Journal Article (Review Article)

DZNE-2020-06847

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Unsupervised excitation: GABAergic dysfunctions in Alzheimer's disease.

Ambrad Giovannetti, E. (First author)DZNE* ; Fuhrmann, M. (Last author)DZNE*

2019
Elsevier Amsterdam

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Please use a persistent id in citations: doi:10.1016/j.brainres.2018.11.042  doi:10.60944/dzne-2020-06847

Abstract: Alzheimer's disease (AD) is characterized by the classical hallmarks of Aβ-deposition and tau-pathology that are thought to ultimately lead to synapse and neuron loss. Although long known, neuroinflammation has recently attracted a substantial amount of attention by researchers due to genome wide association studies (GWAS) that identified microglia associated genes to be correlated with sporadic AD. Besides that, cholinergic degeneration and gamma-aminobutyric acid (GABA) abnormalities have been identified in the brains of AD patients already decades ago, but have not received much attention over the last ten years. Recently, the neuronal network dysfunction hypothesis has revived interest in how impairments of neuronal communication at the network level lead to epileptiform activity and disrupted oscillations observed in the brains of AD patients and mouse models. Thereby, deficits in neuronal networks involved in learning and memory might ultimately cause memory impairments. In this context, an imbalance between excitation and inhibition has been hypothesized to contribute to neuronal network dysfunction. Here, disturbances of cholinergic and GABAergic transmission might play a crucial role. In this review, we will focus on GABAergic dysfunction in AD and mouse models of AD and how those might relate to neuronal network aberration and memory impairment.

Keyword(s): Alzheimer Disease: physiopathology (MeSH) ; Amyloid beta-Peptides: metabolism (MeSH) ; Animals (MeSH) ; Brain: metabolism (MeSH) ; Disease Models, Animal (MeSH) ; GABAergic Neurons: metabolism (MeSH) ; Humans (MeSH) ; Memory: physiology (MeSH) ; Memory Disorders: pathology (MeSH) ; Nerve Degeneration: pathology (MeSH) ; Nerve Net: physiopathology (MeSH) ; Neurons: metabolism (MeSH) ; gamma-Aminobutyric Acid: metabolism (MeSH) ; tau Proteins: metabolism (MeSH)

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Contributing Institute(s):

1. Neuroimmunology and Imaging (AG Fuhrmann)

Research Program(s):

1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2019

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Database coverage:
; ; ; ; BIOSIS Previews ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; Ebsco Academic Search ; Green Open Access ; IF < 5 ; JCR ; Nationallizenz ; SCOPUS ; Web of Science Core Collection

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