Physical Activity as Moderator of the Association Between APOE and Cognitive Decline in Older Adults: Results from Three Longitudinal Cohort Studies.
Gene–environment interaction
InCHIANTI
Longitudinal Aging Study Amsterdam
Rotterdam Study
Journal
The journals of gerontology. Series A, Biological sciences and medical sciences
ISSN: 1758-535X
Titre abrégé: J Gerontol A Biol Sci Med Sci
Pays: United States
ID NLM: 9502837
Informations de publication
Date de publication:
25 09 2020
25 09 2020
Historique:
received:
07
05
2019
pubmed:
29
2
2020
medline:
17
2
2021
entrez:
29
2
2020
Statut:
ppublish
Résumé
Previous studies have suggested that the association between APOE ɛ 4 and dementia is moderated by physical activity (PA), but the results remain inconclusive and longitudinal data on cognitive decline are missing. In this study, we examine whether there is a gene-environment interaction between APOE and PA on cognitive decline in older adults using 9-year follow-up data of three cohort studies. We followed 7,176 participants from three longitudinal cohort studies: Longitudinal Aging Study Amsterdam (LASA), InCHIANTI, and Rotterdam Study for 9 years. PA was assessed with self-reported questionnaires and was categorized in low, moderate, and high PA. Cognitive function was assessed with the Mini-Mental State Examination (MMSE) and cognitive decline was defined as a decrease of three points or more on the MMSE during 3 years follow-up. We fitted logistic regression models using generalized estimating equations adjusting for age, sex, education, depressive symptoms, and number of chronic disease. Interaction between APOE and PA was tested on multiplicative and additive scale. Cohorts were similar in most aspects but InCHIANTI participants were on average older and had lower education. APOE ɛ 4 carriers had higher odds of cognitive decline (odds ratio [OR] = 1.46, 95% confidence interval [CI]: 1.29-1.64) while PA was not significantly associated with cognitive decline overall (moderate PA: OR = 0.87, 0.67-1.13; high PA: OR = 0.71, 0.36-1.40). There was no evidence for an interaction effect between PA and APOE ɛ 4 in cognitive decline in older adults (APOE × moderate PA: p = .83; APOE × high PA: p = .90). Previous claims of a gene-environment interaction between APOE ɛ 4 and PA in cognitive decline are not supported by our results.
Sections du résumé
BACKGROUND
Previous studies have suggested that the association between APOE ɛ 4 and dementia is moderated by physical activity (PA), but the results remain inconclusive and longitudinal data on cognitive decline are missing. In this study, we examine whether there is a gene-environment interaction between APOE and PA on cognitive decline in older adults using 9-year follow-up data of three cohort studies.
METHODS
We followed 7,176 participants from three longitudinal cohort studies: Longitudinal Aging Study Amsterdam (LASA), InCHIANTI, and Rotterdam Study for 9 years. PA was assessed with self-reported questionnaires and was categorized in low, moderate, and high PA. Cognitive function was assessed with the Mini-Mental State Examination (MMSE) and cognitive decline was defined as a decrease of three points or more on the MMSE during 3 years follow-up. We fitted logistic regression models using generalized estimating equations adjusting for age, sex, education, depressive symptoms, and number of chronic disease. Interaction between APOE and PA was tested on multiplicative and additive scale.
RESULTS
Cohorts were similar in most aspects but InCHIANTI participants were on average older and had lower education. APOE ɛ 4 carriers had higher odds of cognitive decline (odds ratio [OR] = 1.46, 95% confidence interval [CI]: 1.29-1.64) while PA was not significantly associated with cognitive decline overall (moderate PA: OR = 0.87, 0.67-1.13; high PA: OR = 0.71, 0.36-1.40). There was no evidence for an interaction effect between PA and APOE ɛ 4 in cognitive decline in older adults (APOE × moderate PA: p = .83; APOE × high PA: p = .90).
CONCLUSIONS
Previous claims of a gene-environment interaction between APOE ɛ 4 and PA in cognitive decline are not supported by our results.
Identifiants
pubmed: 32110803
pii: 5763509
doi: 10.1093/gerona/glaa054
pmc: PMC7518558
doi:
Substances chimiques
Apolipoprotein E4
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1880-1886Subventions
Organisme : NIA NIH HHS
ID : N01 AG050002
Pays : United States
Informations de copyright
© The Author(s) 2020. Published by Oxford University Press on behalf of The Gerontological Society of America.
Références
J Gerontol A Biol Sci Med Sci. 2005 Jun;60(6):760-7
pubmed: 15983180
Arch Neurol. 2010 Jan;67(1):71-9
pubmed: 20065132
Clin Epidemiol. 2017 Dec 18;10:1-16
pubmed: 29296097
BMJ. 2017 Jun 22;357:j2709
pubmed: 28642251
Stroke. 2000 Oct;31(10):2431-6
pubmed: 11022076
Eur J Epidemiol. 2005;20(7):575-9
pubmed: 16119429
Am J Epidemiol. 2007 Jun 1;165(11):1231-8
pubmed: 17431012
Am J Epidemiol. 2005 Apr 1;161(7):639-51
pubmed: 15781953
J Neurol Neurosurg Psychiatry. 2007 Dec;78(12):1298-303
pubmed: 17442763
Curr Opin Psychiatry. 2006 Mar;19(2):190-3
pubmed: 16612202
J Gerontol A Biol Sci Med Sci. 2018 Oct 8;73(11):1504-1511
pubmed: 29216339
Lancet. 1995 Nov 25;346(8987):1387-90
pubmed: 7475820
Eur J Epidemiol. 2013 Mar;28(3):277-83
pubmed: 23385659
Lancet Neurol. 2005 Nov;4(11):705-11
pubmed: 16239176
J Clin Epidemiol. 2004 Mar;57(3):252-8
pubmed: 15066685
J Psychiatr Res. 1975 Nov;12(3):189-98
pubmed: 1202204
Med Sci Sports Exerc. 1991 Aug;23(8):974-9
pubmed: 1956274
Int J Epidemiol. 2002 Feb;31(1):168-74
pubmed: 11914316
Int J Epidemiol. 2007 Oct;36(5):1111-8
pubmed: 17726040
Proc Natl Acad Sci U S A. 2013 May 7;110(19):E1807-16
pubmed: 23620513
Med Sci Sports Exerc. 2001 May;33(5):772-7
pubmed: 11323547
Psychol Aging. 1999 Dec;14(4):539-51
pubmed: 10632143
Am J Epidemiol. 1991 Jun 1;133(11):1078-92
pubmed: 2035512
Arch Neurol. 2012 May;69(5):636-43
pubmed: 22232206
J Gerontol A Biol Sci Med Sci. 2019 Jan 1;74(1):99-107
pubmed: 30321297
BMC Geriatr. 2019 Jun 27;19(1):179
pubmed: 31248370
Proc Natl Acad Sci U S A. 1993 Oct 15;90(20):9649-53
pubmed: 8415756
N Engl J Med. 1995 Nov 9;333(19):1242-7
pubmed: 7566000
Cell Mol Neurobiol. 2010 May;30(4):493-503
pubmed: 20041290
Arch Neurol. 1998 Jul;55(7):964-8
pubmed: 9678314
J Alzheimers Dis. 2017;56(1):297-303
pubmed: 27911292
Z Gerontol Geriatr. 2012 Jan;45(1):11-6
pubmed: 22278001
Neurology. 2019 Jun 4;92(23):e2691-e2698
pubmed: 31028125
Neuron. 2008 Jun 12;58(5):681-93
pubmed: 18549781
Psychol Med. 2014 Apr;44(6):1319-29
pubmed: 23883793
Alzheimer Dis Assoc Disord. 2004 Apr-Jun;18(2):57-64
pubmed: 15249848
J Cell Mol Med. 2008 Dec;12(6B):2762-71
pubmed: 18318693
Mol Neurodegener. 2010 Jun 01;5:23
pubmed: 20515477
BMJ. 2003 Sep 6;327(7414):557-60
pubmed: 12958120