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帕金森病认知障碍的神经生物学。

Neurobiology of cognitive impairment in Parkinson's disease.

机构信息

Institute of Clinical Neurobiology, Kenyongasse 18, A-1070 Vienna, Austria.

出版信息

Expert Rev Neurother. 2012 Dec;12(12):1451-66. doi: 10.1586/ern.12.131.

Abstract

Cognitive impairment is a frequent complication of Parkinson's disease (PD). Mild cognitive impairment (MCI) may progress to dementia more frequently and rapidly. PD dementia (PDD) and PD-MCI have a mean prevalence up to 75% each; a four- to six-times increased incidence rate compared with controls. Recent diagnostic clinical criteria for both PDD and PD-MCI require validation. Cognitive decline in PD can be probed clinically, comprehensive neuropsychological assessment being the best way to define it. Neuroimaging in both disorders revealed cortical atrophy, hypometabolism, white matter changes, dopaminergic/cholinergic dysfunction and increased amyloid burden. Combined analysis of imaging and cerebrospinal fluid markers (tau and Aβ-42) is the most promising method for indentifying PD-MCI and PDD. Morphological substrates are a combination of Lewy and Alzheimer pathologies causing destruction of essential neuronal networks. PDD and dementia with Lewy bodies are considered similar parts of a disease spectrum. Treatment with cholinesterase inhibitors revealed mild-to-moderate results.

摘要

认知障碍是帕金森病(PD)的常见并发症。轻度认知障碍(MCI)可能更频繁、更迅速地进展为痴呆症。PD 痴呆(PDD)和 PD-MCI 的患病率分别高达 75%;与对照组相比,发病率增加了四到六倍。最近的 PDD 和 PD-MCI 的诊断临床标准需要验证。PD 中的认知下降可以通过临床检测来探究,全面的神经心理学评估是定义认知下降的最佳方法。这两种疾病的神经影像学显示皮质萎缩、代谢低下、白质变化、多巴胺能/胆碱能功能障碍和淀粉样蛋白负荷增加。对影像学和脑脊液标志物(tau 和 Aβ-42)的综合分析是识别 PD-MCI 和 PDD 的最有前途的方法。形态学底物是路易体和阿尔茨海默病病理学的组合,导致关键神经元网络的破坏。PDD 和路易体痴呆被认为是疾病谱的相似部分。胆碱酯酶抑制剂的治疗显示出轻度至中度的效果。

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