The impact of cerebral amyloid angiopathy on the occurrence of cerebrovascular lesions in demented patients with Alzheimer features: a neuropathological study

被引:53
作者
De Reuck, J. [1 ]
Deramecourt, V. [1 ,2 ,3 ,4 ]
Cordonnier, C. [1 ,5 ]
Leys, D. [1 ,5 ]
Maurage, C. A. [1 ,2 ,4 ]
Pasquier, F. [1 ,3 ]
机构
[1] Univ Lille Nord France, UDSL, EA 1056, Lille, France
[2] Lille Univ Hosp, Dept Pathol, Lille, France
[3] Lille Univ Hosp, Memory Clin, Lille, France
[4] INSERM, U837, F-59045 Lille, France
[5] Lille Univ Hosp, Neurovasc Dept, Lille, France
关键词
Alzheimer dementia; cerebral amyloid angiopathy; cortical infarcts; haematomas; micro-bleeds; neuropathology; white matter changes; VASCULAR DEMENTIA; MICROBLEEDS; DISEASE; MICROINFARCTS; HYPERTENSION; PATHOLOGY; SEVERITY;
D O I
10.1111/j.1468-1331.2010.03329.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
100204 [神经病学];
摘要
Objective: The aim of this neuropathological study was to determine the prevalence of the different cerebrovascular lesions to be attributed to cerebral amyloid angiopathy (CAA) and of those associated with the severity of the Alzheimer dementia (AD) itself. Patients and methods: The cerebrovascular lesions were compared separately in 40 brains of patients with mild and 50 with severe AD features. In the two groups, the number of lesions were compared between the brains with severe and those with mild of absent CAA. Results: The age of the patients, the vascular risk factors and antithrombotic treatment were similar in all the compared groups. The brains with mild and severe AD features and with CAA contained more haematomas, cortical micro-infarcts and micro-bleeds, and more severe white matter changes, and cortico-subcortical and white matter mini-bleeds. In the CAA brains with severe AD features, also more cortical territorial infarcts were observed, compared to those with mild AD features. Conclusions: The increase in cortical infarcts cannot be attributed to the CAA alone, but also to the severity of the degenerative features, implying additional vascular factors in the pathogenesis of AD.
引用
收藏
页码:913 / 918
页数:6
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