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Overexpression of α-synuclein in oligodendrocytes does not increase susceptibility to focal striatal excitotoxicity.

Kuzdas-Wood, Daniela; Fellner, Lisa; Premstaller, Melanie; Borm, Carlijn; Bloem, Bastiaan; Kirik, Deniz LU ; Wenning, Gregor K and Stefanova, Nadia (2015) In BMC Neuroscience 16(1).
Abstract
Multiple system atrophy (MSA) is a fatal adult-onset neurodegenerative disease characterized by α-synuclein (α-syn) positive oligodendroglial cytoplasmic inclusions. The latter are associated with a neuronal multisystem neurodegeneration targeting central autonomic, olivopontocerebellar and striatonigral pathways, however the underlying mechanisms of neuronal cell death are poorly understood. Previous experiments have shown that oligodendroglial α-syn pathology increases the susceptibility to mitochondrial stress and proteasomal dysfunction leading to enhanced MSA-like neurodegeneration. Here we analyzed whether oligodendroglial α-syn overexpression in a transgenic mouse model of MSA synergistically interacts with focal neuronal... (More)
Multiple system atrophy (MSA) is a fatal adult-onset neurodegenerative disease characterized by α-synuclein (α-syn) positive oligodendroglial cytoplasmic inclusions. The latter are associated with a neuronal multisystem neurodegeneration targeting central autonomic, olivopontocerebellar and striatonigral pathways, however the underlying mechanisms of neuronal cell death are poorly understood. Previous experiments have shown that oligodendroglial α-syn pathology increases the susceptibility to mitochondrial stress and proteasomal dysfunction leading to enhanced MSA-like neurodegeneration. Here we analyzed whether oligodendroglial α-syn overexpression in a transgenic mouse model of MSA synergistically interacts with focal neuronal excitotoxic damage generated by a striatal injection of quinolinic acid (QA) to affect the degree of striatal neuronal loss. (Less)
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organization
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type
Contribution to journal
publication status
published
subject
in
BMC Neuroscience
volume
16
issue
1
publisher
BioMed Central
external identifiers
  • pmid:26627686
  • wos:000365855200001
  • scopus:84949187635
ISSN
1471-2202
DOI
10.1186/s12868-015-0227-6
language
English
LU publication?
yes
id
35486abc-ce20-4076-8fc3-3e36f0190ab4 (old id 8505878)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/26627686?dopt=Abstract
date added to LUP
2016-01-04 20:15:35
date last changed
2017-01-01 05:21:37
@article{35486abc-ce20-4076-8fc3-3e36f0190ab4,
  abstract     = {Multiple system atrophy (MSA) is a fatal adult-onset neurodegenerative disease characterized by α-synuclein (α-syn) positive oligodendroglial cytoplasmic inclusions. The latter are associated with a neuronal multisystem neurodegeneration targeting central autonomic, olivopontocerebellar and striatonigral pathways, however the underlying mechanisms of neuronal cell death are poorly understood. Previous experiments have shown that oligodendroglial α-syn pathology increases the susceptibility to mitochondrial stress and proteasomal dysfunction leading to enhanced MSA-like neurodegeneration. Here we analyzed whether oligodendroglial α-syn overexpression in a transgenic mouse model of MSA synergistically interacts with focal neuronal excitotoxic damage generated by a striatal injection of quinolinic acid (QA) to affect the degree of striatal neuronal loss.},
  articleno    = {86},
  author       = {Kuzdas-Wood, Daniela and Fellner, Lisa and Premstaller, Melanie and Borm, Carlijn and Bloem, Bastiaan and Kirik, Deniz and Wenning, Gregor K and Stefanova, Nadia},
  issn         = {1471-2202},
  language     = {eng},
  number       = {1},
  publisher    = {BioMed Central},
  series       = {BMC Neuroscience},
  title        = {Overexpression of α-synuclein in oligodendrocytes does not increase susceptibility to focal striatal excitotoxicity.},
  url          = {http://dx.doi.org/10.1186/s12868-015-0227-6},
  volume       = {16},
  year         = {2015},
}