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Am J Psychiatry 1997; 154:165-172
Copyright © 1997 by American Psychiatric Association
Association of premorbid intellectual function with cerebral metabolism in Alzheimer's disease: implications for the cognitive reserve hypothesis
GE Alexander, ML Furey, CL Grady, P Pietrini, DR Brady, MJ Mentis and MB Schapiro
Laboratory of Neurosciences, National Institute on Aging, Bethesda, MD 20892, USA.
OBJECTIVE: Clinical heterogeneity in Alzheimer's disease has been widely
observed. One factor that may influence the expression of dementia in
Alzheimer's disease is premorbid intellectual ability. It has been
hypothesized that premorbid ability, as measured by educational experience,
reflects a cognitive reserve that can affect the clinical expression of
Alzheimer's disease. The authors investigated the relation between
estimates of premorbid intellectual function and cerebral glucose
metabolism in patients with Alzheimer's disease to test the effect of
differing levels of premorbid ability on neurophysiological dysfunction.
METHOD: In a resting state with eyes closed and ears occluded, 46 patients
with Alzheimer's disease were evaluated with positron emission tomography
and [18F]-2-fluoro-2-deoxy- D-glucose to determine cerebral metabolism.
Premorbid intellectual ability was assessed by a demographics-based IQ
estimate and performance on a measure of word-reading ability. RESULTS:
After the authors controlled for demographic characteristics and dementia
severity, both estimates of premorbid intellectual ability were inversely
correlated with cerebral metabolism in the prefrontal, pre- motor, and left
superior parietal association regions. In addition, the performance-based
estimate (i.e., reading ability) was inversely correlated with metabolism
in the anterior cingulate, paracentral, right orbitofrontal, and left
thalamic regions, after demographic and clinical variables were controlled
for. CONCLUSIONS: The results suggest that higher levels of premorbid
ability are associated with greater pathophysiological effects of
Alzheimer's disease among patients of similar dementia severity levels.
These findings provide support for a cognitive reserve that can alter the
clinical expression of dementia and influence the neurophysiological
heterogeneity observed in Alzheimer's disease.
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