CAP2 overexpression in hippocampal neurons prevents actin abnormalities and cognitive defects in an Alzheimer’s disease model
Ramona Stringhi, Filippo La Greca, Laura D'Andrea, Elisa Zianni, Lina Vandermeulen, Miriam Ascagni, Michela Carola Speciani, Valeria Edefonti, Diego Scheggia, Monica Di Luca, Silvia Pelucchi, Elena Marcello · FENS Forum 2024
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
ePoster · Neuroscience