Valproic Acid Modifies Synaptic Structure and Accelerates Neurite Outgrowth Via the Glycogen Synthase Kinase-3 Signaling Pathway in an Alzheimer's Disease Model

摘要

AimTau hyperphosphorylation and amyloid -peptide overproduction, caused by altered localization or abnormal activation of glycogen synthase kinase-3 (GSK-3), is a pathogenic mechanism in Alzheimer's disease (AD). Valproic acid (VPA) attenuates senile plaques and neuronal loss. Here, we confirmed that VPA treatment improved spatial memory in amyloid precursor protein (APP)/presenilin 1 (PS 1) double-transgenic mice and investigated the effect of VPA on synaptic structure and neurite outgrowth.