Translational Stroke Research

, Volume 5, Issue 3, pp 330–337

Alzheimer’s Silent Partner: Cerebral Amyloid Angiopathy

Authors

  • Tanya L. Cupino
    • Neurosurgery Center for Research, Education and TrainingLoma Linda University
    • Department of Pathology and Human AnatomyLoma Linda University
Original Article

DOI: 10.1007/s12975-013-0309-7

Cite this article as:
Cupino, T.L. & Zabel, M.K. Transl. Stroke Res. (2014) 5: 330. doi:10.1007/s12975-013-0309-7

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.

Keywords

ComplementMicrobleedMembrane attack complexC3LRP1RAGE

Abbreviations

Amyloid beta

AD

Alzheimer’s disease

APP

Amyloid precursor protein

BMB

Brain microbleed

C3

Complement component 3

CAA

Cerebral amyloid angiopathy

ICH

Intracerebral hemorrhage

MAC

Membrane attack complex

SMC

Smooth muscle cell

Copyright information

© Springer Science+Business Media New York 2013