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The pattern of changes in cerebral glucose metabolism occurring with normal aging has been unclear. Advances in imaging technology, such as improved resolution and anatomical referencing, allow for more precise regional measurement than previously possible. This study explored cerebral glucose metabolism in 17 normal controls ranging in age from 20 to 74 years. High resolution PET scanning, with MRI-based regions of interest correcting for partial volume and atrophy effects, revealed a linear association between advancing age and declining cerebral glucose metabolism. The decline averaged 8% per decade for the whole brain. Changes were most pronounced in limbic structures, and could be implicated in age-associated memory loss.

Regional cerebral glucose metabolism was surveyed in 37 Alzheimer''s disease (AD) patients and 21 normal controls using positron emission tomography. Where possible, brain regions were specified according to their neurobehavioral function rather than as anatomically demarcated structures. Absolute metabolic values revealed significant differences (p < 0.05) between AD patients and controls for whole brain and the more superior supratentorial brain slices. Normalized values (region/brain stem) showed the most striking declines (p < 0.001) in the association cortex (heteromodal region -21%; unimodal region -19%) and the primary sensory-motor cortex (-13%), with motor, auditory, and visual areas more affected than somatosensory areas. Limbic and para-limbic systems were equally affected (-14%; -11%; p < 0.001). Thalamus, striatum, cerebellum and brain stem were minimally or not affected. Neurobehaviorally defined hypometabolic regions largely parallel affected areas noted in anatomic and previous metabolic studies, with the possible exception of metabolic deficits in the primary sensory-motor complex. Conceivably, brain areas unaffected morphologically by the pathophysiological processes of AD may become dysfunctional due to a disruption of connectivity between regions.