期刊
NEUROLOGY
卷 79, 期 24, 页码 2307-2314出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e318278fe32
关键词
-
资金
- Biomedical Laboratory Research and Development Service of the Department of Veterans Affairs
- United States Department of the Army [DAMD17-98-1-8621]
- National Institutes of Health: National Institute of Neurological Disorders and Stroke [5 R01 NS041265]
- National Institute on Aging [1 U01 AG19349, 5 R01 AG017155]
- Office of Research and Development, Medical Research Service Department of Veterans Affairs
- Department of Defense
- NINDS, NIH
- NIA, NIH
- Northwestern Foundation
- Michael J. Fox Foundation
- Department of Veterans Affairs
- NIH
- Michael J. Fox Foundation for Parkinson Research
- Samueli Institute
Objective: To determine whether evidence of neuronal dysfunction or demise preceded deposition of Lewy pathology in vulnerable neurons in Parkinson disease (PD). Methods: We examined the extent of nigral dysfunction and degeneration among 63 normal, incidental Lewy body disease (ILBD), and PD cases based on tyrosine hydroxylase (TH) immunoreactivity and neuron densities, respectively. The relationship between these markers and Lewy pathology (LP) burden in the substantia nigra (SN) and Braak PD stage was assessed. Results: Compared with normal subjects, ILBD cases displayed a significantly higher percentage of TH-negative cells and lower neuronal densities in the SN as early as Braak PD stages 1 and 2, before LP deposition in the nigrostriatal system. ILBD nigral neuron densities were intermediate between normal subjects and PD cases, and TH-negative percentages were higher in ILBD than either normal or PD cases. Furthermore, neuron density and neuronal dysfunction levels remained relatively constant across Braak PD stages in ILBD. Conclusions: These results suggest that significant neurodegeneration and cellular dysfunction precede LP in the SN, challenging the pathogenic role of LP in PD and the assumption that ILBD always represents preclinical PD. Neurology (R) 2012; 79: 2307-2314
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