CAP2 overexpression in hippocampal neurons prevents actin abnormalities and cognitive defects in an Alzheimer’s disease model
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by Amyloid β (Aβ)-driven synaptic dysfunction in the early phases of pathogenesis. However, cytoskeletal abnormalities, such as cofilin-actin rods, have been described in AD patients. In addition, we demonstrated that the actin-binding protein Cyclase-associated protein 2 (CAP2) is a master regulator of cofilin synaptic localization through the Cys32-dependent CAP2 dimerization. The CAP2 dimer-mediated cofilin translocation is required for synaptic plasticity-driven spine remodelling.This mechanism is altered in AD since CA