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NEUROLOGY 2005;64:102-107
© 2005 American Academy of Neurology

Cerebral glucose metabolism in patients with AD and different APOE genotypes

A. Drzezga, MD*, M. Riemenschneider, MD*, B. Strassner, MD, T. Grimmer, MD, M. Peller, MD, A. Knoll, PhD, S. Wagenpfeil, PhD, S. Minoshima, MD, PhD, M. Schwaiger, MD and A. Kurz, MD

From the Departments of Nuclear Medicine (Drs. Drzezga, Strassner, Peller, and Schwaiger) and Psychiatry and Psychotherapy (Drs. Riemenschneider, Grimmer, and Kurz) and Institute for Medical Statistics and Epidemiology (Dr. Wagenpfeil), Technische Universität München, Munich, and Institute for Information Technology (Dr. Knoll), Department for Robotics and Embedded Systems, Technische Universität München, Garching, Germany; and Department of Radiology (Dr. Minoshima), University of Washington, Seattle.

Address correspondence and reprint requests to Dr. A. Drzezga, Nuklearmedizinische Klinik u. Poliklinik, Klinikum rechts der Isar, Technische Universität München, Ismaninger Strasse 22, 81675 München, Germany; e-mail: a.drzezga{at}lrz.tu-muenchen.de

Objective: To examine the influence of the APOE {epsilon}4 allele on cerebral glucose metabolism in a large series of patients with Alzheimer disease (AD).

Methods: Eighty-three patients (41 APOE {epsilon}4 positive and 42 {epsilon}4 negative) were selected from a pre-existing databank of patients with AD (n > 1,000). The patients were carefully matched for age, age at onset, approximate disease duration, educational level, and overall degree of cognitive impairment. Cerebral [18F]fluorodeoxyglucose PET imaging was performed in all patients by a standardized protocol. Statistical comparison of patient PET data vs a healthy control population was performed as well as an analysis of differences between groups (SPM99; Wellcome Department of Cognitive Imaging, London, UK).

Results: A similar pattern of cerebral hypometabolism was detected in the {epsilon}4-positive and -negative patient groups vs healthy volunteers in regions typically affected by AD (bilateral temporal, parietal, posterior cingulate, and prefrontal cortical areas). The comparison between {epsilon}4-positive and -negative patients additionally revealed stronger abnormalities in {epsilon}4 carriers in parietal, temporal, and posterior cingulate cortical regions.

Conclusions: A generally similar pattern of cerebral hypometabolism was detected in APOE {epsilon}4-positive and -negative patients with Alzheimer disease. However, in direct comparison of the two matched groups, the abnormalities in the {epsilon}4-positive group were demonstrated to be more pronounced.


Received May 18, 2004. Accepted in final form September 9, 2004.

*These authors contributed equally to the manuscript.




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