Abstract
Introduction Cerebral amyloid angiopathy (CAA) is small vessel disease that occurs commonly in the elderly population. It results in thickening of the vessel wall, primarily in small arteries and arterioles of the leptomeninges and cerebral cortex [1]. It can also affect cerebellar vessels [2]. The primary constituent of the vascular amyloid deposits is the beta-amyloid peptide (Aβ), also the main component of the senile plaques observed in Alzheimer's disease (AD). The earliest detectable vascular Aβ deposits typically occur between the smooth muscle cells of the media and the connective tissue of the adventitia. As the disease progresses, amyloid replaces the media with loss of smooth muscle cells [1]. Autopsy studies indicate that CAA is a common pathology of older individuals, with 10-40% prevalence in the general population and at least 80% among individuals with AD [3]. Although the precise origin of the vascular amyloid has not been definitively established, the predominant source appears to be neuronal [4]. According to this model, Aβ derived from amyloid precursor protein can deposit in the brain parenchyma to form senile plaques or can be carried via the interstitial fluid into the perivascular space to become cerebrovascular deposits in CAA [5]. Deposition of Aβ causes injury to the vessel wall, which can give rise to small infarctions [6,7] or to rupture of the vessel wall, with leakage of blood, and formation of small cerebral microbleeds (CMB) or larger symptomatic intracerebral hemorrhage (ICH).
Original language | English (US) |
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Title of host publication | Cerebral Microbleeds |
Subtitle of host publication | Pathophysiology to Clinical Practice |
Publisher | Cambridge University Press |
Pages | 109-116 |
Number of pages | 8 |
ISBN (Electronic) | 9780511974892 |
ISBN (Print) | 9780521198455 |
DOIs | |
State | Published - Jan 1 2011 |
ASJC Scopus subject areas
- General Medicine