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Translational Stroke Research

Erschienen in:

01.06.2014 | Original Article

Alzheimer’s Silent Partner: Cerebral Amyloid Angiopathy

verfasst von: Tanya L. Cupino, Matthew K. Zabel

Erschienen in: Translational Stroke Research | Ausgabe 3/2014

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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.

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Titel: Alzheimer’s Silent Partner: Cerebral Amyloid Angiopathy
verfasst von: Tanya L. Cupino
Matthew K. Zabel
Publikationsdatum: 01.06.2014
Verlag: Springer US
Erschienen in: Translational Stroke Research / Ausgabe 3/2014
Print ISSN: 1868-4483
Elektronische ISSN: 1868-601X
DOI: https://doi.org/10.1007/s12975-013-0309-7

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