Declining brain glucose metabolism in normal individuals with a maternal history of Alzheimer disease Academic Article Article uri icon

Overview

MeSH Major

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

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. © 2009 by AAN Enterprises, Inc.

publication date

  • February 10, 2009

Research

keywords

  • Academic Article

Identity

Digital Object Identifier (DOI)

  • 10.1212/01.wnl.0000333247.51383.43

PubMed ID

  • 19005175

Additional Document Info

start page

  • 513

end page

  • 520

volume

  • 72

number

  • 6