A growing amount of data using light and electron microscopy, immunocytochemistry, uptake of brain markers and metabolic studies suggest that the pathogenesis of Alzheimer's disease may be due to impaired vascular delivery of nutrients to the brain. The bulk of this evidence indicates that cerebral capillary transport of glucose, oxygen and other vital nutrients is dysfunctional in Alzheimer brains due to abnormal hemodynamic flow patterns caused by structural deformities of the capillaries. Clinical disorders which can worsen cerebral blood flow, such as head injury, coronary artery disease, cerebrovascular ischemia or the presence of apolipoprotein E4 allele will increase the risk of Alzheimer's dementia. By contrast, activities that increase cerebral blood flow during aging such as complex thinking patterns or the use of drugs to reduce vascular resistance, such as aspirin or NSAIDs, will reduce the risk or improve the status of Alzheimer's disease. The production of neuritic plaques and neurofibrillary tangles may develop from the hypometabolic abnormalities caused by the impaired cerebromicrovasculature in Alzheimer brains. Such metabolic and cerebral blood flow changes are considerably less significant in age-matched control subjects. The major physiological, pathological and cognitive changes reported for Alzheimer's disease appear to have a common denominator which is reflected by the physically distorted cerebromicrovessels and their inability to optimally deliver nutrients to the brain, a condition which ultimately disturbs neurono-glial homeostasis.