TY - JOUR
T1 - Implications of GABAergic neurotransmission in Alzheimer's disease
AU - Li, Yanfang
AU - Sun, Hao
AU - Chen, Zhicai
AU - Xu, Huaxi
AU - Bu, Guojun
AU - Zheng, Hui
N1 - Publisher Copyright:
© 2016 Li, Sun, Chen, Xu, Bu and Zheng.
PY - 2016
Y1 - 2016
N2 - 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.
AB - 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.
KW - Amyloid beta-peptides
KW - Apolipoproteins E
KW - GABAergic neurotransmission
KW - Neuronal inhibition
KW - Tau proteins
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U2 - 10.3389/fnagi.2016.00031
DO - 10.3389/fnagi.2016.00031
M3 - Review article
AN - SCOPUS:84960085716
SN - 1663-4365
VL - 8
JO - Frontiers in Aging Neuroscience
JF - Frontiers in Aging Neuroscience
IS - FEB
M1 - 31
ER -