Abstract

Cognitive deterioration in the elderly caused by Alzheimer’s disease (AD) represents a great sociological, medical, and economic burden. Although the etiology of the disease remains obscure, there is increasing understanding of the pre- and postmortem brain changes. In vivo computed tomography (CT) studies have shown structural changes in the AD brain that are consistent with the reported gross postmortem findings. These CT changes which are associated with the magnitude of the cognitive dysfunction include increasing ventricular size, increasing sulcal prominence, and decreased discrimination between gray and white matter. However, many of these changes occur with normal aging, thus limiting their diagnostic value. Positron emission tomography (PET) studies have found that regional glucose utilization is significantly reduced in AD. This metabolic diminution is strongly related to the magnitude of the cognitive deficit. Importantly, PET studies have not demonstrated a clear normal aging effect and therefore highlight the potential of PET as a diagnostic tool. With the development of short-lived isotopes, PET studies will increasingly use test-retest paradigms to study the capacity of the aging and diseased brain to respond to chemical and behavioral perturbations. Such studies may further enhance the diagnostic utility of PET in AD.

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