Two consecutive positron emission scans were done in one session using
a double injection method of [F-18]2-fluoro-2-deoxyglucose administra
tion to examine the effects of the antimuscarinic drug scopolamine on
cerebral glucose metabolism in ten older adults. Scopolamine causes te
mporary memory impairment, and its effects have been used to model asp
ects of the cognitive impairment that occur in Alzheimer's disease (AD
). Cortical metabolic rates of patients with AD have been reported to
be depressed, especially in parietal, temporal, and frontal associatio
n areas. After scopolamine administration to the elderly volunteers, a
bsolute and normalized glucose metabolic rates were depressed in prefr
ontal and occipital regions and increased in parietal-occipital cortic
al regions and a left middle temporal region. These changes in the old
er volunteers are generally not consistent with changes seen in AD. We
conclude that deficits in muscarinic system function may contribute t
o some but not all of the hypometabolic changes seen in AD patients.