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Insulin-like growth factor-1 and risk of late-onset Alzheimer's disease: findings from a family study.

Authors: Van Exel, E  Eikelenboom, P  Comijs, H  Deeg, DJ  Stek, ML  Westendorp, RG 
Citation: van Exel E, etal., Neurobiol Aging. 2014 Mar;35(3):725.e7-10. doi: 10.1016/j.neurobiolaging.2013.08.014. Epub 2013 Sep 20.
Pubmed: (View Article at PubMed) PMID:24054991
DOI: Full-text: DOI:10.1016/j.neurobiolaging.2013.08.014

Insulin-like growth factor-1 (IGF-1), part of an evolutionary conserved signaling pathway in both mammalian and non-mammalian species, is inferred in neurodegenerative disorders including Alzheimer's disease (AD). A murine model for AD shows that reduced IGF-1 signaling prevents AD-like characteristics. However, variation in serum levels of IGF-1 and risk of AD in humans has yet to be determined. We used a proven family design, comparing middle-aged offspring with and without a parental history of AD. The offspring under study carry an increased risk of AD but do not yet experience cognitive impairment. A total of 206 offspring from 92 families with a parental history of AD were compared with 200 offspring from 97 families without a parental history of AD. Apolipoprotein-E (APOE) genotypes and serum IGF-1 levels were compared in subjects with and without a parental history of AD using linear regression, adjusted for APOE genotype and other possible demographic and clinical confounders. Offspring with a parental history of AD were more likely to be an APOE epsilon4 allele carrier (46.5% vs. 21%, p = 0.001) than were offspring without such a parental history. Offspring with a parental history of AD had higher IGF-1 levels than subjects without such a history, in both unadjusted and adjusted analyses (18.3 mmol/L vs. 16.7 mmol/L, p = 0.001). In conclusion, higher serum IGF-1 levels in middle age are associated with risk of AD disease in older age, independent of APOE genotype.

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CRRD Object Information
CRRD ID: 10045860
Created: 2015-06-18
Species: All species
Last Modified: 2015-06-18
Status: ACTIVE



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