001     138871
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024 7 _ |a 10.1007/s00115-015-0041-5
|2 doi
024 7 _ |a pmid:26781314
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024 7 _ |a 0028-2804
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024 7 _ |a 1433-0407
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037 _ _ |a DZNE-2020-05193
041 _ _ |a ger
082 _ _ |a 610
100 1 _ |a Busche, M. A.
|0 P:(DE-HGF)0
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|e Corresponding author
245 _ _ |a [Mechanisms of Alzheimer's disease : Neuronal hyperactivity and hypoactivity as new therapeutic targets].
260 _ _ |a Heidelberg
|c 2016
|b Springer
264 _ 1 |3 online
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|b Springer Science and Business Media LLC
|c 2016-01-19
264 _ 1 |3 print
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|b Springer Science and Business Media LLC
|c 2016-11-01
336 7 _ |a article
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336 7 _ |a Journal Article
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336 7 _ |a ARTICLE
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520 _ _ |a 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.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
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542 _ _ |i 2016-01-19
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588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 2 |a Alzheimer Disease: complications
|2 MeSH
650 _ 2 |a Alzheimer Disease: physiopathology
|2 MeSH
650 _ 2 |a Alzheimer Disease: therapy
|2 MeSH
650 _ 2 |a Brain: physiopathology
|2 MeSH
650 _ 2 |a Evidence-Based Medicine
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Psychomotor Agitation: complications
|2 MeSH
650 _ 2 |a Psychomotor Agitation: physiopathology
|2 MeSH
650 _ 2 |a Psychomotor Agitation: therapy
|2 MeSH
650 _ 2 |a Treatment Outcome
|2 MeSH
700 1 _ |a Staufenbiel, M.
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700 1 _ |a Willem, M.
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700 1 _ |a Haass, C.
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700 1 _ |a Förstl, H.
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773 1 8 |a 10.1007/s00115-015-0041-5
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|t Der Nervenarzt
|v 87
|y 2016
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773 _ _ |a 10.1007/s00115-015-0041-5
|g Vol. 87, no. 11, p. 1163 - 1174
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856 4 _ |u https://pub.dzne.de/record/138871/files/DZNE-2020-05193.pdf
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21