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000140525 0247_ $$2doi$$a10.1016/j.brainres.2018.11.042
000140525 0247_ $$2pmid$$apmid:30503351
000140525 0247_ $$2ISSN$$a0006-8993
000140525 0247_ $$2ISSN$$a1872-6240
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000140525 0247_ $$2datacite_doi$$a10.60944/dzne-2020-06847
000140525 037__ $$aDZNE-2020-06847
000140525 041__ $$aEnglish
000140525 082__ $$a610
000140525 1001_ $$0P:(DE-2719)2811489$$aAmbrad Giovannetti, Eleonora$$b0$$eFirst author
000140525 245__ $$aUnsupervised excitation: GABAergic dysfunctions in Alzheimer's disease.
000140525 260__ $$aAmsterdam$$bElsevier$$c2019
000140525 264_1 $$2Crossref$$3print$$bElsevier BV$$c2019-03-01
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000140525 520__ $$aAlzheimer'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.
000140525 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0
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000140525 650_2 $$2MeSH$$aAlzheimer Disease: physiopathology
000140525 650_2 $$2MeSH$$aAmyloid beta-Peptides: metabolism
000140525 650_2 $$2MeSH$$aAnimals
000140525 650_2 $$2MeSH$$aBrain: metabolism
000140525 650_2 $$2MeSH$$aDisease Models, Animal
000140525 650_2 $$2MeSH$$aGABAergic Neurons: metabolism
000140525 650_2 $$2MeSH$$aHumans
000140525 650_2 $$2MeSH$$aMemory: physiology
000140525 650_2 $$2MeSH$$aMemory Disorders: pathology
000140525 650_2 $$2MeSH$$aNerve Degeneration: pathology
000140525 650_2 $$2MeSH$$aNerve Net: physiopathology
000140525 650_2 $$2MeSH$$aNeurons: metabolism
000140525 650_2 $$2MeSH$$agamma-Aminobutyric Acid: metabolism
000140525 650_2 $$2MeSH$$atau Proteins: metabolism
000140525 7001_ $$0P:(DE-2719)2679991$$aFuhrmann, Martin$$b1$$eLast author
000140525 77318 $$2Crossref$$3journal-article$$a10.1016/j.brainres.2018.11.042$$b: Elsevier BV, 2019-03-01$$p216-226$$tBrain Research$$v1707$$x0006-8993$$y2019
000140525 773__ $$0PERI:(DE-600)1462674-3$$a10.1016/j.brainres.2018.11.042$$gVol. 1707, p. 216 - 226$$p216-226$$q1707<216 - 226$$tBrain research$$v1707$$x0006-8993$$y2019
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