TY - T1的单胺氧化酶B型是扮演一个角色在帕金森病多巴胺能神经细胞死亡?摩根富林明首页-神经学乔-神经病学SP - 1262 LP - 1262 - 10.1212 / WNL.46.5.1262六世- 46 - 5非盟- Philippe双色格子AU -安妮Kastner AU -伊夫Agid AU -艾蒂安c·赫希Y1 - 1996/05/01 UR - //www.ez-admanager.com/content/46/5/1262.abstract N2 -证据支持的角色hyperoxidation现象在神经细胞死亡的机制在帕金森病(PD)。多巴胺的氧化降解,催化单胺氧化酶B型(缺氧),产生自由基,从而可以与退化的过程。出于这个原因,我们通过免疫组织化学方法研究了MAO-B-containing细胞的分布在中脑5 PD患者和5个匹配的对照组。MAO-B-like免疫反应性胶质细胞中发现,纤维,神经元。尽管大部分MAO-B-positive神经元可能属于中缝背的,我们证明了双标记immunohisto-chemistry,其中一些也多巴胺。MAO-B-positive多巴胺神经元是存在于所有dopa-minergic组中脑的控制。在黑质致密部多巴胺能神经元大多数是位于背侧结构的一部分。MAO-B-positive PD中脑多巴胺神经元仍发现。与对照组相比,多巴胺神经元的损失包含缺氧(−45%)不高于MAO-B-negative多巴胺神经元(−59%)。 The density of MAO-B-positive glial cells varied in the control midbrains: high in the least affected dopaminergic group (the central gray substance) and low in the most affected region (the substantia nigra pars compacta). The density of MAO-B-positive glial cells within dopaminergic cell subgroups in control midbrains were negatively correlated (r = −0.94; p <0.02) to the estimated neuronal loss in PD. We conclude that the presence of MAO-B in dopamine-containing neurons does not contribute to vulnerability in PD. Moreover, its presence in some glial cells might have a protective effect against oxidative stress induced by dopamine metabolism. ER -