Toggle Main Menu Toggle Search

Open Access padlockePrints

The blood-brain barrier and cerebrovascular pathology in Alzheimer's disease

Lookup NU author(s): Professor Raj KalariaORCiD


Full text for this publication is not currently held within this repository. Alternative links are provided below where available.


The pathology of Alzheimer's disease (AD) is not limited to amyloid plaques and neurofibrillary tangles. Recent evidence suggests that more than 30% of AD cases exhibit cerebrovascular pathology, which involves the cellular elements that represent the blood-brain barrier. Certain vascular lesions such as microvascular degeneration affecting the cerebral endothelium, cerebral amyloid angiopathy and periventricular white matter lesions are evident in virtually all cases of AD. Furthermore, clinical studies have demonstrated blood brain barrier dysfunction in AD patients who exhibit peripheral vascular abnormalities such as hypertension, cardiovascular disease and diabetes. Whether these vascular lesions along with perivascular denervation are coincidental or causal in the pathogenetic processes of AD remains to be defined. In this chapter, I review biochemical and morphological evidence in context with the variable but distinct cerebrovascular pathology described in AD. I also consider genetic influences such as apolipoprotein E in relation to cerebrovascular lesions that may shed light on the pathophysiology of the cerebral vasculature. The compelling vascular pathology associated with AD suggests that transient and focal breach of the blood-brain barrier occurs in late onset AD and may involve an interaction of several factors, which include perivascular mediators as well as peripheral circulation derived factors that perturb the endothelium.

Publication metadata

Author(s): Kalaria RN

Publication type: Conference Proceedings (inc. Abstract)

Publication status: Published

Conference Name: Oxidative/Energy Metabolism in Neurodegenerative Disorders

Year of Conference: 1999

Pages: 113-125

ISSN: 0077-8923

Publisher: Wiley-Blackwell Publishing, Inc.


DOI: 10.1111/j.1749-6632.1999.tb07821.x

PubMed id: 10672233

Library holdings: Search Newcastle University Library for this item

Series Title: Annals of the New York Academy of Sciences

ISBN: 1573312096