The results suggest that oligodendroglial overexpression of alpha-synuclein may induce neuroinflammation related to nitrosive stress which is likely to contribute to neurodegeneration in MSA.
We evaluated the pathological features of 102 MSA cases, and presented the pathological spectrum of MSA and initial features of alpha-synuclein accumulation.
Neurological and neurodegenerative alterations in a transgenic mouse model expressing human alpha-synuclein under oligodendrocyte promoter: implications for multiple system atrophy.