文献类型：期刊文献

英文题名：GABAergic Inhibitory Interneuron Deficits in Alzheimer's Disease: Implications for Treatment

作者：Xu, Yilan[1];Zhao, Manna[1];Han, Yuying[1];Zhang, Heng[1]

机构：[1]Shaoxing Univ, Sch Med, Dept Basic Med, Neurodegenerat & Neuroregenerat Lab, Shaoxing, Peoples R China

年份：2020

卷号：14

外文期刊名：FRONTIERS IN NEUROSCIENCE

收录：SSCI(收录号：WOS:000584639500001)、SCI-EXPANDED(收录号：WOS:000584639500001)、、Scopus(收录号：2-s2.0-85087832141)、WOS

基金：This work was supported by grants from the National Natural Science Foundation of China (No. 31800891 to HZ).

语种：英文

外文关键词：GABA inhibitory interneurons; cognitive deficits; Alzheimer's disease; amyloid beta-protein; PV inhibitory interneurons

外文摘要：Alzheimer's disease (AD) is a neurodegenerative disorder characterized clinically by severe cognitive deficits and pathologically by amyloid plaques, neuronal loss, and neurofibrillary tangles. Abnormal amyloid beta-protein (A beta) deposition in the brain is often thought of as a major initiating factor in AD neuropathology. However, gamma-aminobutyric acid (GABA) inhibitory interneurons are resistant to A beta deposition, and A beta decreases synaptic glutamatergic transmission to decrease neural network activity. Furthermore, there is now evidence suggesting that neural network activity is aberrantly increased in AD patients and animal models due to functional deficits in and decreased activity of GABA inhibitory interneurons, contributing to cognitive deficits. Here we describe the roles played by excitatory neurons and GABA inhibitory interneurons in A beta-induced cognitive deficits and how altered GABA interneurons regulate AD neuropathology. We also comprehensively review recent studies on how GABA interneurons and GABA receptors can be exploited for therapeutic benefit. GABA interneurons are an emerging therapeutic target in AD, with further clinical trials urgently warranted.