Abstract
1. The amyloid B-peptide (AB) is involved in the mechanisms of Alzheimer dementia. This paper reviews experimental evidence indicating that AB exerts profound effects on the regulation of the cerebral circulation. 2. Thus, AB compromises the ability of cerebral endothelial cells to produce vascular relaxing factors, impairs the ability of cerebral blood vessels to maintain adequate flow during hypotension, and attenuates the increases in CBF evoked by enhanced brain activity. 3. Studies in transgenic mice overexpressing the amyloid precursor protein suggest that these cerebrovascular alterations disrupt the delicate balance between the brain's energy requirements and cerebral blood supply, rendering the brain more vulnerable to ischemic injury. 4. The findings support the recently emerged notion that vascular factors play a pathogenic role in the early stages of Alzheimer dementia.