STAT3 ameliorates cognitive deficits via regulation of NMDAR expression in an Alzheimer's disease animal model
Huali Wan, Xiao‐Yue Hong, Zaihua Zhao, Ting Li, Bingge Zhang, Qian Liu, Shi Ping Zhao, Jian‐Zhi Wang, Xuefeng Shen, Gong‐Ping Liu
Abstract
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.
Topics & Concepts
DiseaseNeuroscienceNMDA receptorCognitionAlzheimer's diseaseMedicinePsychologyInternal medicineReceptorCytokine Signaling Pathways and InteractionsGDF15 and Related BiomarkersProtein Tyrosine Phosphatases