本文由小咖机器人翻译整理

期刊来源：Lancet

原文链接：https://doi.org/10.1016/S0140-6736(23)01478-2

摘要内容如下：

帕金森病是一种与聚集的α-突触核蛋白沉积相关的渐进性神经退行性疾病。从遗传学和分子病理学的角度深入了解帕金森病的发病机制。生化研究、帕金森病患者移植神经元的研究以及细胞和动物模型研究表明，α-突触核蛋白的异常聚集以及肠道、脑干和高级脑区之间的病理扩散可能是帕金森病发生和发展的基础。在细胞水平上，线粒体、溶酶体和内涵体功能异常可以在单基因和散发性帕金森病中发现，这提示了多种潜在的治疗方法。最近的研究还强调了可能在肠道中触发的免疫适应不良和炎症反应，这加速了帕金森病的发病机制。虽然目前还没有针对帕金森病的疾病改善疗法，但我们现在有了开发合理的神经保护疗法的坚实基础，我们希望这些疗法能够阻止这种致残性神经疾病的发展。

英文原文如下：

Abstracts

Parkinson's disease is a progressive neurodegenerative condition associated with the deposition of aggregated α-synuclein. Insights into the pathogenesis of Parkinson's disease have been derived from genetics and molecular pathology. Biochemical studies, investigation of transplanted neurons in patients with Parkinson's disease, and cell and animal model studies suggest that abnormal aggregation of α-synuclein and spreading of pathology between the gut, brainstem, and higher brain regions probably underlie the development and progression of Parkinson's disease. At a cellular level, abnormal mitochondrial, lysosomal, and endosomal function can be identified in both monogenic and sporadic Parkinson's disease, suggesting multiple potential treatment approaches. Recent work has also highlighted maladaptive immune and inflammatory responses, possibly triggered in the gut, that accelerate the pathogenesis of Parkinson's disease. Although there are currently no disease-modifying treatments for Parkinson's disease, we now have a solid basis for the development of rational neuroprotective therapies that we hope will halt the progression of this disabling neurological condition.

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