PARKINSON'S DISEASE, AUTOIMMUNITY, AND OLFACTION
PARKINSON'S DISEASE, AUTOIMMUNITY, AND OLFACTION
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DOI：
10.3109/00207450903178786
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发表时间：
2009-01-01
影响因子：
2.2
通讯作者：
Shoenfeld, Yehuda
中科院分区：
文献类型：
--
作者：
Benkler, Michal;Agmon-Levin, Nancy;Shoenfeld, Yehuda
帕金森病（PD）是一种常见的进行性神经退行性疾病，主要分类为运动障碍，表现为嗅觉功能障碍等非运动症状。这种疾病的发病机制尚未阐明，但它似乎与一系列复杂的遗传、环境和免疫相互作用相互关联。本综述通过描述黑质和脑脊液 (CSF) 内的先天免疫成分（包括补体和细胞因子）的增加，揭示了在 PD 患者中观察到的免疫改变。这些改变延伸到适应性免疫反应，PD患者外周血和脑脊液中T细胞和自身抗体（抗α-突触核蛋白和抗GM1神经节苷脂）升高。有趣的是，最近出现了另一种致病三联征，通过嗅觉功能障碍将帕金森病与自身免疫联系起来。嗅觉缺陷是帕金森病最早的症状之一，也是一项独特的观察结果，表明嗅觉下降是自身免疫机制的结果。因此，我们考虑了几种因其嗅觉后果而闻名的无可争议的自身免疫性疾病作为模板示例，这些示例可能会更多地阐明自身免疫与 PD 之间的关系。我们希望了解这种疾病的本质可以为成功阻止进行性神经退行性过程奠定基础。
Parkinson's disease (PD) is a common progressive neurodegenerative disorder, mainly classified as a movement disorder which manifests among others nonmotor symptoms such as olfactory dysfunction. The etiopathogenesis of this disease has yet to be elucidated, though it seems to be interconnected with a complex set of genetic, environmental, and immunological interactions. This review unfolds the immune alterations observed in PD patients by describing the increase in the innate immune components including complement and cytokines within their substantia nigra and cerebrospinal fluid (CSF). These alterations extended to the adaptive immune response with the elevation of T cells and autoantibodies (anti-a-synuclein and anti-GM1-ganglioside) in the peripheral blood and CSF of PD patients. Interestingly, another etiopathogenic triad has recently emerged linking PD to autoimmunity through olfactory dysfunction. Smell deficit is one of the earliest signs of PD and a unique observation suggesting olfactory declines to be a consequence of autoimmune mechanisms. Therefore, we considered several undisputed autoimmune diseases known for their olfactory consequences as template examples that may shed more light on the relationship between autoimmunity and PD. We hope that understanding the nature of this disease may lay the ground for successes in the quest to halt the progressive neurodegenerative process.