精神科药物治疗对帕金森病患者的影响——为什么老年人比年轻人更严重?

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摘要

精神类药物可能引起药物性帕金森病(MIP)。年龄是其最常见的危险因素和预测因素特发性PD。本文综述了这些关系。背景:MIP可能是由诱发亚临床特发性PD引起的,而特发性PD可能是衰老的一种表现。讨论:衰老可能在特发性PD的发病机制中发挥重要作用,涉及非多巴胺能结构,导致黑质内的应激源级联,降低对损伤的反应能力。线粒体功能障碍和蛋白质降解改变对这些神经元的危害可能比大脑其他部位更大。特发性PD的神经元变性与衰老相同。尽管流行病学确定衰老是帕金森病的危险因素,但生物学相关性仍然难以捉摸。来自衰老的非人类灵长类动物的中脑多巴胺神经元显示出PD中多巴胺神经元退化的已知相关标记。Pang等人声称,大多数80多岁的老人没有帕金森病,这在病因学上挑战了年龄。特发性PD仍然是一个临床诊断,质疑他们的身体检查有多详细。Raghunathan等人评估了PD脑中的糖胺聚糖和蛋白质,并与对照组进行了比较,发现特发性PD与对照组不同,这使人们怀疑PD是一种衰老的表达。环境或遗传因素可能很重要,但年龄仍然是关键,一旦诊断出PD就开始治疗。结论:年龄与特发性帕金森病的预后关系大于病程。MIP可能是由先前存在的特发性PD引发的,需要治疗和进一步的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Parkinsonian Consequences in Patients Treated with Psychotropics-Why Does It Affect the Elderly More so than the Young?
Introduction: Psychotropics may provoke medication induced parkinsonism (MIP). Age is its most common risk factor and predictor for idiopathic PD. This paper reviews these relationships. Background: MIP may result from a trigger evoking subclinical idiopathic PD and idiopathic PD may represent an expression of aging. Discussion: Aging may play a substantive role in the pathogenesis of idiopathic PD, involving nondopaminergic structures, causing a cascade of stressors within the substantia nigra, reducing capacity to respond to insults. Mitochondrial dysfunction and altered protein degradation may be more detrimental to these neurons than elsewhere within the brain. The neurons, degenerating in idiopathic PD, are the same as in aging. Despite epidemiology identifying aging, as the PD risk factor, biological correlates remain elusive. Midbrain dopamine neurons, from aging nonhuman primates, show markers of known correlates of dopamine neuron degeneration, found in PD. Pang et al claim most octogenarian do not have PD, challenging age in its aetiology. Idiopathic PD remains a clinical diagnosis, questioning how detailed was their physical examination. Raghunathan et al evaluated glycosaminoglycans and proteins in PD brains, compared with controls, finding idiopathic PD differed from controls, casting doubt that PD is an expression of aging. Environmental or genetic factors may be important but age remains pivotal with treatment started as soon as the diagnosis of PD is made. Conclusions: Age is more relevant to the prognosis of idiopathic PD than is disease duration. MIP may result from a trigger allowing the expression of pre-existing idiopathic PD, requiring treatment and further investigation.
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