Translational Stroke Research

, Volume 5, Issue 3, pp 330–337 | Cite as

Alzheimer’s Silent Partner: Cerebral Amyloid Angiopathy

Original Article


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.


Complement Microbleed Membrane attack complex C3 LRP1 RAGE 


Amyloid beta


Alzheimer’s disease


Amyloid precursor protein


Brain microbleed


Complement component 3


Cerebral amyloid angiopathy


Intracerebral hemorrhage


Membrane attack complex


Smooth muscle cell


Conflict of Interest

This article does not contain any studies with human or animal subjects. Tanya Cupino and Matthew Zabel declare that they have no conflict of interest.


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Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  1. 1.Neurosurgery Center for Research, Education and TrainingLoma Linda UniversityLoma LindaUSA
  2. 2.Department of Pathology and Human AnatomyLoma Linda UniversityLoma LindaUSA

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