Late-life brain volume: a life-course approach. The AGES-Reykjavik study.

To access publisher's full text version of this article click on the hyperlink at the bottom of the page The "fetal-origins-of-adult-disease" hypothesis proposes that an unfavorable intrauterine environment, estimated from small birth size, may induce permanent changes in fetal organs...

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Published in:Neurobiology of Aging
Main Authors: Muller, Majon, Sigurdsson, Sigurdur, Kjartansson, Olafur, Gunnarsdottir, Ingibjorg, Thorsdottir, Inga, Harris, Tamara B, van Buchem, Mark, Gudnason, Vilmundur, Launer, Lenore J
Other Authors: 1 NIA, Intramural Res Program, Lab Epidemiol & Populat Sci, Bethesda, MD 20892 USA 2 Vrije Univ Amsterdam, Med Ctr, Dept Internal Med, Amsterdam, Netherlands 3 Iceland Heart Assoc, Kopavogur, Iceland 4 Landspitali Univ Hosp, Dept Neurol, Reykjavik, Iceland Organization-Enhanced Name(s) Landspitali National University Hospital 5 Landspitali Univ Hosp, Dept Radiol, Reykjavik, Iceland Organization-Enhanced Name(s) Landspitali National University Hospital 6 Univ Iceland, Unit Nutr Res, Reykjavik, Iceland 7 Landspitali Univ Hosp, Reykjavik, Iceland Organization-Enhanced Name(s) Landspitali National University Hospital 8 Leiden Univ, Med Ctr, Dept Radiol, Leiden, Netherlands
Format: Article in Journal/Newspaper
Language:English
Published: Elsevier Science Inc 2016
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Online Access:http://hdl.handle.net/2336/611372
https://doi.org/10.1016/j.neurobiolaging.2016.02.012
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Summary:To access publisher's full text version of this article click on the hyperlink at the bottom of the page The "fetal-origins-of-adult-disease" hypothesis proposes that an unfavorable intrauterine environment, estimated from small birth size, may induce permanent changes in fetal organs, including the brain. These changes in combination with effects of (cardiovascular) exposures during adult life may condition the later risk of brain atrophy. We investigated the combined effect of small birth size and mid-life cardiovascular risk on late-life brain volumes. Archived birth records of weight and height were abstracted for 1348 participants of the age, gene/environment susceptibility-Reykjavik study (RS; 2002-2006) population-based cohort, who participated in the original cohort of the RS (baseline 1967). Mid-life cardiovascular risk factors (CVRF) were collected in the RS. As a part of the late-life age, gene/environment susceptibility-RS examination, a brain magnetic resonance imaging was acquired and from it, volumes of total brain, gray matter, white matter, and white matter lesions were estimated. Adjusting for intracranial volume, demographics, and education showed small birth size (low ponderal index [PI]) and increased mid-life cardiovascular risk had an additive effect on having smaller late-life brain volumes. Compared with the reference group (high PI/absence of mid-life CVRF), participants with lower PI/presence of mid-life CVRF (body mass index >25 kg/m(2), hypertension, diabetes, "ever smokers") had smaller total brain volume later in life; B (95% confidence interval) were -10.9 mL (-21.0 to -0.9), -10.9 mL (-20.4 to -1.4), -20.9 mL (-46.9 to 5.2), and -10.8 mL (-19.3 to -2.2), respectively. These results suggest that exposure to an unfavorable intrauterine environment contributes to the trajectory toward smaller brain volume, adding to the atrophy that may be associated with mid-life cardiovascular risk.