Mitigation of Synaptic and Memory Impairments through F‐Actin Stabilization in an Alzheimer’s Disease Mouse Model

The compelling evidence supporting the stabilization of F-actin suggests a promising strategy for alleviating synaptic impairments in AD, as it not only restores dendritic spines but also increases the surface localization of glutamate receptors. Our findings on complex interplay between cytoskeleton dynamics and synaptic functions may provide potential therapeutic targets aimed at preserving synaptic integrity and ameliorating cognitive decline in AD.