TY  - JOUR
AU  - Busche, M. A.
AU  - Staufenbiel, M.
AU  - Willem, M.
AU  - Haass, C.
AU  - Förstl, H.
TI  - [Mechanisms of Alzheimer's disease : Neuronal hyperactivity and hypoactivity as new therapeutic targets].
JO  - Der Nervenarzt
VL  - 87
IS  - 11
SN  - 0028-2804
CY  - Heidelberg
PB  - Springer
M1  - DZNE-2020-05193
SP  - 1163-1174
PY  - 2016
AB  - 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.
KW  - Alzheimer Disease: complications
KW  - Alzheimer Disease: physiopathology
KW  - Alzheimer Disease: therapy
KW  - Brain: physiopathology
KW  - Evidence-Based Medicine
KW  - Humans
KW  - Psychomotor Agitation: complications
KW  - Psychomotor Agitation: physiopathology
KW  - Psychomotor Agitation: therapy
KW  - Treatment Outcome
LB  - PUB:(DE-HGF)16
C6  - pmid:26781314
DO  - DOI:10.1007/s00115-015-0041-5
UR  - https://pub.dzne.de/record/138871
ER  -