论文部分内容阅读
1.帕金森氏病的研究进展1960年发现本病患者脑纹状体内多巴胺特异性减少,后来发现,黑质中含黑色素的神经元同时有变性、脱落,机理不明。1983年发现1—甲基—4—苯—四氢吡啶(MPTP)可诱发人和猴的帕金森氏综合征,因与帕金森氏病的病理改变极其类似,推测是帕金森氏病的类似模型。目前认为,到达脑的MPTP积聚到神经元的神经末梢部位,经单胺氧化酶B转变为MPP~+,使黑质神经元变性脱落。MPP~+可损害线粒体的辅酶I,抑制线粒体呼吸,阻碍ATP的产生,导致儿茶酚胺神经元的特异性变性。最近发现与MPTP类似的化学物质四氢异喹啉,(TIQ)与帕金森氏病的病因相关。广部等证明鼠脑内存在TIQ和1—甲基TIQ(IMeTIQ),永津等发现TIQ
1. Parkinson’s disease research progress 1960 found that patients with cerebellar striatum dopamine specificity decreased, later found that substantia nigra contains melanin neurons degeneration, shedding, the mechanism is unknown. In 1983, it was found that 1-methyl-4-phenyl-tetrahydropyridine (MPTP) can induce Parkinson’s syndrome in humans and monkeys, which is similar to the pathological changes of Parkinson’s disease and is presumed to be similar to Parkinson’s disease model. At present, it is believed that the MPTP reaching the brain accumulates to the nerve endings of neurons and is converted to MPP ~ + by monoamine oxidase B, which degenerates the substantia nigra neurons. MPP ~ + can damage the mitochondrial coenzyme I, inhibit mitochondrial respiration, hinder the production of ATP, leading to specific degeneration of catecholamine neurons. Recently, tetrahydroisoquinoline (TIQ), a chemical analogous to MPTP, was found to be associated with the etiology of Parkinson’s disease. Department of other evidence of the existence of brain TIQ and 1-methyl TIQ (IMeTIQ), Yongjin found TIQ