Abstract
Cerebral amyloid angiopathy (CAA) is an age-associated disease characterized by amyloid deposition in cerebral and meningeal vessel walls. CAA is detected in the majority of the individuals with dementia and also in a large number of non-demented elderly individuals. In addition, CAA is strongly associated with Alzheimer's disease (AD) pathology. Mechanical consequences including intra-cerebral or subarachnoid hemorrhage remains CAA most feared complication, but only a small fraction of CAA results in severe bleeding. On the hand the non-mechanical consequences in cerebrovascular regulation are prevalent and may be even more deleterious. Studies of animal models have provided strong evidence linking the vasoactive Aβ 1-40, the main species found in CAA, to disturbances in endothelial-dependent factors, disrupting cerebrovascular regulation Here, we aimed to review experimental findings regarding the non-mechanical consequences of CAA for cerebrovascular regulation and discuss the implications of these results to clinical practice.
Original language | English |
---|---|
Pages (from-to) | 838-842 |
Number of pages | 5 |
Journal | Experimental Gerontology |
Volume | 47 |
Issue number | 11 |
DOIs | |
State | Published - Nov 2012 |
Keywords
- Alzheimer's disease
- Amyloid
- Angiopathy
- Animal models
- Blood brain barrier
- Cerebrovascular dysfunction
- Dementia
- Endothelium