THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES CANADIAN NEUROLOGICAL SOCIETY DISTINGUISHED GUEST LECTURE Etiology of Parkinson's Disease: A Research Strategy
THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES CANADIAN NEUROLOGICAL SOCIETY DISTINGUISHED GUEST LECTURE Etiology of Parkinson's Disease: A Research Strategy
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加拿大神经科学杂志加拿大神经病学会杰出客座讲座帕金森病的病因学：研究策略
DOI：
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发表时间：
2003
期刊：
影响因子：
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通讯作者：
A. Barbeau
中科院分区：
文献类型：
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作者：
A. Barbeau
在这篇文章中，我提出了一个新的“全局方法假说”来解释帕金森氏病的病理生理学：“对帕金森氏病的易感性是遗传决定的，并反映在所有细胞中。我认为特发性帕金森病是一个普遍的细胞老化过程的综合结果，在易感个体中，由各种经常重复的触发因素加速。这些因素有一个共同的事实，即它们会导致产生儿茶酚胺的神经元（中枢和外围）的周转短暂增加。这导致这些神经元中自由基的积累。当有毒物质暴露的数量或时间超过细胞的清除能力时，细胞器和膜就会受到损害，通过自身免疫反应对受损的纤维和细胞死亡，特别是脑干的色素神经元，导致路易小体的形成。进行性细胞耗竭导致剩余色素细胞中儿茶酚胺周转量代偿性增加，并不断加速退行性过程。由此导致的基底神经节神经递质失衡解释了帕金森病的症状。”根据这一假设，我们的研究目标应该是：(1)从所有表型中划定真正的帕金森病的界限；(2)识别帕金森易感个体和最常见的触发因素；(3)减少不可避免的触发因素对代谢的影响；(4)通过增加自由基捕获剂的功能利用率来保护易感个体。
In this essay I present a new "global approach hypothesis" to explain the pathophysiology of Parkinson's disease: "Susceptibility to Parkinsonism is genetically determined and is reflected in all cells. I propose that idiopathic Parkinson's disease is the combined result of a generalized cell aging process accelerated, in susceptible individuals, by a variety of often repetitive trigger factors. These factors have in common the fact that they cause a transient increase in turnover within catecholamine producing neurons, centrally as well as peripherally. This results in accumulation within these neurons of free radicals. When the level of the toxic substances, in quantity or in time of exposure, exceeds the scavenging capacity of the cell, damage to organelles and to membranes results, leading to the formation of Lewy bodies through an autoimmune reaction to damaged filaments and to cell death, particularly in the pigmented neurons of the brainstem. The progressive cell depletion leads to a compensatory increase in catecholamine turnover in the remaining pigmented cells, and an ever-accelerating degenerative process. The resulting neurotransmitter imbalance in the basal ganglia explains the symptoms of Parkinson's disease". In the light of this hypothesis, our research objectives should be (1) to delineate the limits of true Parkinson's disease from all phenocopies; (2) to identify individuals susceptible to parkinsonism and the most common trigger factors; (3) to reduce the metabolic effects of unavoidable trigger factors and (4) to protect susceptible individuals by increasing the functional availability of free radical trapping agents.
影响因子：
56.9
作者：
GOLDMAN, JE;YEN, SH;PERESS, NS
通讯作者：
PERESS, NS