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A deadly spread: cellular mechanisms of α-synuclein transfer.

Steiner, Jennifer LU ; Angot, Elodie LU and Brundin, Patrik LU (2011) In Cell Death and Differentiation 18(9). p.1425-1433
Abstract
Classically, Parkinson's disease (PD) is linked to dopamine neuron death in the substantia nigra pars compacta. Intracytoplasmic protein inclusions named Lewy bodies, and corresponding Lewy neurites found in neuronal processes, are also key features of the degenerative process in the substantia nigra. The molecular mechanisms by which substantia nigra dopamine neurons die and whether the Lewy pathology is directly involved in the cell death pathway are open questions. More recently, it has become apparent that Lewy pathology gradually involves greater parts of the PD brain and is widespread in late stages. In this review, we first discuss the role of misfolded α-synuclein protein, which is the main constituent of Lewy bodies, in the... (More)
Classically, Parkinson's disease (PD) is linked to dopamine neuron death in the substantia nigra pars compacta. Intracytoplasmic protein inclusions named Lewy bodies, and corresponding Lewy neurites found in neuronal processes, are also key features of the degenerative process in the substantia nigra. The molecular mechanisms by which substantia nigra dopamine neurons die and whether the Lewy pathology is directly involved in the cell death pathway are open questions. More recently, it has become apparent that Lewy pathology gradually involves greater parts of the PD brain and is widespread in late stages. In this review, we first discuss the role of misfolded α-synuclein protein, which is the main constituent of Lewy bodies, in the pathogenesis of PD. We then describe recent evidence that α-synuclein might transfer between cells in PD brains. We discuss in detail the possible molecular mechanisms underlying the proposed propagation and the likely consequences for cells that take up α-synuclein. Finally, we focus on aspects of the pathogenic process that could be targeted with new pharmaceutical therapies or used to develop biomarkers for early PD detection.Cell Death and Differentiation advance online publication, 13 May 2011; doi:10.1038/cdd.2011.53. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
prion-like, Parkinson's disease, alpha-synuclein, seeding, aggregation
in
Cell Death and Differentiation
volume
18
issue
9
pages
1425 - 1433
publisher
Nature Publishing Group
external identifiers
  • wos:000293998100005
  • pmid:21566660
  • scopus:80051707299
ISSN
1350-9047
DOI
10.1038/cdd.2011.53
language
English
LU publication?
yes
id
a22c7878-f367-40db-9df8-c1713ba3b946 (old id 1972669)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/21566660?dopt=Abstract
date added to LUP
2011-06-07 19:10:09
date last changed
2017-10-22 03:09:23
@article{a22c7878-f367-40db-9df8-c1713ba3b946,
  abstract     = {Classically, Parkinson's disease (PD) is linked to dopamine neuron death in the substantia nigra pars compacta. Intracytoplasmic protein inclusions named Lewy bodies, and corresponding Lewy neurites found in neuronal processes, are also key features of the degenerative process in the substantia nigra. The molecular mechanisms by which substantia nigra dopamine neurons die and whether the Lewy pathology is directly involved in the cell death pathway are open questions. More recently, it has become apparent that Lewy pathology gradually involves greater parts of the PD brain and is widespread in late stages. In this review, we first discuss the role of misfolded α-synuclein protein, which is the main constituent of Lewy bodies, in the pathogenesis of PD. We then describe recent evidence that α-synuclein might transfer between cells in PD brains. We discuss in detail the possible molecular mechanisms underlying the proposed propagation and the likely consequences for cells that take up α-synuclein. Finally, we focus on aspects of the pathogenic process that could be targeted with new pharmaceutical therapies or used to develop biomarkers for early PD detection.Cell Death and Differentiation advance online publication, 13 May 2011; doi:10.1038/cdd.2011.53.},
  author       = {Steiner, Jennifer and Angot, Elodie and Brundin, Patrik},
  issn         = {1350-9047},
  keyword      = {prion-like,Parkinson's disease,alpha-synuclein,seeding,aggregation},
  language     = {eng},
  number       = {9},
  pages        = {1425--1433},
  publisher    = {Nature Publishing Group},
  series       = {Cell Death and Differentiation},
  title        = {A deadly spread: cellular mechanisms of α-synuclein transfer.},
  url          = {http://dx.doi.org/10.1038/cdd.2011.53},
  volume       = {18},
  year         = {2011},
}