Implications of GABAergic neurotransmission in Alzheimer's disease

Yanfang Li, Hao Sun, Zhicai Chen, Huaxi Xu, Guojun Bu, Hui Zheng

Research output: Contribution to journalReview articlepeer-review

100 Scopus citations


Alzheimer's disease (AD) is characterized pathologically by the deposition of β-amyloid peptides (Aβ) and the accumulation of neurofibrillary tangles (NFTs) composed of hyper-phosphorylated tau. Regardless of the pathological hallmarks, synaptic dysfunction is widely accepted as a causal event in AD. Of the two major types of synapses in the central nervous system (CNS): glutamatergic and GABAergic, which provide excitatory and inhibitory outputs respectively, abundant data implicate an impaired glutamatergic system during disease progression. However, emerging evidence supports the notion that disrupted default neuronal network underlies impaired memory, and that alterations of GABAergic circuits, either plays a primary role or as a compensatory response to excitotoxicity, may also contribute to AD by disrupting the overall network function. The goal of this review is to provide an overview of the involvement of Aβ, tau and apolipoprotein E4 (apoE4), the major genetic risk factor in late-onset AD (LOAD), in GABAergic neurotransmission and the potential of modulating the GABAergic function as AD therapy.

Original languageEnglish (US)
Article number31
JournalFrontiers in Aging Neuroscience
Issue numberFEB
StatePublished - 2016


  • Amyloid beta-peptides
  • Apolipoproteins E
  • GABAergic neurotransmission
  • Neuronal inhibition
  • Tau proteins

ASJC Scopus subject areas

  • Aging
  • Cognitive Neuroscience


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