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目的帕金森病是一种常见的神经变性性疾病,其病理特征为中脑黑质多巴胺能神经元的选择性和进行性变性。而近来的临床资料提示,在帕金森病早期,脑桥蓝斑核的去甲肾上腺素能神经元先于黑质发生病变。实验室研究也发现,蓝斑变性后,黑质多巴胺能神经元的电生理状态、神经递质代谢活动会发生改变,对损伤因素的易感性增高,促进了帕金森病的发病。其原因可能为蓝斑通过调节递质释放、摄取毒物、分泌营养物质等方式影响黑质多巴胺能神经元以及该区域的神经胶质细胞,对多巴胺系统起到保护作用。本文综述了帕金森病临床资料中蓝斑的病理表现、以及基础研究中蓝斑与黑质的关系以及蓝斑对黑质起保护作用的可能机制。本综述应能为深入研究帕金森病的发病机制提供参考。
Purpose Parkinson’s disease is a common neurodegenerative disease characterized by its selective and progressive degeneration of mesencephalic dopaminergic neurons. Recent clinical data suggest that in the early stages of Parkinson’s disease, noradrenergic neurons in the Pontine nucleus undergo lesion prior to substantia nigra. Laboratory studies have also found that after the blue spot degeneration, dopaminergic neurons nigral electrophysiological state, neurotransmitter metabolic activity will change, increased susceptibility to injury, and promote the incidence of Parkinson’s disease. The reason may be the blue plaque by regulating the release of neurotransmitters, taking poison, secretion of nutrients and other means affect the substantia nigra dopaminergic neurons and glial cells in the region, play a protective effect on the dopamine system. This review summarizes the pathological findings of blue plaques in clinical data of Parkinson’s disease, as well as the relationship between plaques and substantia nigra in basic research and the possible mechanism by which plaque plays a protective role against the substantia nigra. This review should provide a reference for further study on the pathogenesis of Parkinson’s disease.