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Brain Advance Access published online on May 11, 2005
Brain, doi:10.1093/brain/awh539
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© The Author (2005). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Received November 19, 2004
Revised February 15, 2005
Accepted April 8, 2005

Article

Glucose metabolism in early onset versus late onset Alzheimer's disease: an SPM analysis of 120 patients

E. J. Kim 1*, S. S. Cho 2, Y. Jeong 3, K. C. Park 4, S. J. Kang 5, E. Kang 2, S. E. Kim 2, K. H. Lee 6, and D. L. Na 1

1 Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
2 Department of Nuclear Medicine, Seoul National University College of Medicine, Seoul, Korea
3 Department of Neurology, University of Florida and Veterans Affairs Medical Center, Gainesville, FL, USA
4 Department of Neurology, College of Medicine, Kyung Hee University, Seoul, Korea
5 Department of Psychology, Kangwon National University, Chuncheon, Korea
6 Department of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

* To whom correspondence should be addressed.
E. J. Kim, E-mail: dukna{at}smc.samsung.co.kr


  Abstract

The aims of this cross-sectional study were (i) to compare the overall glucose metabolism between early onset and late onset Alzheimer's disease in a large sample of patients; and (ii) to investigate the pattern of glucose metabolism as a function of dementia severity in early onset versus late onset Alzheimer's disease, using a statistical parametric mapping (SPM) analysis. Subjects consisted of four groups: 74 patients with early onset Alzheimer's disease, 46 patients with late onset of the disease, and two control groups age matched to each patient group. All the subjects underwent 2-[18F]fluoro-2-deoxy-D-glucose (FDG)-PET under the same scanning conditions. Severity of dementia was rated with the Clincial Dementia Rating (CDR). Voxel-based SPM99 was used for statistical analyses. Overall glucose hypometabolism of early onset Alzheimer's disease patients was much greater in magnitude and extent than that of late onset patients, though both groups were similar in dementia severity: the early onset group showed more severe hypometabolism in parietal, frontal and subcortical (basal ganglia and thalamus) areas. When the decline of glucose metabolism was compared as a function of CDR stage, the slope was steeper in early onset than in late onset Alzheimer's disease. The rapid decline occurred at CDR 0.5-1 in the early onset group, whereas similar changes occurred at CDR 2-3 in the late onset group. The greater hypometabolism in early onset than in late onset patients is required to reach the same severity of dementia, probably reflecting greater functional reserve in younger than in older subjects. Alternatively, the metabolic decline curve suggests that the early onset patients may take a more rapid course in the reduction of glucose metabolism than the late onset patients.

Keywords: Alzheimer's disease; early onset; late onset; PET; statistical parametric mapping.
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