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Synaptic retrogenesis and amyloid-beta in Alzheimer's disease

Wasling, Pontus; Daborg, Jonny; Riebe, Ilse; Andersson, My LU ; Portelius, Erik; Blennow, Kaj LU ; Hanse, Eric and Zetterberg, Henrik LU (2009) In Journal of Alzheimer's Disease 16(1). p.1-14
Abstract

Pathological hallmarks of Alzheimer's disease (AD) include synaptic and neuronal degeneration and the presence of extracellular deposits of amyloid-beta (Abeta) in senile plaques in the cerebral cortex. Although these brain lesions may be seen also in aged non-demented individuals, the increase in brain Abeta is believed by many to represent the earliest event in the disease process. Accumulating evidence suggests that Abeta, which is highly conserved by evolution, may have an important physiological role in synapse elimination during brain development. An intriguing idea is that this putative function can become pathogenic if activated in the aging brain. Here, we review the literature on the possible physiological roles of Abeta and... (More)

Pathological hallmarks of Alzheimer's disease (AD) include synaptic and neuronal degeneration and the presence of extracellular deposits of amyloid-beta (Abeta) in senile plaques in the cerebral cortex. Although these brain lesions may be seen also in aged non-demented individuals, the increase in brain Abeta is believed by many to represent the earliest event in the disease process. Accumulating evidence suggests that Abeta, which is highly conserved by evolution, may have an important physiological role in synapse elimination during brain development. An intriguing idea is that this putative function can become pathogenic if activated in the aging brain. Here, we review the literature on the possible physiological roles of Abeta and its precursor protein AbetaPP during development with special focus on electrophysiological findings.

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author
publishing date
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Contribution to journal
publication status
published
keywords
Alzheimer Disease, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Animals, Brain, Cell Proliferation, Glutamic Acid, Humans, Long-Term Potentiation, Memory, Neuronal Plasticity, Synapses, Journal Article, Research Support, Non-U.S. Gov't, Review
in
Journal of Alzheimer's Disease
volume
16
issue
1
pages
14 pages
publisher
IOS Press
external identifiers
  • scopus:58849151716
ISSN
1387-2877
DOI
10.3233/JAD-2009-0918
language
English
LU publication?
no
id
20ed8f4c-bab5-4790-a345-f4f4bff2c675
date added to LUP
2017-03-30 17:03:16
date last changed
2017-10-08 05:00:33
@article{20ed8f4c-bab5-4790-a345-f4f4bff2c675,
  abstract     = {<p>Pathological hallmarks of Alzheimer's disease (AD) include synaptic and neuronal degeneration and the presence of extracellular deposits of amyloid-beta (Abeta) in senile plaques in the cerebral cortex. Although these brain lesions may be seen also in aged non-demented individuals, the increase in brain Abeta is believed by many to represent the earliest event in the disease process. Accumulating evidence suggests that Abeta, which is highly conserved by evolution, may have an important physiological role in synapse elimination during brain development. An intriguing idea is that this putative function can become pathogenic if activated in the aging brain. Here, we review the literature on the possible physiological roles of Abeta and its precursor protein AbetaPP during development with special focus on electrophysiological findings.</p>},
  author       = {Wasling, Pontus and Daborg, Jonny and Riebe, Ilse and Andersson, My and Portelius, Erik and Blennow, Kaj and Hanse, Eric and Zetterberg, Henrik},
  issn         = {1387-2877},
  keyword      = {Alzheimer Disease,Amyloid beta-Peptides,Amyloid beta-Protein Precursor,Animals,Brain,Cell Proliferation,Glutamic Acid,Humans,Long-Term Potentiation,Memory,Neuronal Plasticity,Synapses,Journal Article,Research Support, Non-U.S. Gov't,Review},
  language     = {eng},
  number       = {1},
  pages        = {1--14},
  publisher    = {IOS Press},
  series       = {Journal of Alzheimer's Disease},
  title        = {Synaptic retrogenesis and amyloid-beta in Alzheimer's disease},
  url          = {http://dx.doi.org/10.3233/JAD-2009-0918},
  volume       = {16},
  year         = {2009},
}