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

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Author

  • Daniela Kuzdas-Wood
  • Lisa Fellner
  • Melanie Premstaller
  • Carlijn Borm
  • Bastiaan Bloem
  • Deniz Kirik
  • Gregor K Wenning
  • Nadia Stefanova

Summary, in English

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.

Publishing year

2015

Language

English

Publication/Series

BMC Neuroscience

Volume

16

Issue

1

Document type

Journal article

Publisher

BioMed Central (BMC)

Topic

  • Neurosciences

Status

Published

Research group

  • Brain Repair and Imaging in Neural Systems (BRAINS)

ISBN/ISSN/Other

  • ISSN: 1471-2202