title: No difference in cerebral glucose metabolism in patients with Alzheimer disease and differing apolipoprotein E genotypes.
abstract: BACKGROUND
  Recent findings of a reduced cerebral metabolic rate of glucose (CMRGlu) in at-risk relatives of patients with Alzheimer disease (AD) who carry the apolipoprotein E (APOE) epsilon 4 allele suggest a causative role for the E4 isoform in cognitive changes that lead to AD. It is not known whether epsilon 4 allele-associated deficits exist in patients with clinical AD.
  
  
  OBJECTIVE
  To determine whether distinct patterns of cerebral hypometabolism exist in patients who carry the epsilon 4 allele.
  
  
  METHODS
  Information on the CMRGlu and APOE genotype was available for 46 patients at a memory disorders clinic: 31 patients were diagnosed as having probable AD, 3 demented patients did not meet criteria for AD, and 12 patients had mild memory complaints. Positron emission tomography with the use of 18F-fludeoxyglucose was used to calculate the CMRGlu in the frontal and temporoparietal regions of the cortex. Estimates were standardized to the sensorimotor area of the cortex. Linear regression models were constructed to relate the APOE genotype to the CMRGlu, adjusting for cognitive status (ie, the Mini-Mental State Examination score).
  
  
  RESULTS
  Distinct patterns of the CMRGlu did not emerge for patients with different APOE genotypes. Bilateral deficits in the CMRGlu were found in the patients with AD. Left-right asymmetry was found in 8 of 12 patients with mild memory complaints: 7 of 8 had CMRGlu ratio less than 0.85 in the left side of the temporoparietal region of the cortex.
  
  
  CONCLUSIONS
  The APOE epsilon 4 allele does not appear to be associated with specific deficits in brain metabolism in patients with AD despite evidence that the epsilon 4 allele is associated with preclinical alterations. This finding is consistent with previous epidemiologic results that have demonstrated a higher risk for AD in carriers of the epsilon 4 allele, but no change in the rate of progression of AD.
authors.affiliation: Department of Clinical Neuroscience and Family Medicine, Karolinska Institute, Huddinge University Hospital, Sweden.
authors.forename: E H
authors.initials: EH
authors.lastname: Corder
authors.forename: V
authors.initials: V
authors.lastname: Jelic
authors.forename: H
authors.initials: H
authors.lastname: Basun
authors.forename: L
authors.initials: L
authors.lastname: Lannfelt
authors.forename: S
authors.initials: S
authors.lastname: Valind
authors.forename: B
authors.initials: B
authors.lastname: Winblad
authors.forename: A
authors.initials: A
authors.lastname: Nordberg
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D000544:Alzheimer Disease / Q000235:genetics* / Q000378:metabolism*; D001057:Apolipoproteins E / Q000235:genetics*; D001921:Brain / Q000000981:diagnostic imaging / Q000378:metabolism*; D005838:Genotype; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D008875:Middle Aged; D011877:Radionuclide Imaging
chemical_list: D001057:Apolipoproteins E; D005947:Glucose