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

• Published in: European journal of neurology Vol. 18; no. 6; pp. 913 - 918
• Main Authors: De Reuck, J., Deramecourt, V., Cordonnier, C., Leys, D., Maurage, C. A., Pasquier, F.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.06.2011; John Wiley & Sons, Inc
• Subjects: Age; Aged; Aged, 80 and over; Alzheimer dementia; Alzheimer Disease - drug therapy; Alzheimer Disease - epidemiology; Alzheimer Disease - pathology; Alzheimer's disease; Brain; Brain Infarction - epidemiology; Brain Infarction - pathology; Brain Infarction - physiopathology; Cerebral amyloid angiopathy; Cerebral Amyloid Angiopathy - drug therapy; Cerebral Amyloid Angiopathy - epidemiology; Cerebral Amyloid Angiopathy - pathology; Cerebral Arteries - pathology; Cerebral Arteries - physiopathology; Comorbidity; cortical infarcts; Dementia disorders; Female; Fibrinolytic Agents - therapeutic use; haematomas; Hematoma; Humans; Male; micro-bleeds; Neurodegenerative diseases; Neuropathology; Prevalence; Risk factors; Severity of Illness Index; Substantia alba; white matter changes
• ISSN: 1351-5101; 1468-1331
• DOI: 10.1111/j.1468-1331.2010.03329.x

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.