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Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer's disease

Gouras, Gunnar K. LU orcid ; Tampellini, Davide LU ; Takahashi, Reisuke H. and Capetillo-Zarate, Estibaliz (2010) In Acta Neuropathologica 119(5). p.523-541
Abstract

The aberrant accumulation of aggregated β-amyloid peptides (Aβ) as plaques is a hallmark of Alzheimer's disease (AD) neuropathology and reduction of Ab has become a leading direction of emerging experimental therapies for the disease. The mechanism(s) whereby Aβ is involved in the pathophysiology of the disease remain(s) poorly understood. Initially fibrils, and subsequently oligomers of extracellular Aβ have been viewed as the most important pathogenic form of Aβ in AD. More recently, the intraneuronal accumulation of Aβ has been described in the brain, although technical considerations and its relevance in AD have made this a controversial topic. Here, we review the emerging evidence linking intraneuronal Aβ accumulation to the... (More)

The aberrant accumulation of aggregated β-amyloid peptides (Aβ) as plaques is a hallmark of Alzheimer's disease (AD) neuropathology and reduction of Ab has become a leading direction of emerging experimental therapies for the disease. The mechanism(s) whereby Aβ is involved in the pathophysiology of the disease remain(s) poorly understood. Initially fibrils, and subsequently oligomers of extracellular Aβ have been viewed as the most important pathogenic form of Aβ in AD. More recently, the intraneuronal accumulation of Aβ has been described in the brain, although technical considerations and its relevance in AD have made this a controversial topic. Here, we review the emerging evidence linking intraneuronal Aβ accumulation to the development of synaptic pathology and plaques in AD, and discuss the implications of intraneuronal β-amyloid for AD pathology, biology, diagnosis and therapy.

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author
; ; and
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Amyloid, Dementia pugilistica, Endosome, Head injury, Synapse, Tau
in
Acta Neuropathologica
volume
119
issue
5
pages
523 - 541
publisher
Springer
external identifiers
  • scopus:77953019895
  • pmid:20354705
ISSN
0001-6322
DOI
10.1007/s00401-010-0679-9
language
English
LU publication?
no
id
75bec51f-6466-40ce-9fa6-7c5917d059a2
date added to LUP
2020-02-20 14:19:17
date last changed
2024-09-18 19:29:11
@article{75bec51f-6466-40ce-9fa6-7c5917d059a2,
  abstract     = {{<p>The aberrant accumulation of aggregated β-amyloid peptides (Aβ) as plaques is a hallmark of Alzheimer's disease (AD) neuropathology and reduction of Ab has become a leading direction of emerging experimental therapies for the disease. The mechanism(s) whereby Aβ is involved in the pathophysiology of the disease remain(s) poorly understood. Initially fibrils, and subsequently oligomers of extracellular Aβ have been viewed as the most important pathogenic form of Aβ in AD. More recently, the intraneuronal accumulation of Aβ has been described in the brain, although technical considerations and its relevance in AD have made this a controversial topic. Here, we review the emerging evidence linking intraneuronal Aβ accumulation to the development of synaptic pathology and plaques in AD, and discuss the implications of intraneuronal β-amyloid for AD pathology, biology, diagnosis and therapy.</p>}},
  author       = {{Gouras, Gunnar K. and Tampellini, Davide and Takahashi, Reisuke H. and Capetillo-Zarate, Estibaliz}},
  issn         = {{0001-6322}},
  keywords     = {{Amyloid; Dementia pugilistica; Endosome; Head injury; Synapse; Tau}},
  language     = {{eng}},
  month        = {{05}},
  number       = {{5}},
  pages        = {{523--541}},
  publisher    = {{Springer}},
  series       = {{Acta Neuropathologica}},
  title        = {{Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer's disease}},
  url          = {{http://dx.doi.org/10.1007/s00401-010-0679-9}},
  doi          = {{10.1007/s00401-010-0679-9}},
  volume       = {{119}},
  year         = {{2010}},
}