Cited by 237Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsCancer-related cognitive impairment studies

Maternal family history of Alzheimer's disease predisposes to reduced brain glucose metabolism

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Mosconi, Lisa, Brys, Miroslaw, Switalski, Remigiusz, Mistur, Rachel, Glodzik, Lidia, Pirraglia, Elizabeth, Tsui, Wai, De Santi, Susan +1 more·2007·Proceedings of the National Academy of Sciences

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-[(18)F]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.

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Authors
Mosconi, L., Brys, M., Switalski, R., Mistur, R., Glodzik, L., Pirraglia, E., Tsui, W., De Santi, S., & de Leon, M. J.
Affiliations
  • New York University (US)
  • *Department of Psychiatry, New York University School of Medicine, 560 First Avenue, New York, NY 10016; and
  • Nathan Kline Institute for Psychiatric Research (US)
Venue
Proceedings of the National Academy of Sciences
Published
2007-11-27
Volume
104
Issue
48
Pages
19067-19072
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W1983761458
Cited by
237
References
56
Citations by year
2026: 7 · 2025: 5 · 2024: 3 · 2023: 7 · 2022: 8 · 2021: 14 · 2020: 18 · 2019: 7 · 2018: 14 · 2017: 11 · 2016: 8 · 2015: 10 · 2014: 21 · 2013: 17 · 2012: 19
FWCI
8.27
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Alzheimer's Association
  • National Institutes of Health (AG12101, AG08051)
  • National Institute on Aging (AG022374, R01AG022374, AG 12101, R01AG012101, P30AG008051, AG 08051, R01AG013616, AG 13616)
  • National Center for Research Resources (M01RR000096)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Cancer-related cognitive impairment studies
Keywords
Alzheimer's disease, family history (medicine), maternal inheritance, brain glucose metabolism, cognitively normal older adults, parental risk, posterior cingulate cortex, precuneus, medial temporal lobe, temporoparietal cortex, apolipoprotein E, gender differences
MeSH terms
Aged, Aged, 80 and over, Alzheimer Disease, Brain Mapping, Cerebral Cortex, Female, Fluorine Radioisotopes, Glucose, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Mothers, Retrospective Studies, Risk, Genomic Imprinting, Genetic Heterogeneity, Fluorodeoxyglucose F18, Genetic Predisposition to Disease, Positron-Emission Tomography, Genes, Mitochondrial, Apolipoprotein E4

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