β-amyloid Peptides and Amyloid Plaques in Alzheimer's Disease.
Gouras, Gunnar LU
; Olsson, Tomas
LU
and Hansson, Oskar
LU
(2015)
In Neurotherapeutics
12(1).
p.3-11
- Abstract
- Many lines of evidence support that β-amyloid (Aβ) peptides play an important role in Alzheimer's disease (AD), the most common cause of dementia. But despite much effort the molecular mechanisms of how Aβ contributes to AD remain unclear. While Aβ is generated from its precursor protein throughout life, the peptide is best known as the main component of amyloid plaques, the neuropathological hallmark of AD. Reduction in Aβ has been the major target of recent experimental therapies against AD. Unfortunately, human clinical trials targeting Aβ have not shown the hoped-for benefits. Thus, doubts have been growing about the role of Aβ as a therapeutic target. Here we review evidence supporting the involvement of Aβ in AD, highlight the... (More)
- Many lines of evidence support that β-amyloid (Aβ) peptides play an important role in Alzheimer's disease (AD), the most common cause of dementia. But despite much effort the molecular mechanisms of how Aβ contributes to AD remain unclear. While Aβ is generated from its precursor protein throughout life, the peptide is best known as the main component of amyloid plaques, the neuropathological hallmark of AD. Reduction in Aβ has been the major target of recent experimental therapies against AD. Unfortunately, human clinical trials targeting Aβ have not shown the hoped-for benefits. Thus, doubts have been growing about the role of Aβ as a therapeutic target. Here we review evidence supporting the involvement of Aβ in AD, highlight the importance of differentiating between various forms of Aβ, and suggest that a better understanding of Aβ's precise pathophysiological role in the disease is important for correctly targeting it for potential future therapy. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4820247
- author
- Gouras, Gunnar
LU
; Olsson, Tomas
LU
and Hansson, Oskar
LU
- organization
- publishing date
- 2015
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Neurotherapeutics
- volume
- 12
- issue
- 1
- pages
- 3 - 11
- publisher
- Springer
- external identifiers
-
- pmid:25371168
- wos:000349541800002
- scopus:84939980592
- pmid:25371168
- ISSN
- 1878-7479
- DOI
- 10.1007/s13311-014-0313-y
- language
- English
- LU publication?
- yes
- id
- 3be7e559-3f38-4cdd-bcac-4b3511f30071 (old id 4820247)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/25371168?dopt=Abstract
- date added to LUP
- 2016-04-01 11:00:44
- date last changed
- 2022-05-18 03:57:18
@article{3be7e559-3f38-4cdd-bcac-4b3511f30071,
abstract = {{Many lines of evidence support that β-amyloid (Aβ) peptides play an important role in Alzheimer's disease (AD), the most common cause of dementia. But despite much effort the molecular mechanisms of how Aβ contributes to AD remain unclear. While Aβ is generated from its precursor protein throughout life, the peptide is best known as the main component of amyloid plaques, the neuropathological hallmark of AD. Reduction in Aβ has been the major target of recent experimental therapies against AD. Unfortunately, human clinical trials targeting Aβ have not shown the hoped-for benefits. Thus, doubts have been growing about the role of Aβ as a therapeutic target. Here we review evidence supporting the involvement of Aβ in AD, highlight the importance of differentiating between various forms of Aβ, and suggest that a better understanding of Aβ's precise pathophysiological role in the disease is important for correctly targeting it for potential future therapy.}},
author = {{Gouras, Gunnar and Olsson, Tomas and Hansson, Oskar}},
issn = {{1878-7479}},
language = {{eng}},
number = {{1}},
pages = {{3--11}},
publisher = {{Springer}},
series = {{Neurotherapeutics}},
title = {{β-amyloid Peptides and Amyloid Plaques in Alzheimer's Disease.}},
url = {{http://dx.doi.org/10.1007/s13311-014-0313-y}},
doi = {{10.1007/s13311-014-0313-y}},
volume = {{12}},
year = {{2015}},
}