Titre : | Social disorder, APOE-E4 genotype, and change in cognitive function among older adults living in Chicago. (2012) |
Auteurs : | BOARDMAN (Jasond) : USA. Institute of Behavioral Science. University of Colorado. Boulder. CO. ; Lisal BARNES ; EVANS (Denis-A) : USA. Rush Institute for Healthy Aging. Rush University Medical Center. Chicago. IL. ; MENDES DE LEON (Carlos-F) : USA. Department of Epidemiology. University of Michigan. Ann Arbor. MI. ; Robert-S WILSON ; Department of Behavioral Sciences. Rush University Medical Center. Chicago. IL. USA ; Department of Neurological Sciences. Rush University Medical Center. Chicago. IL. USA ; Rush Alzheimer's Disease Center. Rush University Medical Center. Chicago. IL. USA |
Type de document : | Article |
Dans : | Social science and medicine (vol. 74, n° 10, 2012) |
Pagination : | 1584-1590 |
Langues: | Anglais |
Mots-clés : | Changement ; Fonction cognitive ; Personne âgée ; Santé environnementale ; Homme ; Amérique ; Amérique du Nord |
Résumé : | [BDSP. Notice produite par INIST-CNRS R0xk9BlI. Diffusion soumise à autorisation]. The goal of this paper is to describe the simultaneous influence of social and genetic risk factors on declines in cognitive functioning among older American adults. We use detailed information about the social characteristics of older adults'neighborhoods from the Chicago Health and Aging Project (n=1655 ; ages 65+) in conjunction with information about respondent's APOE genotype to predict changes in cognitive function over time. Results indicate that the presence of the epsilon4 allele is associated with a significantly lower cognitive function score at baseline and greater declines in cognitive function compared to those without this risk allele. Importantly, we also show significant variation in the effect of the epsilon4 allele across neighborhoods and our results indicate that this genotype is more strongly associated with cognitive function for residents of neighborhoods with the lowest levels of social disorder. Our findings support the non-causal social push gene-environment interaction model. |