Intraneuronal Aβ accumulation and origin of plaques in Alzheimer's disease
Gouras, Gunnar K. LU
; Almeida, Claudia G.
and Takahashi, Reisuke H.
(2005)
In Neurobiology of Aging
26(9).
p.1235-1244
- Abstract
Plaques are a defining neuropathological hallmark of Alzheimer's disease (AD) and the major constituent of plaques, the β-amyloid peptide (Aβ), is considered to play an important role in the pathophysiology of AD. But the biological origin of Aβ plaques and the mechanism whereby Aβ is involved in pathogenesis have been unknown. Aβ plaques were thought to form from the gradual accumulation and aggregation of secreted Aβ in the extracellular space. More recently, the accumulation of Aβ has been demonstrated to occur within neurons with AD pathogenesis. Moreover, intraneuronal Aβ accumulation has been reported to be critical in the synaptic dysfunction, cognitive dysfunction and the formation of plaques in AD. Here we provide a historical... (More)
Plaques are a defining neuropathological hallmark of Alzheimer's disease (AD) and the major constituent of plaques, the β-amyloid peptide (Aβ), is considered to play an important role in the pathophysiology of AD. But the biological origin of Aβ plaques and the mechanism whereby Aβ is involved in pathogenesis have been unknown. Aβ plaques were thought to form from the gradual accumulation and aggregation of secreted Aβ in the extracellular space. More recently, the accumulation of Aβ has been demonstrated to occur within neurons with AD pathogenesis. Moreover, intraneuronal Aβ accumulation has been reported to be critical in the synaptic dysfunction, cognitive dysfunction and the formation of plaques in AD. Here we provide a historical overview on the origin of plaques and a discussion on potential biological and therapeutic implications of intraneuronal Aβ accumulation for AD.
(Less)
- author
- Gouras, Gunnar K.
LU
; Almeida, Claudia G.
and Takahashi, Reisuke H.
- publishing date
- 2005-10
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Alzheimer, Amyloid, Endosome, Multivesicular body, Proteasome, Synapse, Ubiquitin
- in
- Neurobiology of Aging
- volume
- 26
- issue
- 9
- pages
- 1235 - 1244
- publisher
- Elsevier
- external identifiers
-
- pmid:16023263
- scopus:25144501662
- ISSN
- 0197-4580
- DOI
- 10.1016/j.neurobiolaging.2005.05.022
- language
- English
- LU publication?
- no
- id
- 63c709a0-e9f0-44bf-95a7-826493b08d78
- date added to LUP
- 2020-02-20 14:23:24
- date last changed
- 2024-06-12 10:17:21
@article{63c709a0-e9f0-44bf-95a7-826493b08d78,
abstract = {{<p>Plaques are a defining neuropathological hallmark of Alzheimer's disease (AD) and the major constituent of plaques, the β-amyloid peptide (Aβ), is considered to play an important role in the pathophysiology of AD. But the biological origin of Aβ plaques and the mechanism whereby Aβ is involved in pathogenesis have been unknown. Aβ plaques were thought to form from the gradual accumulation and aggregation of secreted Aβ in the extracellular space. More recently, the accumulation of Aβ has been demonstrated to occur within neurons with AD pathogenesis. Moreover, intraneuronal Aβ accumulation has been reported to be critical in the synaptic dysfunction, cognitive dysfunction and the formation of plaques in AD. Here we provide a historical overview on the origin of plaques and a discussion on potential biological and therapeutic implications of intraneuronal Aβ accumulation for AD.</p>}},
author = {{Gouras, Gunnar K. and Almeida, Claudia G. and Takahashi, Reisuke H.}},
issn = {{0197-4580}},
keywords = {{Alzheimer; Amyloid; Endosome; Multivesicular body; Proteasome; Synapse; Ubiquitin}},
language = {{eng}},
number = {{9}},
pages = {{1235--1244}},
publisher = {{Elsevier}},
series = {{Neurobiology of Aging}},
title = {{Intraneuronal Aβ accumulation and origin of plaques in Alzheimer's disease}},
url = {{http://dx.doi.org/10.1016/j.neurobiolaging.2005.05.022}},
doi = {{10.1016/j.neurobiolaging.2005.05.022}},
volume = {{26}},
year = {{2005}},
}