G-protein coupled receptor regulates cytoskeletal remodelling of extracellular Tau in Alzheimer's disease.

Alzheimer's disease, a neurodegenerative disorder, is marked by amyloid-β plaques and Tau-induced neurofibrillary tangles, which disrupt cytoskeletal dynamics. This study highlights the role of G-protein coupled receptors (GPCRs) in regulating Tau-induced actin and microtubule remodeling within microglia. GPCR activation influences key cytoskeletal processes via Rho GTPase signaling, modulating structures like lamellipodia and filopodia, essential for cellular migration and phagocytosis. Dysregulation of GPCR pathways impairs microglial function, exacerbating Tau aggregation and neuroinflammation. Therapeutic approaches targeting GPCR-mediated pathways, actin stability, and microtubule dynamics offer potential for mitigating Tau pathology and stabilizing the cytoskeleton. This study provides insights into GPCR-based strategies as promising interventions to address neurodegeneration in AD.