Premium
The relationship between cerebral amyloid angiopathy and cortical microinfarcts in brain ageing and A lzheimer's disease
Author(s) -
Kövari E.,
Herrmann F. R.,
Hof P. R.,
Bouras C.
Publication year - 2013
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/nan.12003
Subject(s) - cerebral amyloid angiopathy , pathology , autopsy , dementia , medicine , pathogenesis , population , angiopathy , alzheimer's disease , pittsburgh compound b , amyloid (mycology) , lesion , cerebral cortex , disease , endocrinology , diabetes mellitus , environmental health
Aims Cerebral amyloid angiopathy ( CAA ) represents the deposition of amyloid β protein ( Aβ ) in the meningeal and intracerebral vessels. It is often observed as an accompanying lesion of Alzheimer's disease ( AD ) or in the brain of elderly individuals even in the absence of dementia. CAA is largely age‐dependent. In subjects with severe CAA a higher frequency of vascular lesions has been reported. The goal of our study was to define the frequency and distribution of CAA in a 1‐year autopsy population (91 cases) from the D epartment of I nternal M edicine, R ehabilitation, and G eriatrics, G eneva. Materials and methods Five brain regions were examined, including the hippocampus, and the inferior temporal, frontal, parietal and occipital cortex, using an antibody against Aβ, and simultaneously assessing the severity of AD ‐type pathology with B raak stages for neurofibrillary tangles identified with an anti‐tau antibody. In parallel, the relationships of CAA with vascular brain lesions were established. Results CAA was present in 53.8% of the studied population, even in cases without AD (50.6%). The strongest correlation was seen between CAA and age, followed by the severity of amyloid plaques deposition. Microinfarcts were more frequent in cases with CAA ; however, our results did not confirm a correlation between these parameters. Conclusion The present data show that CAA plays a role in the development of microvascular lesions in the ageing brain, but cannot be considered as the most important factor in this vascular pathology, suggesting that other mechanisms also contribute importantly to the pathogenesis of microvascular changes.