Amyloid Beta and the Cerebral Vasculature

Abstract

The vascular pattern of amyloid beta (Aβ) deposition in the brain is commonly referred to as cerebral amyloid angiopathy (CAA) (1). CAA is an important cause of cerebral hemorrhages and may lead to ischemic infarction and dementia (2). A pure form of CAA, without parenchymal lesions, has been documented in hereditary cerebral hemorrhage, Dutch type, sporadic idiopathic CAA and in cerebrovascular malformations (3, 4, 5). Cerebrovascular amyloid deposition is associated with aging, and CAA is an important feature of several disorders associated with mutations in the amyloid precursor protein (APP) gene, as well as in Down’s syndrome and Alzheimer’s disease (AD) (6, 7, 8). Indeed, CAA is a key pathologic finding in 80–90% of AD cases (9,10). A recent study of 201 autopsy cases of elderly Japanese shows that the incidence and severity of CAA are significantly higher in AD cases compared to non-AD cases (11). Also, some genetic risk factors associated with the AD are involved in the pathogenesis of CAA, including apolipoprotein E (apoE) genotype, presenilin 1, and apantichymotrypsin (12, 13, 14).