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大量饮酒与神经病理学损伤:一项人体死后研究。

Heavy alcohol consumption and neuropathological lesions: a post-mortem human study.

机构信息

Department of Clinical Medicine, Unit of Neurology, Kuopio University, Kuopio, Finland.

出版信息

J Neurosci Res. 2009 Sep;87(12):2786-92. doi: 10.1002/jnr.22091.

Abstract

Epidemiological studies have indicated that excessive alcohol consumption leads to cognitive impairment, but the specific pathological mechanism involved remains unknown. The present study evaluated the association between heavy alcohol intake and the neuropathological hallmark lesions of the three most common neurodegenerative disorders, i.e., Alzheimer's disease (AD), dementia with Lewy bodies (DLB), and vascular cognitive impairment (VCI), in post-mortem human brains. The study cohort was sampled from the subjects who underwent a medicolegal autopsy during a 6-month period in 1999 and it included 54 heavy alcohol consumers and 54 age- and gender-matched control subjects. Immunohistochemical methodology was used to visualize the aggregation of beta-amyloid, hyperphosphorylated tau, and alpha-synuclein and the extent of infarcts. In the present study, no statistically significant influence was observed for alcohol consumption on the extent of neuropathological lesions encountered in the three most common degenerative disorders. Our results indicate that alcohol-related dementia differs from VCI, AD, and DLB; i.e., it has a different etiology and pathogenesis.

摘要

流行病学研究表明,过量饮酒可导致认知障碍,但具体的病理机制尚不清楚。本研究评估了大量饮酒与三种最常见的神经退行性疾病(即阿尔茨海默病(AD)、路易体痴呆(DLB)和血管性认知障碍(VCI))的神经病理学标志病变之间的关联,这些病变取自于 1999 年 6 个月期间进行法医解剖的受试者的脑组织样本。研究队列包括 54 名大量饮酒者和 54 名年龄和性别匹配的对照组。免疫组织化学方法用于可视化β-淀粉样蛋白、过度磷酸化的 tau 和α-突触核蛋白的聚集以及梗死的程度。在本研究中,未观察到饮酒对三种最常见退行性疾病中遇到的神经病理学病变程度有统计学显著影响。我们的结果表明,酒精相关痴呆与 VCI、AD 和 DLB 不同;即,它具有不同的病因和发病机制。

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