文章基本信息

标题：Axon pathology in Parkinson’s disease and Lewy body dementia hippocampus contains α-, β-, and γ-synuclein
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作者：James E. Galvin ; Kunihiro Uryu ; Virginia M.-Y. Lee 等
期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1999
卷号：96
期号：23
页码：13450-13455
DOI：10.1073/pnas.96.23.13450
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Pathogenic -synuclein (S) gene mutations occur in rare familial Parkinson's disease (PD) kindreds, and wild-type S is a major component of Lewy bodies (LBs) in sporadic PD, dementia with LBs (DLB), and the LB variant of Alzheimer's disease, but {beta}-synuclein ({beta}S) and {gamma}-synuclein ({gamma}S) have not yet been implicated in neurological disorders. Here we show that in PD and DLB, but not normal brains, antibodies to S and {beta}S reveal novel presynaptic axon terminal pathology in the hippocampal dentate, hilar, and CA2/3 regions, whereas antibodies to {gamma}S detect previously unrecognized axonal spheroid-like lesions in the hippocampal dentate molecular layer. The aggregation of other synaptic proteins and synaptic vesicle-like structures in the S- and {beta}S-labeled hilar dystrophic neurites suggests that synaptic dysfunction may result from these lesions. Our findings broaden the concept of neurodegenerative "synucleinopathies" by implicating {beta}S and {gamma}S, in addition to S, in the onset/progression of PD and DLB.
关键词：perforant pathway ; mossy fibers