期刊
JOURNAL OF PARKINSONS DISEASE
卷 5, 期 1, 页码 1-19出版社
IOS PRESS
DOI: 10.3233/JPD-140491
关键词
Parkinson disease; alpha-synuclein; post-translational modifications; microglia; T-lymphocyte; innate immunity; adaptive immunity; antigen presentation
资金
- Parkinson Association of Alabama
- National Institute of Neurological Disorders and Stroke [F31-NS076017]
Alpha-synuclein (alpha-syn) is central to the pathogenesis of Parkinson disease (PD). Gene duplications, triplications and point mutations in SNCA1, the gene encoding alpha-syn, cause autosomal dominant forms of PD. Aggregated and post-translationally modified forms of alpha-syn are present in Lewy bodies and Lewy neurites in both sporadic and familial PD, and recent work has emphasized the prion-like ability of aggregated alpha-syn to produce spreading pathology. Accumulation of abnormal forms of alpha-syn is a trigger for PD, but recent evidence suggests that much of the downstream neurodegeneration may result from inflammatory responses. Components of both the innate and adaptive immune systems are activated in PD, and influencing interactions between innate and adaptive immune components has been shown to modify the pathological process in animal models of PD. Understanding the relationship between alpha-syn and subsequent inflammation may reveal novel targets for neuroprotective interventions. In this review, we examine the role of alpha-syn and modified forms of this protein in the initiation of innate and adaptive immune responses.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据