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Decreased cortical glucose metabolism in converters from CDR 0.5 to Alzheimer's disease in a community: the Osaki-Tajiri Project

Published online by Cambridge University Press:  01 December 2008

Hiroshi Ishii
Affiliation:
Department of Geriatric Behavioral Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan Kawasaki Kokoro Hospital, Kawasaki, Japan
Hiroyasu Ishikawa
Affiliation:
Department of Geriatric Behavioral Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan The Osaki-Tajiri SKIP Center, Osaki, Japan
Kenichi Meguro*
Affiliation:
Department of Geriatric Behavioral Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan The Osaki-Tajiri SKIP Center, Osaki, Japan
Manabu Tashiro
Affiliation:
Division of Nuclear Medicine, Cyclotron Radioisotope Center, Tohoku University, Sendai, Japan
Satoshi Yamaguchi
Affiliation:
Department of Geriatric Behavioral Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan The Osaki-Tajiri SKIP Center, Osaki, Japan
*
Correspondence should be addressed to: Kenichi Meguro, MD, PhD, Department of Geriatric Behavioral Neurology, Tohoku University Graduate School of Medicine, 2-1, Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan. Email: [email protected].
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Abstract

Background: Several follow-up [18F]fluorodeoxy glucose (FDG)-positron emission tomography (PET) studies have been performed in patients with mild cognitive impairment, but none have examined subjects with a Clinical Dementia Rating (CDR) of 0.5. Therefore, we used FDG-PET to investigate whether baseline glucose metabolism (CMRglc) in CDR 0.5 converters to dementia showed changes consistent with early Alzheimer's disease (AD).

Methods: Based on our earlier study, which we refer to as Prevalence Study 1998, we were able to examine 14 CDR 0, 42 CDR 0.5, and 12 AD subjects with PET and follow these subjects for five years. Baseline neuropsychological and CMRglc values were compared among groups of CDR 0, CDR 0.5/converters, CDR 0.5/non-converters, and AD subjects.

Results: All CDR 0 subjects were reassessed as CDR 0 after the five-year period. For CDR 0.5 subjects, 20 had converted to AD and 22 remained as CDR 0.5. In cognitive tests, CDR 0.5/converters showed significantly deteriorated recent memory function compared with CDR 0.5/non-converters at the baseline evaluation. Most brain areas showed decreased CMRglc in AD patients. CDR 0.5/converters had a significantly lower baseline CMRglc in the right cingulate, left inferior parietal and left temporal gyrus compared with CDR 0.5/non-converters.

Conclusions: Our findings suggest that CDR 0.5/converters have a baseline metabolic decline in areas that might be specific to AD.

Type
Research Article
Copyright
Copyright © International Psychogeriatric Association 2008

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