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From the Department of Clinical Pathophysiology, Nuclear Medicine Unit (Drs. Mosconi, De Cristofaro, Fayyaz, and Pupi), and Department of Neurological and Psychiatric Sciences (Drs. Sorbi, Nacmias, Cellini, Bagnoli, and Bracco), University of Florence, Italy; and University of Cologne (Dr. Herholz), Neurological Clinic and Max-Planck-Institute for Neurological Research, Köln, Germany.
Address correspondence and reprint requests to Dr. Prof. Alberto Pupi, Department of Clinical Pathophysiology, Nuclear Medicine Unit, University of Florence, viale Morgagni 85, 50134 Florence, Italy; e-mail: a.pupi{at}dfc.unifi.it
This FDG-PET study with SPM99 compared 46 patients with sporadic Alzheimer disease (SAD) to 40 patients with familial AD (FAD) and to 35 matched controls. AD groups had equivalent metabolic (METglu) reductions in several cortical and limbic areas with respect to the controls. Patients with FAD showed decreased METglu in the posterior cingulate, parahippocampal, and occipital cortex as compared to the patients with SAD (p < 0.001). Genetic factors lead to phenotypic differences in AD.
Received February 14, 2003. Accepted in final form June 23, 2003.
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