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Lookup NU author(s): Professor Raj KalariaORCiD
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Vascular involvement in Alzheimer disease (AD) is not necessarily coincident. Current evidence suggests the neuropathology of Alzheimer type of dementia comprises more than amyloid plaques and neurofibrillary tangles. At least a third of recognized AD cases may exhibit cerebrovascular pathology, which also constitutes distinct small vessel disease. Cerebral amyloid angiopathy, microvascular degeneration affecting the cerebral endothelium and smooth muscle cells, basal lamina alterations, hyalinosis, and fibrosis are frequently evident in AD. These changes may be accompanied by perivascular denervation that is causal in the cognitive decline of AD. In addition, amyloid β protein appears directly involved in the degeneration of both the larger perforating arterial vessels as well as cerebral capillaries, which represent the blood-brain barrier. The cerebrovascular pathology in AD also encompasses macro- and micro-infarctions, hemorrhages, lacunas, and ischemic white-matter changes. An interaction of both perivascular mediators and derived factors would perturb the brain vasculature. Peripheral vascular factors such as long-standing hypertension, atrial fibrillation, coronary or carotid artery disease, and diabetes mellitus are also apparent in AD. These factors would modify the cerebral circulation such that a sustained hypoperfusion or oligemia is impacted upon the aging processes to induce the characteristic pathology.
Author(s): Kalaria RN
Publication type: Article
Publication status: Published
Journal: International Psychogeriatrics
Year: 2003
Volume: 15
Issue: 1
Pages: 47-52
Print publication date: 01/01/2003
ISSN (print): 1041-6102
ISSN (electronic): 1741-203X
Publisher: Cambridge University Press
URL: http://dx.doi.org/10.1017/S1041610203008950
DOI: 10.1017/S1041610203008950
PubMed id: 16191216
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