Journal Article (Review Article) DZNE-2020-05193

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[Mechanisms of Alzheimer's disease : Neuronal hyperactivity and hypoactivity as new therapeutic targets].

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2016
Springer Heidelberg

Der Nervenarzt 87(11), 1163-1174 () [10.1007/s00115-015-0041-5]

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Abstract: Alzheimer's disease (AD) is characterized by the pathological accumulation of amyloid-beta (Abeta) and tau peptides in the brain. Recent evidence suggests that the soluble peptide amyloid-eta (Aeta) may have an additional role in the pathogenesis of AD. The detailed investigation of the cellular and neurophysiological mechanisms underlying AD has revealed surprising results that may become highly relevant for the early diagnosis and treatment of the disease. By analyzing the function of single neurons and large-scale networks in intact brains in vivo it has been shown that A-beta, tau and A-eta abnormally modulate brain activity and obviously unfold contrasting effects: while A-beta promotes neuronal hyperactivity as well as epileptiform activity, tau and A-eta reduce the activity of neurons. Promising new evidence from animal studies and humans with AD indicates that the treatment of hyperactivity may improve cognitive dysfunctions and even slow the underlying disease process.

Keyword(s): Alzheimer Disease: complications (MeSH) ; Alzheimer Disease: physiopathology (MeSH) ; Alzheimer Disease: therapy (MeSH) ; Brain: physiopathology (MeSH) ; Evidence-Based Medicine (MeSH) ; Humans (MeSH) ; Psychomotor Agitation: complications (MeSH) ; Psychomotor Agitation: physiopathology (MeSH) ; Psychomotor Agitation: therapy (MeSH) ; Treatment Outcome (MeSH)

Classification:

Contributing Institute(s):
  1. Ext Ludwig-Maximilians-University (Ext LMU)
  2. Molecular Neurodegeneration (AG Haass)
Research Program(s):
  1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2016
Database coverage:
Medline ; BIOSIS Previews ; Clarivate Analytics Master Journal List ; Current Contents - Clinical Medicine ; Ebsco Academic Search ; IF < 5 ; JCR ; NCBI Molecular Biology Database ; NationallizenzNationallizenz ; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Web of Science Core Collection
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Document types > Articles > Journal Article
Institute Collections > M DZNE > M DZNE-AG Haass
Institute Collections > M DZNE > M DZNE-Ext LMU
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 Record created 2020-02-18, last modified 2024-01-09


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