Cellular and Arrhythmogenic Ventricular Cardiomyopathy Pathway in Alzheimer's Disease: Implications for Cardiovascular and Cellular Dysfunction

Differential RNA expression analysis revealed significant upregulation of several pathways in AD compared to controls. The Focal Adhesion pathway (hsa04510) was notably upregulated (FDR p = 0.00079, strength = 0.67), indicating altered cell-extracellular matrix interactions. The Arrhythmogenic Right Ventricular Cardiomyopathy pathway (hsa05412) also showed upregulation (FDR p = 0.0019, strength = 0.65), suggesting cardiovascular dysfunction. Additionally, pathways related to extracellular matrix (ECM)-receptor interaction (hsa04512, FDR p = 0.0031) and Hippo signaling (hsa04390, FDR p = 0.0119) were upregulated, highlighting cellular proliferation and tissue repair mechanisms. Pathways linked to vascular function, such as Vascular Smooth Muscle Contraction (hsa04270, FDR p = 0.0146) and Fluid Shear Stress and Atherosclerosis (hsa05418, FDR p = 0.0052), were also significantly altered, pointing to potential vascular dysfunction in AD patients CONCLUSION: The upregulation of pathways involved in cellular adhesion, cardiovascular function, and tissue repair suggests that AD may disrupt vascular integrity and cellular interactions beyond the central nervous system. These findings provide insight into cardiovascular disease and cardiomyopathy in AD and support the need for further research into these pathways as potential therapeutic targets for managing vascular and cellular dysfunction in AD.