STAT3 ameliorates cognitive deficits via regulation of NMDAR expression in an Alzheimer's disease animal model

Conclusions: Taken together, our study indicates that hTau accumulation impaired synaptic plasticity through STAT3 inactivation induced suppression of NMDARs expression, revealing a novel mechanism for hTau-associated synapse and memory deficits.

Source: Theranostics - April 19, 2021 Category: Molecular Biology Authors: Hua-Li Wan, Xiao-Yue Hong, Zai-Hua Zhao, Ting Li, Bing-Ge Zhang, Qian Liu, Qun Wang, Shi Zhao, Jian-Zhi Wang, Xue-Feng Shen, Gong-Ping Liu Tags: Research Paper Source Type: research