families, and the generalizability to other family configurations, including single-parent families, same-sex parents, and families with non-parental caregivers, requires further investigation. Finally, although power analyses indicated adequate statistical sensitivity for the primary analyses, the trend-level alpha band interaction (\u003cem\u003ep =\u003c/em\u003e .085) suggests that replication in larger samples is warranted to evaluate whether the compensatory reorganization extends across frequency bands.\u003c/p\u003e\n\u003cp\u003eIn conclusion, the present study demonstrates that parent–child neural synchrony operates as a family-level coordination system characterized by mechanisms of complementarity between the maternal and paternal pathways. When childhood anxiety disrupts the normative balance, the family system actively reorganizes, and fathers assume an enhanced neural regulatory role that complements the attenuated mother–child coupling. Such complementarity is not merely reactive to the immediate interaction context but is sensitive to the broader caregiving familial dynamics, including the behavior of the co-parent who is not present during the interaction. These findings extend the \u003cem\u003ebiobehavioral synchrony\u003c/em\u003e framework from a dyadic to whole-family level analysis and provide neural evidence that human parenting operates as an integrated system where the contributions of each parent are continuously calibrated to the needs of the child and the coparental dynamics.\u003c/p\u003e"},{"header":"4. Methods","content":"\u003cp\u003eThe project has been pre-registered: https://osf.io/fzxs4/files/92spu\u003c/p\u003e\n\u003ch2\u003e4.1. Participants and Study Design\u003c/h2\u003e\n\u003cp\u003eThe study included a total of 83 two-parent family triads stratified into two groups: 53 families with children aged 3–7 years diagnosed with an anxiety disorder and 30 families with typically developing children of the same age range. After applying EEG quality criteria, the final analytic sample comprised 77 families (49 clinical, 28 control).\u003c/p\u003e\n\u003cp\u003eThe mean age of the mothers was 39.05 years (SD = 4.16) in the control group and 39.87 years (SD = 4.20) in the clinical group (total: M = 39.50, SD = 4.15). For the fathers, mean age was 42.16 years (SD = 4.55) in the control group and 41.14 years (SD = 3.73) in the clinical group.\u003c/p\u003e\n\u003cp\u003eAmong children in the final analytic sample, mean age was 5.52 years (SD = 1.20) in the control group and 5.41 years (SD = 1.14) in the clinical group (total: M = 5.45, SD = 1.16; range: 3.0–7.6 years), with no significant group difference (\u003cem\u003et\u003c/em\u003e(72) = 0.40, \u003cem\u003eP =\u003c/em\u003e .689; age data available for 74 of 77 children). Across the sample, 53.2% were boys (\u003cem\u003en =\u003c/em\u003e 41) and 46.8% were girls (\u003cem\u003en =\u003c/em\u003e 36); sex distributions were comparable across groups (control: 64.3% boys; clinical: 46.9% boys; χ²(1) = 1.51, \u003cem\u003eP =\u003c/em\u003e .219).\u003c/p\u003e\n\u003cp\u003eAll participating families consisted of children living with two heterosexual parents in the same household, with all family members fluent in the local language. Children in the anxiety group met DSM-5 criteria for an anxiety disorder as confirmed through comprehensive clinical assessment, with anxiety symptoms of sufficient severity to warrant therapeutic intervention and no concurrent participation in other psychological treatments. Control group children were screened to ensure absence of clinically significant behavioural or emotional difficulties, no history of psychiatric diagnosis, and no current psychological interventions. Exclusion criteria for all participants included neurological disorders or head injuries in any family member, uncorrected vision or hearing impairments, and inability to tolerate EEG equipment. Anxiety group participants were recruited through clinical referral sources, with all children undergoing comprehensive psychological assessment including structured clinical interviews and standardized questionnaires administered by licensed clinicians. Control group families were recruited through community sources and screened via detailed intake interviews with parents to confirm absence of psychological concerns and ensure demographic matching with the anxiety group. The study was approved by the institutional ethics committee and all participants provided written informed consent (parents) and age-appropriate assent (children).\u003c/p\u003e\n\u003cp\u003eOf the total 83 family triads that were enrolled, the data of 6 families were excluded due to EEG signal quality, yielding a total of 77 families (49 clinical, 28 control). Within these families, mother–child EEG data were unavailable for three dyads (in which the mother did not participate in the EEG recording), and father–child data were unavailable for two dyads (in which the fathers were not present or did not participate in the recording), resulting in 74 and 75 usable mother–child and father–child dyads, respectively.\u003c/p\u003e\n\u003ch2\u003e\u0026nbsp;4.2. Experimental Design and Procedure\u003c/h2\u003e\n\u003cp\u003eLaboratory sessions were scheduled during afternoon hours (14:00–16:00) to optimize child cooperation and minimize fatigue effects, conducted in a standardized laboratory environment equipped with synchronized four-camera recording systems. Upon arrival, families completed informed consent procedures while children acclimated to the laboratory environment for approximately 45 minutes. The preparation phase included detailed protocol explanation and systematic EEG cap application following a standardized protocol, beginning with parents to model the procedure for children, followed by child cap placement only after demonstrated comfort with the environment. Electrode impedances were verified and adjusted to maintain signal quality throughout the session. Following successful EEG preparation, experimenters exited the observation room to minimize interference with naturalistic family interactions. The experimental session comprised several sequential phases designed to assess neural synchrony across different interaction contexts (Figure 1). Phase 1 began with a 3-minute free-play interaction between the child and the same parent, during which the parent received standardized instructions to engage in naturalistic play using a pre-selected set of age-appropriate toys placed on a designated table. Phase 2 involved parents switching, with the first parent exiting to the waiting area and the second parent entering to engage in a sequential free-play interaction with the child. The order of parent participation was counterbalanced across families to control for potential order effects. EEG data were continuously recorded throughout all phases, with behavioral interactions simultaneously captured via the four-camera system with synchronized timestamps. Real-time monitoring of EEG signal quality ensured data integrity, with sessions discontinued and rescheduled if signal quality could not be maintained or if child distress occurred.\u003c/p\u003e\n\u003ch2\u003e4.3. EEG Data Acquisition\u003c/h2\u003e\n\u003cp\u003eSimultaneous EEG recording was conducted using three Acticap helmets, each equipped with 32 active electrodes arranged according to the international 10/20 system and integrated chin stabilization to minimize movement artifacts. Within the scope of the study, only two interactors were present at any given interaction. Signal acquisition parameters included analog bandpass filtering between 0.1 and 500 Hz with continuous sampling at 1000 Hz. Electrode impedances were maintained below 10 kΩ throughout recording sessions, with the common ground electrode positioned at AFz. To ensure temporal precision essential for cross-brain measurements, the two EEG caps used in each interaction were connected to a single amplifier unit, enabling millisecond-level synchronization accuracy between participant recordings.\u003c/p\u003e\n\u003ch2\u003e4.4. Data Preprocessing\u003c/h2\u003e\n\u003cp\u003eEEG data preprocessing was conducted using Python 3.8 with the MNE software package (v0.17.0). Initial preprocessing involved separation of dual-participant data files to two separate files to enable individual artifact detection and signal optimization. All EEG recordings underwent digital bandpass filtering between 1 and 50 Hz using finite impulse response filter to eliminate low-frequency drift and high-frequency noise while preserving neural oscillations of interest. Data were segmented into 1000 ms epochs with 500 ms sliding windows to maximize data utilization while maintaining temporal resolution for connectivity analyses. Artifact removal proceeded in two sequential stages: first, an unsupervised Bayesian optimization algorithm (AutoReject) eliminated trials containing transient jumps in isolated channels and artifacts affecting channel groups; second, Independent Component Analysis (ICA) using MNE’s implementations of FastICA and CORRMAP \u003csup\u003e94\u003c/sup\u003e removed systematic physiological artifacts. ICA-based artifact removal targeted ocular artifacts, muscular activity components and non-physiological artifacts. Independent components corresponding to these artifact sources were manually identified by trained analysts and served as templates for automated detection and removal of similar components across all participants, ensuring consistent artifact removal criteria throughout the dataset.\u003c/p\u003e\n\u003ch2\u003e4.5. Inter-Brain Synchrony Quantification\u003c/h2\u003e\n\u003cp\u003eInter-brain neural synchrony was quantified using the weighted Phase Lag Index (wPLI; \u003csup\u003e95\u003c/sup\u003e), a measure that indexes the consistency of phase relationships between neural oscillations while minimizing the influence of volume conduction and shared environmental noise through a weighting scheme that attenuates phase differences near zero. wPLI has been shown to outperform traditional coherence-based measures in naturalistic recording conditions \u003csup\u003e95,96\u003c/sup\u003e and has been validated extensively for hyperscanning applications across different samples and developmental stages \u003csup\u003e28–32,37,38,97,98\u003c/sup\u003e.\u003c/p\u003e\n\u003cp\u003eAnalysis focused on two rhythms of interest: the alpha rhythm (8–12 Hz) and beta rhythm (13–30 Hz). Our focus on alpha and beta frequency bands was motivated by converging evidence: in mother-child and adult-child dyads, inter-brain synchrony is often observed in the alpha band, linked to empathy, shared attention and joint engagement \u003csup\u003e32,65,75,99\u003c/sup\u003e. Beta rhythms were additionally evaluated based on evidence of beta-band activation in mother–child dyads with older children \u003csup\u003e30–32,37,38\u003c/sup\u003e and the arousal characteristics of father–child interactions \u003csup\u003e9\u003c/sup\u003e.\u003c/p\u003e\n\u003cp\u003eAnalytic signal computation employed finite impulse response (FIR) filtering with Hamming window application to minimize spectral leakage and edge artifacts, followed by Hilbert transform to extract instantaneous phase information. Spatial analysis was restricted to theoretically motivated regions of interest based on established literature regarding social cognition and interpersonal neural coupling. The analysis incorporated four bilateral ROIs encompassing frontal regions (Fp1, F3, F7 for the left hemisphere; Fp2, F4, F8 for the right hemisphere), associated with executive control and social cognition\u003cem\u003e\u0026nbsp;\u003csup\u003e100–103\u003c/sup\u003e\u003c/em\u003e, and temporo-parietal regions (P7, T7, P3 for left hemisphere; P8, T8, P4 for right hemisphere), implicated in theory of mind, attention, and sensorimotor integration \u003csup\u003e104,105\u003c/sup\u003e. The wPLI for each inter-brain link was calculated as the mean connectivity of each of the 3 electrodes in one target ROI with each of the 3 electrodes in the second target ROI, resulting in 9 connectivity values averaged for each ROI combination into one inter-brain link. Inter-brain connectivity was examined across all possible ROI pairings between the two interactors’ neural networks, including ipsilateral and contralateral connections across frontal and temporo-parietal regions. Individual wPLI values were computed for each inter-brain link, followed by network-level aggregation through averaging of all linkages to generate a composite whole-network inter-brain synchrony measure in the fronto-temporo-parietal network.\u003c/p\u003e\n\u003ch2\u003e4.6. Surrogate Data Generation\u003c/h2\u003e\n\u003cp\u003eTo validate the specificity of neural synchrony during real parent–child interactions, surrogate data were generated by computing wPLI values between one member of a dyad and the second member from a different dyad within the same sample. This process was repeated for all possible cross-dyad combinations. A stringent quality control criterion required surrogate dyads to share at least 50% clean epochs from the entire interaction period, with dyads did not meet the minimum epoch-sharing threshold removed from analyses. For each original dyad, surrogate values were averaged across all valid permutations to create a single representative surrogate value matched to the real connectivity value of the dyad.\u003c/p\u003e\n\u003ch2\u003e4.7. Behavioral Coding\u003c/h2\u003e\n\u003cp\u003eParent–child interactions were coded using the Coding Interactive Behavior system (CIB; \u003csup\u003e60\u003c/sup\u003e), a well-validated global rating system for social interactions across the lifespan with over 300 published applications across diverse populations and contexts \u003csup\u003e18,67\u003c/sup\u003e and has been successfully implemented in hyperscanning research \u003csup\u003e28–32,38,97,98,106\u003c/sup\u003e. The CIB employs 52 codes rated on 5-point scales that were averaged into theoretically-based constructs. This study utilized the Maternal Sensitive Support and Paternal Exploratory Encouragement constructs, adapted for each sample’s relational context. Based on the theoretical framework of Feldman \u003csup\u003e9\u003c/sup\u003e, maternal and paternal behaviors differ in arousal, regulation and intensity, with mother–child interaction framed as “rhythms of safety”, versus the father’s more engaging and stimulating “rhythms of exploration”. In accordance with this framework, the \u003cem\u003eMaternal Sensitive Support\u003c/em\u003e construct comprised the following codes: mother positive affect, maternal lead, vocal appropriateness, and elaboration. The \u003cem\u003ePaternal\u0026nbsp;Exploratory Encouragement\u003c/em\u003e construct, in line, included positive social exploration of environment and father’s adaptability (reverse coded from over-consistency), as well as the reverse codes of constriction, tension, over-regulation, and structure limit. Both constructs were coded such that higher scores reflected more positive parental behaviors, in line with the theoretical literature. Coding was performed by trained raters blind to study hypotheses. Inter-rater reliability was established on 20% of interactions, with all codes achieving \u0026gt;90% agreement (mean ICC = 0.93, range = 0.89–0.99).\u003c/p\u003e\n\u003ch2\u003e4.8. Statistical Analysis\u003c/h2\u003e\n\u003cp\u003eAnalysis proceeded in three stages. In the first stage, inter-brain synchrony was validated by comparing real versus surrogate wPLI values. Shapiro-Wilk tests indicated significant deviations from normality for difference scores across all comparisons (all P \u0026lt; 0.03), justifying the use of Wilcoxon signed-rank tests with rank-biserial correlations (\u003cem\u003er\u003csub\u003erb\u003c/sub\u003e\u003c/em\u003e) as effect sizes, applying False Discovery Rate \u003cem\u003e(FDR)\u003c/em\u003e correction across four comparisons (two parents × two frequency bands). In the second stage, differential synchrony patterns were examined using 2×2 mixed ANOVAs on Δ synchrony scores (real minus surrogate) with Parent (mother–child, father–child) as a within-subjects factor and Child Anxiety (clinical, control) as a between-subjects factor, separately for alpha and beta bands. Partial eta-squared (η²p) effect sizes are reported with 90% confidence intervals, consistent with the convention for ANOVA effect sizes. The significant beta interaction was decomposed through: (a) an independent-samples comparison of the mother-minus-father difference score between groups (Welch’s t-test with 95% CI for Cohen’s d derived from the non-central t-distribution, justified by Shapiro-Wilk confirmation of normality in both groups, P \u0026gt; .13), and (b) within-sample paired Wilcoxon signed-rank tests comparing mother–child versus father–child synchrony (FDR-corrected).\u003c/p\u003e\n\u003cp\u003ePrior to analysis, univariate outliers were identified separately for each parent–child dyad type (mother–child, father–child) and sample (control, clinical) on the beta Δ synchrony scores, and the same exclusions were applied uniformly across both frequency bands. This dyad-level approach was adopted on the grounds that extreme synchrony values likely reflect session-level characteristics — such as atypical interaction dynamics or residual signal artifacts — that are not specific to a single frequency band; applying consistent exclusions also ensures a comparable analytic sample across the alpha and beta analyses reported in Table 1. Participants with values exceeding 2.5 standard deviations above the group mean were excluded from the relevant dyad-specific analyses (3 families from mother–child analyses, 2 from father–child analyses), resulting in analytic samples of \u003cem\u003eN\u003c/em\u003e = 71 for mother–child and \u003cem\u003eN\u003c/em\u003e = 73 for father–child comparisons, with \u003cem\u003eN\u003c/em\u003e = 68 families providing complete data for both dyads. A supplementary sensitivity analysis retaining the full sample without any exclusions confirmed that the beta-band interaction remained significant and that the same crossover direction greater mother–child synchrony in control families and greater father–child synchrony in clinical families was preserved in the alpha band (Supplementary Sensitivity Analysis, Tables S-SA1–S-SA2, Figures S-SA1–S-SA3).\u003c/p\u003e\n\u003cp\u003eThis analysis was evaluated again as an omnibus 2×2×2 mixed ANOVA incorporating both the validation (real vs. surrogate) and differential balance including parent (mother-child, father-child) and sample (clinical, control) components (Supplementary Analysis 3; Supplementary Table S3; Supplementary Figure S8). This analysis yielded a highly significant three-way Parent × Data Type × Child Anxiety interaction for beta synchrony, confirming that the crossover pattern of our results reflects genuine differential neural coupling rather than non-specific group differences.\u003c/p\u003e\n\u003cp\u003eFinally, in the third stage of analysis, hierarchical regression models examined brain–behavior coupling, predicting parent–child beta Δ synchrony from Child Anxiety (Step 1), Maternal and paternal parenting quality (Step 2), and all two-way interactions (Step 3). Analyses were conducted using Python 3.8 (scipy v1.7, \u003csup\u003e107\u003c/sup\u003e; statsmodels v0.13, \u003csup\u003e108\u003c/sup\u003e and JASP v0.18 (JASP Team, 2024).\u003c/p\u003e\n\u003ch2\u003e4.9. Power Analysis\u003c/h2\u003e\n\u003cp\u003ePost-hoc power analyses were conducted to evaluate the statistical sensitivity of the study given the final analytic sample. For the primary analysis, in which the Parent × Child Anxiety interaction on beta Δ synchrony (F(1,66) = 12.68, η²\u003cem\u003ep =\u003c/em\u003e 0.161), observed power exceeded 0.93, well above the conventional 0.8 threshold. A sensitivity analysis indicated that the study was powered at 80% to detect interaction effects as small as η²\u003cem\u003ep =\u003c/em\u003e 0.108 (F ≥ 8.08) for the 2×2 mixed ANOVA design. The between-group comparison of the Δ mother-child minus father-child neural synchrony balance score (\u003cem\u003ed\u0026nbsp;\u003c/em\u003e= 0.81) yielded power of 0.87 with the observed sample sizes (\u003cem\u003en =\u003c/em\u003e 25 control, \u003cem\u003en =\u003c/em\u003e 43 clinical). For the within-sample Wilcoxon signed-rank tests comparing mother–child versus father–child beta synchrony (r_rb = 0.53 and −0.49 for control and clinical samples, respectively), post-hoc power was computed using the equivalent paired effect sizes (d_z = 0.43 and 0.45), as standard power analysis frameworks require parametric effect size input. This yielded power of 0.53 for the control comparison (\u003cem\u003en =\u003c/em\u003e 25) and 0.82 for the clinical comparison (\u003cem\u003en =\u003c/em\u003e 43). Although power for the smaller control subsample was moderate, both tests achieved statistical significance, and these decomposition tests serve to characterize a significant omnibus interaction rather than standing as independent primary hypotheses. All four validation analyses (real vs. surrogate) achieved power exceeding 0.999, reflecting large effect sizes (\u003cem\u003er\u003csub\u003erb\u003c/sub\u003e\u003c/em\u003e= 0.85–1.00). For the hierarchical regression models, the full models predicting mother–child synchrony (R² = 0.306, f² = 0.44) and father–child synchrony (R² = 0.353, f² = 0.55) yielded power of 0.97 and 0.99, respectively (\u003cem\u003eN =\u003c/em\u003e 65, 6 predictors). The Step 3 interaction increments (ΔR² = 0.152 and 0.143, f²change = 0.22) both achieved power of 0.84. Collectively, these analyses confirm that the study was adequately powered for the primary and secondary analyses, with the exception of the alpha interaction trend (F = 3.06, power = 0.41), which has been interpreted cautiously and warrants replication in larger samples. A supplementary sensitivity analysis confirmed that all key findings were robust when retaining the full sample without outlier exclusions (see Supplementary Sensitivity Analysis).\u003c/p\u003e"},{"header":"Declarations","content":"\u003ch2\u003eData Availability\u003c/h2\u003e\n\u003cp\u003eThe data generated in this study cannot be made publicly available due to participant privacy protections under our ethical approval (IRB) protocol. Requests for access to anonymized, aggregated data may be directed to the corresponding author and will be evaluated on a case-by-case basis. Data sharing requests must include: (1) a research proposal outlining intended use, (2) confirmation of institutional ethics approval, and (3) a data use agreement. Requests will be fulfilled within 30 days where feasible and compliant with privacy regulations.\u003c/p\u003e\n\u003ch2\u003eCode Availability\u003c/h2\u003e\n\u003cp\u003eAll analysis code is publicly available at https://github.com/Yoavshapira1/FelmanLabEEGpipeline. The repository includes preprocessing scripts, neural synchrony analysis pipelines, statistical analysis code, and visualization functions.\u003c/p\u003e\n\u003ch2\u003eAcknowledgements\u003c/h2\u003e\n\u003cp\u003eThe study was supported by the Simms/Mann Foundation Chair to Ruth Feldman and by the Bezos Family Foundation. The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript.\u003c/p\u003e\n\u003ch2\u003eAuthor Contributions\u003c/h2\u003e\n\u003cp\u003eConceptualization: L.S. and R.F.; methodology: L.S. and R.F.; investigation and data curation: L.S., C.S., O.S-R., Y.A.; formal analysis: L.S., C.S., O.H., I.P.; writing: L.S. and R.F.; writing – review and editing: R.F., C.S., O.H., O.S-R, Y.A.\u003c/p\u003e\n\u003ch2\u003eCompeting Interests\u003c/h2\u003e\n\u003cp\u003eThe authors declare no competing interests.\u003c/p\u003e\n\u003ch2\u003eResource Availability\u003c/h2\u003e\n\u003cp\u003eAny requests for further information and resources that would not compromise the participants’ privacy should be directed to and will be fulfilled by the corresponding author.\u003c/p\u003e\n\u003ch2\u003eDeclaration of Generative AI and AI-Assisted Technologies\u003c/h2\u003e\n\u003cp\u003eDuring the preparation of this work we employed AI tools only to improve the language and readability of the paper. After using this tool, humans reviewed and edited the content as needed, and take full responsibility for the content of the publication.\u003c/p\u003e\n"},{"header":"References","content":"\u003col\u003e\n \u003cli\u003eAbraham, E., Hendler, T., Shapira-Lichter, I., Kanat-Maymon, Y., Zagoory-Sharon, O., \u0026amp; Feldman, R. (2014). Father\u0026rsquo;s brain is sensitive to childcare experiences. Proceedings of the National Academy of Sciences, 111(27), 9792\u0026ndash;9797.\u003c/li\u003e\n \u003cli\u003eAtzil, S., Gao, W., Fradkin, I., \u0026amp; Barrett, L. F. (2018). Growing a social brain. Nature Human Behaviour, 2(9), 624\u0026ndash;636.\u003c/li\u003e\n \u003cli\u003eAytuglu, A., Graham-Engeland, J. E., Feinberg, M. E., Murray-Perdue, S. A., Conway, C. A., \u0026amp; Schreier, H. M. C. (2025). Longitudinal associations between father\u0026ndash; and mother\u0026ndash;child interactions, coparenting, and child cardiometabolic health. 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Father involvement moderates the effect of Maternal depression during a child\u0026rsquo;s infancy on child behavior problems in kindergarten. Journal of Family Psychology, 18(4), 575\u0026ndash;588.\u003c/li\u003e\n \u003cli\u003eMinuchin, P. (1985). Families and individual development: Provocations from the field of family therapy. Child Development, 56(2), 289\u0026ndash;302.\u003c/li\u003e\n \u003cli\u003eMu\u0026ntilde;oz-Moldes, S., \u0026amp; Bhatt, A. (2023). Neural oscillations in social interaction: Current trends and future directions. In A. Czeszumski et al. (Eds.), Hyperscanning and Brain-to-Brain Coupling. Springer.\u003c/li\u003e\n \u003cli\u003eNguyen, T., Schleihauf, H., Kungl, M., Kayhan, E., Hoehl, S., \u0026amp; Vrtička, P. (2021). Interpersonal neural synchrony during father\u0026ndash;child problem solving: an fNIRS hyperscanning study.\u0026nbsp;Child development,\u0026nbsp;92(4), e565-e580.\u003c/li\u003e\n \u003cli\u003eNguyen, T., Schleihauf, H., Kayhan, E., Matthes, D., Vrtička, P., \u0026amp; Bhatt, R. (2020). The effects of interaction quality on neural synchrony during mother-child problem solving. Cortex, 124, 235\u0026ndash;249.\u003c/li\u003e\n \u003cli\u003ePaquette, D. (2004). Theorizing the father\u0026ndash;child relationship: Mechanisms and developmental outcomes. Human Development, 47(4), 193\u0026ndash;219.\u003c/li\u003e\n \u003cli\u003ePiazza, E. A., Hasenfratz, L., Hasson, U., \u0026amp; Lew-Williams, C. (2020). Infant and adult brains are coupled to the dynamics of natural communication. Proceedings of the National Academy of Sciences, 117(20), 23058\u0026ndash;23065.\u003c/li\u003e\n \u003cli\u003eRamchandani, P. G., Psychogiou, L., Vlachos, H., Iles, J., Sethna, V., Netsi, E., \u0026amp; Lodder, A. (2013). Paternal depression: An examination of its links with father, child and family functioning in the postnatal period. Depression and Anxiety, 30(8), 798\u0026ndash;807.\u003c/li\u003e\n \u003cli\u003eRapee, R. M., Schniering, C. A., \u0026amp; Hudson, J. L. (2009). Anxiety disorders during childhood and adolescence: Origins and treatment. Annual Review of Clinical Psychology, 5, 311\u0026ndash;341.\u003c/li\u003e\n \u003cli\u003eReindl, V., Gerloff, C., Scharke, W., \u0026amp; Konrad, K. (2018). Brain-to-brain synchrony in parent-child dyads and the relationship with emotion regulation revealed by fNIRS-based hyperscanning. NeuroImage, 178, 493\u0026ndash;502.\u003c/li\u003e\n \u003cli\u003eRilling, J. K. (2013). The neural and hormonal bases of human paternal care. Neuropsychologia, 51(4), 731\u0026ndash;747.\u003c/li\u003e\n \u003cli\u003eRogers, F. D., \u0026amp; Bales, K. L. (2019). 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Brain Research, 1856, 149856.\u003c/li\u003e\n \u003cli\u003eStGeorge, J., \u0026amp; Freeman, E. (2017). Measurement of father\u0026ndash;child rough-and-tumble play and its relations to child behavior. Infant Mental Health Journal, 38(6), 709\u0026ndash;725.\u003c/li\u003e\n \u003cli\u003eSun, X., Qian, X., Li, Y., Wang, Y., \u0026amp; Fu, S. (2022). A dataset of parent\u0026ndash;child hyperscanning functional near-infrared spectroscopy during free play and video watching. Scientific Data, 9, 627.\u003c/li\u003e\n \u003cli\u003eTrivers, R. L. (1972). Parental investment and sexual selection. In B. Campbell (Ed.), Sexual Selection and the Descent of Man (pp. 136\u0026ndash;179). Aldine.\u003c/li\u003e\n \u003cli\u003eUlmer-Yaniv, A., Salomon, R., Waidergoren, S., Shimon-Raz, O., Djalovski, A., \u0026amp; Feldman, R. (2021). Synchronous caregiving from birth to adulthood tunes humans\u0026rsquo; social brain. Proceedings of the National Academy of Sciences, 118(14), e2012900118.\u003c/li\u003e\n \u003cli\u003eVinck, M., Oostenveld, R., van Wingerden, M., Battaglia, F., \u0026amp; Pennartz, C. M. (2011). An improved index of phase-synchronization for electrophysiological data in the presence of volume-conduction, noise and sample-size bias. NeuroImage, 55(4), 1548\u0026ndash;1565.\u003c/li\u003e\n \u003cli\u003eViola, F. C., Thorne, J., Edmonds, B., Schneider, T., Eichele, T., \u0026amp; Debener, S. (2009). Semi-automatic identification of independent components representing EEG artifact. Clinical Neurophysiology, 120(5), 868\u0026ndash;877.\u003c/li\u003e\n \u003cli\u003eWoodroffe, R., \u0026amp; Vincent, A. (1994). Mother\u0026rsquo;s little helpers: Patterns of male care in mammals. Trends in Ecology \u0026amp; Evolution, 9(8), 294\u0026ndash;297.\u003c/li\u003e\n \u003cli\u003eZhang, M., Liu, J., \u0026amp; Hu, Y. (2025). Inter-brain synchrony and psychological distress in dyadic interactions: A systematic review. Neuroscience \u0026amp; Biobehavioral Reviews, 154, 105320.\u003c/li\u003e\n \u003cli\u003eZhao, Z., Salesse, R. N., Gueugnon, M., Schmidt, R. C., Marin, L., \u0026amp; Bardy, B. G. (2024). Parent\u0026ndash;child neural synchrony: A comprehensive review of hyperscanning studies. Neuroscience \u0026amp; Biobehavioral Reviews, 157, 105523.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"
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