Maternal family history of Alzheimer's disease predisposes to reduced brain glucose metabolism Academic Article Article uri icon

Overview

MeSH Major

  • Adenocarcinoma
  • Antineoplastic Agents
  • Drug Resistance, Neoplasm
  • Esophageal Neoplasms
  • Esophagogastric Junction
  • Niacinamide
  • Phenylurea Compounds
  • Stomach Neoplasms

abstract

  • Having a parent affected with late-onset Alzheimer's disease (AD) is a risk factor for developing AD among cognitively normal subjects. We examined whether cognitively normal subjects with a parental family history of AD show cerebral metabolic rate of glucose (CMRglc) reductions consistent with AD as compared with those without a family history and whether there are parent gender effects. Forty-nine 50- to 80-year-old normal subjects were examined who received clinical, neuropsychological, and 2-[18F]fluoro-2-deoxy-D-glucose- positron emission tomography examinations, including 16 subjects with a maternal (FHm) and eight with a paternal (FHp) family history of AD and 25 with no family history (FH-). FH groups were comparable for demographic and neuropsychological measures. As compared with both FH-and FHp groups, FHm subjects showed CMRglc reductions in the same regions as clinically affected AD patients, involving the posterior cingulate cortex/precuneus, parietotemporal and frontal cortices, and medial temporal lobes (P < 0.05, corrected for multiple comparisons). These effects remained significant after accounting for possible risk factors for AD, including age, gender, education, apolipoprotein E genotype, and subjective memory complaints. No CMRglc differences were found between FHp and FH-subjects. This study shows a relationship between reduced CMRglc in AD-vulnerable brain regions and a maternal family history of AD in cognitively normal individuals. © 2007 by The National Academy of Sciences of the USA.

publication date

  • November 27, 2007

Research

keywords

  • Academic Article

Identity

Digital Object Identifier (DOI)

  • 10.1073/pnas.0705036104

PubMed ID

  • 18003925

Additional Document Info

start page

  • 19067

end page

  • 19072

volume

  • 104

number

  • 48