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- W3100852457 endingPage "8704" @default.
- W3100852457 startingPage "8704" @default.
- W3100852457 abstract "γ-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter, playing a central role in the regulation of cortical excitability and the maintenance of the excitatory/inhibitory (E/I) balance. Several lines of evidence point to a remodeling of the cerebral GABAergic system in Alzheimer’s disease (AD), with past studies demonstrating alterations in GABA receptor and transporter expression, GABA synthesizing enzyme activity and focal GABA concentrations in post-mortem tissue. AD is a chronic neurodegenerative disorder with a poorly understood etiology and the temporal cortex is one of the earliest regions in the brain to be affected by AD neurodegeneration. Utilizing NanoString nCounter analysis, we demonstrate here the transcriptional downregulation of several GABA signaling components in the post-mortem human middle temporal gyrus (MTG) in AD, including the GABAA receptor α1, α2, α3, α5, β1, β2, β3, δ, γ2, γ3, and θ subunits and the GABAB receptor 2 (GABABR2) subunit. In addition to this, we note the transcriptional upregulation of the betaine-GABA transporter (BGT1) and GABA transporter 2 (GAT2), and the downregulation of the 67 kDa isoform of glutamate decarboxylase (GAD67), the primary GABA synthesizing enzyme. The functional consequences of these changes require further investigation, but such alterations may underlie disruptions to the E/I balance that are believed to contribute to cognitive decline in AD." @default.
- W3100852457 created "2020-11-23" @default.
- W3100852457 creator A5019752279 @default.
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- W3100852457 creator A5049161020 @default.
- W3100852457 creator A5085058765 @default.
- W3100852457 creator A5088282584 @default.
- W3100852457 date "2020-11-18" @default.
- W3100852457 modified "2023-09-23" @default.
- W3100852457 title "Impaired Expression of GABA Signaling Components in the Alzheimer’s Disease Middle Temporal Gyrus" @default.
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