title: Declining brain glucose metabolism in normal individuals with a maternal history of Alzheimer disease.
abstract: BACKGROUND
  At cross-section, cognitively normal individuals (NL) with a maternal history of late-onset Alzheimer disease (AD) have reduced glucose metabolism (CMRglc) on FDG-PET in the same brain regions as patients with clinical AD as compared to those with a paternal and a negative family history (FH) of AD. This longitudinal FDG-PET study examines whether CMRglc reductions in NL subjects with a maternal history of AD are progressive.
  
  
  METHODS
  Seventy-five 50- to 82-year-old NL received 2-year follow-up clinical, neuropsychological, and FDG-PET examinations. These included 37 subjects with negative family history of AD (FH-), 9 with paternal (FHp), and 20 with maternal AD (FHm). Two subjects had parents with postmortem confirmed AD. Statistical parametric mapping was used to compare CMRglc across FH groups at baseline, follow-up, and longitudinally.
  
  
  RESULTS
  At both time points, the FH groups were comparable for demographic and neuropsychological characteristics. At baseline and at follow-up, FHm subjects showed CMRglc reductions in the parieto-temporal, posterior cingulate, and medial temporal cortices as compared to FH- and FHp (p < 0.001). Longitudinally, FHm had significant CMRglc declines in these regions, which were significantly greater than those in FH- and FHp (p < 0.05).
  
  
  CONCLUSIONS
  A maternal history of Alzheimer disease (AD) predisposes normal individuals to progressive CMRglc reductions in AD-vulnerable brain regions, which may be related to a higher risk for developing AD.
authors.affiliation: Department of Psychiatry, NYU School of Medicine, 550 First Avenue, New York, NY 10016, USA. lisa.mosconi@med.nyu.edu
authors.forename: L
authors.initials: L
authors.lastname: Mosconi
authors.forename: R
authors.initials: R
authors.lastname: Mistur
authors.forename: R
authors.initials: R
authors.lastname: Switalski
authors.forename: M
authors.initials: M
authors.lastname: Brys
authors.forename: L
authors.initials: L
authors.lastname: Glodzik
authors.forename: K
authors.initials: K
authors.lastname: Rich
authors.forename: E
authors.initials: E
authors.lastname: Pirraglia
authors.forename: W
authors.initials: W
authors.lastname: Tsui
authors.forename: S
authors.initials: S
authors.lastname: De Santi
authors.forename: M J
authors.initials: MJ
authors.lastname: de Leon
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000378:metabolism*; D000544:Alzheimer Disease / Q000151:congenital* / Q000378:metabolism*; D001921:Brain / Q000378:metabolism*; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005947:Glucose / Q000378:metabolism*; D006579:Heterozygote; D006801:Humans; D008297:Male; D008875:Middle Aged; D009035:Mothers
chemical_list: D005947:Glucose