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Lookup NU author(s): Professor Raj KalariaORCiD
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Current evidence suggests that the neuropathology of Alzheimer type of dementia comprises more than amyloid plaques and neurofibrillary tangles. At least a third of Alzheimer disease (AD) cases may exhibit significant cerebrovascular pathology, which constitutes distinct small vessel disease (SVD). Cerebral amyloid angiopathy, microvascular degeneration affecting the cerebral endothelium and smooth muscle cells, basal lamina alterations, hyalinosis and fibrosis are often evident in AD. These changes may be accompanied by perivascular denervation that is causal in the cognitive decline of AD. Amyloid β protein may cause degeneration of both the larger perforating arterial vessels as well as cerebral capillaries, which represent the blood-brain barrier. In addition, macro- and microinfarctions, haemorrhages, lacunes and ischaemic white matter changes are also present in AD. The development of SVD in late-onset AD may engage an interaction of perivascular mediators as well as circulation-derived factors that perturb the brain vasculature. Peripheral vascular disease such as longstanding hypertension, atrial fibrillation, coronary or carotid artery disease and diabetes could further modify the cerebral circulation such that a sustained hypoperfusion or oligaemia is impacted upon the ageing brain. Copyright © 2002 S. Karger AG, Basel.
Author(s): Kalaria RN
Publication type: Article
Publication status: Published
Journal: Cerebrovascular Diseases
Year: 2002
Volume: 13
Issue: Suppl. 2
Pages: 48-52
Print publication date: 01/01/2002
ISSN (print): 1015-9770
ISSN (electronic): 1421-9786
Publisher: S. Karger AG
URL: http://dx.doi.org/10.1159/000049150
DOI: 10.1159/000049150
PubMed id: 11901243
Notes: Issue title: Small Vessel Diseases, White Matter Lesions and Vascular Cognitive Impairment, edited by Timo Erkinjuntti and Helmuth Steinmetz. ISBN: 978-3-8055-7390-0.
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