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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)
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author
organization
publishing date
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
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
2014-12-01 19:12:31
date last changed
2017-11-05 03:22:39
@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},
  volume       = {12},
  year         = {2015},
}