Prevalence and impact of cerebrovascular pathology in Alzheimer's disease and parkinsonism
Article first published online: 5 JUN 2006
Acta Neurologica Scandinavica
Volume 114, Issue 1, pages 38–46, July 2006
How to Cite
Jellinger, K. A. and Attems, J. (2006), Prevalence and impact of cerebrovascular pathology in Alzheimer's disease and parkinsonism. Acta Neurologica Scandinavica, 114: 38–46. doi: 10.1111/j.1600-0404.2006.00665.x
- Issue published online: 5 JUN 2006
- Article first published online: 5 JUN 2006
- Accepted for publication March 17, 2006
- Alzheimer's disease;
- Braak staging;
- cerebral amyloid angiopathy;
- cerebrovascular pathology;
- clinico-pathological correlations;
- Parkinson's disease
Objective – To study the prevalence and impact of cerebrovascular lesions (CVL) in Alzheimer's disease (AD) and their effects on cognitive impairment.
Material and methods – In study I, the prevalence of vascular lesions in a prospective series of 244 autopsy-proved AD cases (mean age 83.1 ± 8.4 years) and 230 age-matched non-demented controls was examined using immunochemistry and current morphological diagnostic criteria. In study II, in 100 consecutive autopsy cases (mean age 84.3 ± 9.3 years), the incidence of general and capillary cerebral amyloid angiopathy (CAA, CapCAA) was examined.
Results – In study I, AD cases showed significantly more frequent CVL than age-matched controls without differences in the Braak stages, but the severity of CAA was significantly higher in AD brain with associated vascular lesions. In study II, CAA was more frequent in demented than in non-demented patients, but did neither correlate with high-grade AD pathology nor with clinical dementia, whereas CapCAA correlated with both dementia and high Braak stages; the severity of both types of CAA showed only low correlation with each other.
Conclusions – The present data and other studies confirm the importance of CVL in AD and Parkinson's disease without considerable impact on cognitive impairment in progressed stages of AD, and the close association of CapCAA but not of general CAA with clinical dementia and AD pathology.