科研之友
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摘要
Multiple systems atrophy (MSA) is a neurodegenerative disorder characterized by oligodendrocytic accumulations of alpha-synuclein (alpha syn). Oxidative stress is a key mechanism proposed to underlie MSA pathology. To address the role of asyn modifications, over and above general oxidative modifications, this study examined the effects of 3-nitropropionic acid (3NP) administration, a technique used to model MSA, in knock-out mice lacking alpha syn (alpha synKO). Although susceptible to 3NP-induced oxidative stress, asynKO mice display reduced neuronal loss and dendritic pathology. The alpha synKO mice are resistant to 3NP-induced motor deficits and display attenuated loss of tyrosine hydroxylase and dopamine transporter striatal immunoreactivity. The results suggest that deficits in MSA are not due to general oxidative protein modification but in addition may be related to specific alpha syn modifications.
- 出版日期2010-4-21
