The Blood-Brain Barrier and Cerebrovascular Pathology in Alzheimer's Disease

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 lesio...

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Bibliographic Details
Published in:Annals of the New York Academy of Sciences 1999-11, Vol.893 (1), p.113-125
Main Author: KALARIA, RAJ N.
Format: Article
Language:English
Subjects:
Alzheimer Disease - pathology
Alzheimer Disease - physiopathology
Blood-Brain Barrier
Brain - pathology
Cerebrovascular Circulation
Endothelium, Vascular - pathology
Humans
Microcirculation - pathology
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Summary: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. These vascular abnormalities are likely to worsen cognitive disability in AD.
ISSN:0077-8923
1749-6632
DOI:10.1111/j.1749-6632.1999.tb07821.x