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by claude@2026-06, 2026-06-24
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This study evaluated the effects of repetitive mild traumatic brain injury delivered using the CHIMERA closed-head rotational acceleration model versus sham treatment in 6-month-old APP/PS1 mice, assessing outcomes one month later. EEG/EMG recordings for 72 hours were used to characterize sleep architecture and epileptiform activity, and blood plasma and brain tissue were analyzed for neuropathology markers. The main findings were that time in vigilance during sleep was unchanged, but NREM sleep showed a shift toward higher-frequency EEG power; epileptiform activity did not differ between groups, while blood plasma neurofilament light increased and brain amyloid pathology did not change. A key limitation explicitly reflected in the timing is that the assessments were performed one month post-injury, leaving longer-term effects on amyloid, sleep, or epileptiform activity unaddressed. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.
Abstract
Traumatic Brain Injury (TBI) is a known risk factor for Alzheimer’s disease and related neurodegenerative diseases. Sleep disturbances and epileptiform abnormalities can appear after TBI and may contribute to the development of neuropathology. In this study, we characterized sleep, epileptiform activity, and neuropathology after repetitive mild traumatic brain injury (rmTBI) in a mouse model of Alzheimer’s disease. We used the Closed Head Impact Model of Engineered Rotational Acceleration (CHIMERA) to deliver rmTBI or sham (control) treatment to 6-month-old APP/PS1 mice (N=19). One month post-injury, we implanted electroencephalogram (EEG) and electromyographic (EMG) electrodes, recorded for 72 hours, and then collected brain tissue and blood plasma. Our assessment of sleep architecture showed that time spent in vigilance state was not affected by the rmTBI one month post-injury; however, power spectra analysis showed a shift towards higher frequencies in the rmTBI group during non-rapid eye movement (NREM) sleep. Epileptiform activity did not differ between sham and rmTBI. Compared to sham controls, the rmTBI group showed higher neurofilament light (NF-L), but not glial-fibrillary acidic protein (GFAP) in blood plasma and no change in Aβ pathology. These results indicate sustained neurological injury in the APP/PS1 mice one month after rmTBI without affecting amyloid deposition in the brain. Our study suggests that rmTBI can induce neural injury without causing enduring sleep disruption, seizures, and exacerbation of amyloidosis in the APP/PS1 mouse model.
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Abstract
Traumatic Brain Injury (TBI) is a known risk factor for Alzheimer’s disease and related neurodegenerative diseases. Sleep disturbances and epileptiform abnormalities can appear after TBI and may contribute to the development of neuropathology. In this study, we characterized sleep, epileptiform activity, and neuropathology after repetitive mild traumatic brain injury (rmTBI) in a mouse model of Alzheimer’s disease. We used the Closed Head Impact Model of Engineered Rotational Acceleration (CHIMERA) to deliver rmTBI or sham (control) treatment to 6-month-old APP/PS1 mice (N=19). One month post-injury, we implanted electroencephalogram (EEG) and electromyographic (EMG) electrodes, recorded for 72 hours, and then collected brain tissue and blood plasma. Our assessment of sleep architecture showed that time spent in vigilance state was not affected by the rmTBI one month post-injury; however, power spectra analysis showed a shift towards higher frequencies in the rmTBI group during non-rapid eye movement (NREM) sleep. Epileptiform activity did not differ between sham and rmTBI. Compared to sham controls, the rmTBI group showed higher neurofilament light (NF-L), but not glial-fibrillary acidic protein (GFAP) in blood plasma and no change in Aβ pathology. These results indicate sustained neurological injury in the APP/PS1 mice one month after rmTBI without affecting amyloid deposition in the brain. Our study suggests that rmTBI can induce neural injury without causing enduring sleep disruption, seizures, and exacerbation of amyloidosis in the APP/PS1 mouse model.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
-Introduction: to add population data -Methods: CHIMERA: to add procedure details such as injury location, type of injury, rational for age at injury. Some details in biosample and histology data. -Discussion: more elaboration on results and tone-down claims. All of these revisions were suggested by the reviewers of the journal where we have submitted our paper (not published yet).
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