title: Reduced gray matter volume in normal adults with a maternal family history of Alzheimer disease.
abstract: OBJECTIVE
  A consistently identified risk factor for Alzheimer disease (AD) is family history of dementia, with maternal transmission significantly more frequent than paternal transmission. A history of maternal AD may be related to AD-like glucose consumption in cognitively healthy subjects. In this cross-sectional study, we tested whether cognitively healthy people with a family history of AD have less gray matter volume (GMV), an endophenotype for late-onset AD, than individuals with no family history, and whether decreases in GMV are different in subjects with a maternal family history.
  
  
  METHODS
  As part of the Kansas University Brain Aging Project, 67 cognitively intact individuals with a maternal history of late-onset AD (FHm, n = 16), a paternal history of AD (FHp, n = 8), or no parental history of AD (FH-, n = 43), similar in age, gender, education, and Mini-Mental State Examination score, were scanned at 3 T. We used voxel-based morphometry to examine GMV differences between groups, controlling for age, gender, and apoE4.
  
  
  RESULTS
  Cognitively healthy individuals with a family history of late-onset AD had significantly decreased GMV in the precuneus, middle frontal, inferior frontal, and superior frontal gyri compared with FH- individuals. FHm subjects had significantly smaller inferior frontal, middle frontal, precuneus, and lingual gyri compared with FH- and FHp subjects.
  
  
  CONCLUSIONS
  Overall, maternal family history of Alzheimer disease (AD) in cognitively normal individuals is associated with lower gray matter volume in AD-vulnerable brain regions. These data complement and extend reports of cerebral metabolic differences in subjects with a maternal family history.
authors.affiliation: University of Kansas School of Medicine, Department of Neurology, 2100 West 36th Ave., Suite 110, Kansas City, KS 66160, USA. rhonea@kumc.edu
authors.forename: R A
authors.initials: RA
authors.lastname: Honea
authors.forename: R H
authors.initials: RH
authors.lastname: Swerdlow
authors.forename: E D
authors.initials: ED
authors.lastname: Vidoni
authors.forename: J
authors.initials: J
authors.lastname: Goodwin
authors.forename: J M
authors.initials: JM
authors.lastname: Burns
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000175:diagnosis* / Q000235:genetics* / Q000503:physiopathology; D053327:Apolipoprotein E4 / Q000235:genetics; D001284:Atrophy / Q000235:genetics* / Q000473:pathology* / Q000503:physiopathology; D001921:Brain / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D001931:Brain Mapping; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D042241:Early Diagnosis; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D006801:Humans; D007091:Image Processing, Computer-Assisted; D040582:Inheritance Patterns / Q000235:genetics*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009035:Mothers; D009483:Neuropsychological Tests; D012307:Risk Factors
chemical_list: D053327:Apolipoprotein E4