ArticleBMC neuroscience2015
Overexpression of α-synuclein in oligodendrocytes does not increase susceptibility to focal striatal excitotoxicity.
Article in BMC neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Multiple System Atrophy: An Oligodendroglioneural Synucleinopathy1.Journal of Alzheimer's disease : JAD · 2018Review
- Multiple system atrophy: pathogenic mechanisms and biomarkers.Journal of neural transmission (Vienna, Austria : 1996) · 2016Review
- Review: Multiple system atrophy: emerging targets for interventional therapies.Neuropathology and applied neurobiology · 2016Review
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundMultiple 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.
resultsQA injury led to comparable striatal neuronal loss and optical density of astro- and microgliosis in the striatum of transgenic and control mice. Respectively, no differences were identified in drug-induced rotation behavior or open field behavior between the groups.
conclusionsThe failure of oligodendroglial α-syn pathology to exacerbate striatal neuronal loss resulting from QA excitotoxicity contrasts with enhanced striatal neurodegeneration due to oxidative or proteolytic stress, suggesting that enhanced vulnerability to excitotoxicity does not occur in oligodendroglial α-synucleinopathy like MSA.
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