Abstract

A solid body of evidence has accumulated over the past 20 years confirming the critical role of cerebrovascular disease in Alzheimer disease (AD) and other dementias of the aged.1–6 Most recently, data from the National Alzheimer's Coordinating Center7 demonstrated the presence of vascular pathology in 79.9% of 4,629 brains from patients with neuropathologically confirmed AD. Lesions included atherosclerosis in the circle of Willis, arteriosclerotic leukoencephalopathy, arteriolosclerosis, large infarcts, lacunes, multiple microinfarcts, and hemorrhages. Notably, cerebral amyloid angiopathy was present in less than half of the brains (40.8%). Given the absence of an effective treatment to halt the progression of AD, the current emphasis is on dementia prevention by appropriate treatment of vascular risk factors for stroke.8,9 Once stroke occurs, optimal treatment of the acute ictus with prompt restoration of flow in the occluded vessels improves the cognitive outcome. In contrast, stroke complications such as aspiration pneumonia, hypoxemia, seizures, hypotension, or cardiac arrhythmias increase the risk of poststroke cognitive impairment 4-fold.10

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