title: Alzheimer's silent partner: cerebral amyloid angiopathy.
abstract: Alzheimer's disease (AD) is the most common form of dementia, which completely lacks a viable, long-term therapeutic intervention. This is partly due to an incomplete understanding of AD etiology and the possible confounding factors associated with its genotypic and phenotypic heterogeneity. Cerebral amyloid angiopathy (CAA) is a common, yet frequently overlooked, pathology associated with AD. CAA manifests with deposition amyloid-beta (Aβ) within the smooth muscle layer of cerebral arteries and arterioles. The role of Aβ in AD and CAA pathophysiology has long been controversial. Although it has demonstrated toxicity at super-physiological levels in vitro, Aβ load does not necessarily correlate with cognitive demise in humans. In this review, we describe the contributions of CAA to AD pathophysiology and important pathomechanisms that may lead to vascular fragility and hemorrhages. Additionally, we discuss the effect of Aβ on smooth muscle cell phenotype and viability, especially in terms of the complement cascade.
authors: Neurosurgery Center for Research, Education and Training, Loma Linda University, Loma Linda, CA, USA.
authors: Tanya L
authors: TL
authors: Cupino
authors: Matthew K
authors: MK
authors: Zabel
mesh_terms: D000544:Alzheimer Disease / Q000150:complications* / Q000378:metabolism; D016657:Cerebral Amyloid Angiopathy / Q000150:complications* / Q000378:metabolism; D006801:Humans; D032389:Myocytes, Smooth Muscle / Q000473:pathology