The Link Between β-catenin/Wnt Signaling Pathway and Cognitive Function in Chronic Kidney Disease

Chronic Kidney Disease (CKD), which is marked by impaired kidney function, is recognized as a significant public health issue, and individuals with this condition are at a heightened risk of experiencing cognitive problems simultaneously. This research evaluated the functional importance of the β-catenin signaling pathway in cognitive function in mice with chronic renal disease caused by adenine. The study also aimed to determine the relevance of the influence of the β-catenin signaling system on cognitive function and its underlying processes. Firstly, a mouse model of CKD was created. Subsequently, the cognitive capacity of mice with CKD was assessed using a water maze. Following that, immunofluorescence labeling and protein blot analysis were used to quantify the levels of β-catenin and Dickkopf-related protein -1 (DKK1) expression in the brain and kidney of mice with CKD. This study aims to investigate the role of β-catenin in cognitive impairment in CKD mice. CKD mice exhibited neuronal injury and cognitive impairment, which correlated with a significant decrease in the number of nuclei in the frontal lobe. These nuclei had pale staining, blurred boundaries, a hazy appearance, and, in some cases, swelling or disintegration. Furthermore, it was proven that DKK1 exacerbates cognitive impairment in mice with CKD by blocking the β-catenin/Wnt signaling pathway. To summarize, the study revealed that the β-catenin signaling pathway impacts cognitive function in mice with CKD induced by adenine. Additionally, it was observed that increased levels of DKK1 resulted in neuronal damage in the brain tissue of mice with CKD.