title: Cerebral glucose metabolism in patients with AD and different APOE genotypes.
abstract: OBJECTIVE
  To examine the influence of the APOE epsilon4 allele on cerebral glucose metabolism in a large series of patients with Alzheimer disease (AD).
  
  
  METHODS
  Eighty-three patients (41 APOE epsilon4 positive and 42 epsilon4 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 epsilon4-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 epsilon4-positive and -negative patients additionally revealed stronger abnormalities in epsilon4 carriers in parietal, temporal, and posterior cingulate cortical regions.
  
  
  CONCLUSIONS
  A generally similar pattern of cerebral hypometabolism was detected in APOE epsilon4-positive and -negative patients with Alzheimer disease. However, in direct comparison of the two matched groups, the abnormalities in the epsilon4-positive group were demonstrated to be more pronounced.
authors.affiliation: Department of Nuclear Medicine, Technische Universität München, Munich, Germany. a.drzezga@lrz.tu-muenchen.de
authors.forename: A
authors.initials: A
authors.lastname: Drzezga
authors.forename: M
authors.initials: M
authors.lastname: Riemenschneider
authors.forename: B
authors.initials: B
authors.lastname: Strassner
authors.forename: T
authors.initials: T
authors.lastname: Grimmer
authors.forename: M
authors.initials: M
authors.lastname: Peller
authors.forename: A
authors.initials: A
authors.lastname: Knoll
authors.forename: S
authors.initials: S
authors.lastname: Wagenpfeil
authors.forename: S
authors.initials: S
authors.lastname: Minoshima
authors.forename: M
authors.initials: M
authors.lastname: Schwaiger
authors.forename: A
authors.initials: A
authors.lastname: Kurz
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000235:genetics / Q000378:metabolism*; D053327:Apolipoprotein E4; D001057:Apolipoproteins E / Q000235:genetics*; D002540:Cerebral Cortex / Q000737:chemistry*; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000378:metabolism; D005838:Genotype; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography / Q000379:methods
chemical_list: D053327:Apolipoprotein E4; D001057:Apolipoproteins E; D019788:Fluorodeoxyglucose F18; D005947:Glucose