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阿尔茨海默病中皮质微梗死与认知障碍的关系。

Relationship between cortical microinfarcts and cognitive impairment in Alzheimer's disease.

作者信息

Damasceno Benito P

机构信息

Professor of the Department of Neurology, Medical School, State University of Campinas (UNICAMP), Campinas SP, Brazil.

出版信息

Dement Neuropsychol. 2012 Jul-Sep;6(3):131-136. doi: 10.1590/S1980-57642012DN06030004.

DOI:10.1590/S1980-57642012DN06030004
PMID:29213786
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5618959/
Abstract

Cerebrovascular disease and AD pathology co-exist in most dementia cases, and microinfarcts (MIs), particularly if cortical and multiple, play an additive and independent role in AD cognitive impairment. The main cause of cortical MIs is chronic cerebral hypoperfusion but occlusive vascular diseases, embolism and blood-brain barrier disruptions, isolated or combined, may also play a role. The precise mechanisms by which MIs cause cognitive impairment are not well known, but one plausible explanation is that they are widespread and accompanied by diffuse hypoperfusion, hypoxia, oxidative stress and inflammation, particularly in the watershed areas of the tertiary association cortex, and hence could damage cognition networks and explain many of AD's cognitive and behavioral disturbances. Therefore, it is crucial to control vascular risk factors and avoid uncontrolled use of the antihypertensives, neuroleptics and other sedative drugs frequently prescribed to AD patients.

摘要

在大多数痴呆病例中,脑血管疾病与阿尔茨海默病(AD)病理共存,微梗死灶(MIs),尤其是皮质微梗死灶且为多发时,在AD认知障碍中起累加和独立作用。皮质MIs的主要原因是慢性脑灌注不足,但闭塞性血管疾病、栓塞和血脑屏障破坏,单独或合并出现时也可能起作用。MIs导致认知障碍的确切机制尚不清楚,但一种合理的解释是,它们广泛存在并伴有弥漫性灌注不足、缺氧、氧化应激和炎症,特别是在三级联合皮质的分水岭区域,因此可能损害认知网络,并解释AD的许多认知和行为障碍。因此,控制血管危险因素并避免无节制地使用经常给AD患者开的抗高血压药、抗精神病药和其他镇静药物至关重要。

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本文引用的文献

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