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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 ,
Hiroyasu Ishikawa ,
Kenichi Meguro ,
Manabu Tashiro  and
Satoshi Yamaguchi
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: k-meg@umin.ac.jp.
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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.

Keywords

MCICDR 0.5FDGPETAlzheimer's disease
Type
Research Article
Information
International Psychogeriatrics , Volume 21 , Issue 1 , February 2009 , pp. 148 - 156
Copyright
Copyright © International Psychogeriatric Association 2008

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References

American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorders, 4th edn. Washington, DC: American Psychiatric Association.Google Scholar
Arnaiz, E. et al. (2001). Impaired cerebral glucose metabolism and cognitive functioning predict deterioration in mild cognitive impairment. NeuroReport, 12, 851–855.Google Scholar
Chen, P., Ratcliff, G., Belle, S. H., Cauley, J. A., DeKosky, S. T., and Ganguli, M. (2000). Cognitive tests that best discriminate between presymptomatic AD and those who remain nondemented. Neurology, 55, 1847–1853.CrossRefGoogle ScholarPubMed
Chetelat, G., Desgranges, B., de la Sayette, V., Viader, F., Eustache, F. and Baron, J. C. (2003). Mild cognitive impairment: can FDG-PET predict who is to rapidly convert to Alzheimer's disease? Neurology, 60, 1374–1377.CrossRefGoogle ScholarPubMed
Drzezga, A. et al. (2003). Cerebral metabolic changes accompanying conversion of mild cognitive impairment into Alzheimer's disease: a PET follow-up study. European Journal of Nuclear Medicine and Molecular Imaging, 30, 1104–1113.Google ScholarPubMed
Evans, A. D. et al. (1994). 3D statistical neuroanatomical models from 305 MRI volumes. IEEE Nuclear Science Symposium Medical Imaging Conference, 3, 1813–1817.Google Scholar
Fellgiebel, A., Scheurich, A., Bartenstein, P. and Muller, M. J. (2007). FDG-PET and CSF phospho-tau for prediction of cognitive decline in mild cognitive impairment. Psychiatry Research, 155, 167–171.Google Scholar
Folstein, M. F., Folstein, S. E. and McHugh, P. R. (1975). “Mini-mental state”: a practical method for grading the cognitive state of patients for the clinician. Journal of Psychiatric Research, 12, 189–198.CrossRefGoogle Scholar
Hoffman, J. M. et al. (2000). FDG PET imaging in patients with pathologically verified dementia. Journal of Nuclear Medicine, 41, 1920–1928.Google ScholarPubMed
Ishiwata, A., Sakayori, O., Minoshima, S., Mizumura, S., Kitamura, S. and Katayama, Y. (2006). Preclinical evidence of Alzheimer changes in progressive mild cognitive impairment: a qualitative and quantitative SPECT study. Acta Neurologica Scandinavica, 114, 91–96.CrossRefGoogle ScholarPubMed
Larrieu, S. et al. (2002). Incidence and outcome of mild cognitive impairment in a population-based prospective cohort. Neurology, 59, 1594–1599.Google Scholar
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D. and Stadlan, E. M. (1984). Clinical diagnosis of AD: report of the NINCDS-ADRDA work group under the auspices of department of health and human services task force on AD. Neurology, 34, 939–944.CrossRefGoogle Scholar
Meguro, K. (2004). A Clinical Approach to Dementia: An Instruction of CDR Worksheet. Tokyo: Igaku-Shoin.Google Scholar
Meguro, K. et al. (2002). Prevalence of dementia and dementing diseases in Japan: the Tajiri Project. Archives of Neurology, 59, 1109–1114.CrossRefGoogle ScholarPubMed
Meguro, K. et al. (2004). Prevalence and cognitive performances of Clinical Dementia Rating 0.5 and mild cognitive impairment in Japan: the Tajiri Project. Alzheimer Disease and Associate Disorders, 18, 3–10.CrossRefGoogle ScholarPubMed
Meguro, K. et al. (2007) Incidence of dementia and associated risk factors in Japan: The Osaki-Tajiri Project. Journal of Neurological Sciences, 260, 175–182.Google Scholar
Morris, J. C. (1993). The Clinical Dementia Rating (CDR): current version and scoring rules. Neurology, 43, 2412–2414.Google Scholar
Morris, J. C. et al. (2001). Mild cognitive impairment represents early-stage Alzheimer's disease. Archives of Neurology, 58, 397–405.CrossRefGoogle Scholar
Mosconi, L. et al. (2004). MCI conversion to dementia and the APOE genotype: a prediction study with FDG-PET. Neurology, 63, 2332–2340.Google Scholar
Perneczky, R., Hartmann, J., Grimmer, T., Drzezga, A. and Kurz, A. (2007). Cerebral metabolic correlates of the Clinical Dementia Rating scale in mild cognitive impairment. Journal of Geriatric Psychiatry and Neurology, 20, 84–88.Google Scholar
Petersen, R. C., Smith, G. E., Waring, S. C., Ivnik, R. J., Kokmen, E. and Tangelos, E. G. (1997). Aging, memory, and mild cognitive impairment. International Psychogeriatrics, 9, 65–69.CrossRefGoogle ScholarPubMed
Phelps, M. E., Huang, S. C., Hoffman, E. J., Selin, C., Sokoloff, L. and Kuhl, D. E. (1979). Tomographic measurement of local glucose metabolic rate in humans with (FO-18)2-fluoro-2-deoxy-D-glucose: validation of method. Annals of Neurology, 6, 371–388.Google Scholar
Reisberg, B., Ferris, S. H. and de Leon, M. J. (1982). The global deterioration scale for assessment of primary degenerative dementia. American Journal of Psychiatry, 139, 1136–1139.Google Scholar
Reivich, M. et al. (1979). The 18F-fluoro-deoxyglucose method for the measurement of local cerebral glucose utilization in man. Circulation Research, 44, 127–137.CrossRefGoogle Scholar
Silverman, D. H. et al. (2001). Positron emission tomography in evaluation of dementia: regional brain metabolism and long-term outcome. JAMA, 286, 2120–2127.Google Scholar
Talairach, J. and Trournoux, P. (1988). Co-planar Stereotaxic Atlas of the Human Brain: 3-dimensional Proportional System: An Approach to Cerebral Imaging. New York: Thieme Medical.Google Scholar
Teng, E. L. et al. (1994). The Cognitive Ability Screening Instrument (CASI): a practical test for cross-cultural epidemiological studies of dementia. International Psychogeriatrics, 6, 45–58.Google Scholar
Visser, P. J., Verhey, F. R., Hofman, P. A., Scheltens, P. and Jolles, J. (2002). Medial temporal lobe atrophy predicts Alzheimer's disease in patients with minor cognitive impairment. Journal of Neurology, Neurosurgery, and Psychiatry, 72, 491–497.Google ScholarPubMed
Yamaguchi, S. et al. (1997). Decreased cortical glucose metabolism correlated with hippocampal atrophy in Alzheimer's disease as shown by MRI and PET. Journal of Neurology, Neurosurgery, and Psychiatry, 62, 596–600.Google Scholar