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Ojalehto, E., Finkel, D., Russ, T. C., Karlsson, I. K. & Ericsson, M. (2023). Influences of genetically predicted and attained education on geographic mobility and their association with mortality. Social Science and Medicine, 324, Article ID 115882.
Open this publication in new window or tab >>Influences of genetically predicted and attained education on geographic mobility and their association with mortality
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2023 (English)In: Social Science and Medicine, ISSN 0277-9536, E-ISSN 1873-5347, Vol. 324, article id 115882Article in journal (Refereed) Published
Abstract [en]

Introduction: Both educational attainment and genetic propensity to education (PGSEdu) have been associated with geographic mobility. Socioeconomic conditions are, in turn, associated with individuals’ health. Geographic mobility could therefore lead to better health for some since it could provide better opportunities, like education. Our aim was to study how attained education and genetic predisposition for higher education are related to geographic mobility, and how they affect the association between geographic mobility and mortality. Methods: We used data from the Swedish Twin Registry (twins born 1926–1955; n = 14,211) in logistic regression models to test if attained education and PGSEdu predicted geographic mobility. Cox regression models were then performed to test if geographic mobility, attained education, and PGSEdu were associated with mortality. Results: The results show that both attained education and PGSEdu predicted geographic mobility, in both independent and joint effect models, with higher education associated with higher mobility. Geographic mobility was associated with lower mortality in the independent effect model, but joint effect models showed that this association was completely explained by attained education. Conclusions: To conclude, both attained education and PGSEdu were associated with geographic mobility. Moreover, attained education explained the relationship between geographic mobility and mortality.

Place, publisher, year, edition, pages
Elsevier, 2023
Keywords
adult, article, education, educational status, genetic risk score, human, human experiment, major clinical study, mortality, social status, tertiary education, Attained education, Geographic mobility, Polygenic score, Socioeconomic status
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:hj:diva-60153 (URN)10.1016/j.socscimed.2023.115882 (DOI)000975172700001 ()37030096 (PubMedID)2-s2.0-85151519861 (Scopus ID)HOA;intsam;875670 (Local ID)HOA;intsam;875670 (Archive number)HOA;intsam;875670 (OAI)
Funder
NIH (National Institutes of Health), R01 AG059329, R01 AG060470Swedish Research Council, 2017-00641
Available from: 2023-04-17 Created: 2023-04-17 Last updated: 2023-05-15Bibliographically approved
Karlsson, I. K., Zhan, Y., Wang, Y., Li, X., Jylhava, J., Hägg, S., . . . Reynolds, C. A. (2022). Adiposity and the risk of dementia: mediating effects from inflammation and lipid levels. European Journal of Epidemiology, 37, 1261-1271
Open this publication in new window or tab >>Adiposity and the risk of dementia: mediating effects from inflammation and lipid levels
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2022 (English)In: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 37, p. 1261-1271Article in journal (Refereed) Published
Abstract [en]

While midlife adiposity is a risk factor for dementia, adiposity in late-life appears to be associated with lower risk. What drives the associations is poorly understood, especially the inverse association in late-life. Using results from genome-wide association studies, we identified inflammation and lipid metabolism as biological pathways involved in both adiposity and dementia. To test if these factors mediate the effect of midlife and/or late-life adiposity on dementia, we then used cohort data from the Swedish Twin Registry, with measures of adiposity and potential mediators taken in midlife (age 40-64, n = 5999) or late-life (age 65-90, n = 7257). Associations between body-mass index (BMI), waist-hip ratio (WHR), C-reactive protein (CRP), lipid levels, and dementia were tested in survival and mediation analyses. Age was used as the underlying time scale, and sex and education included as covariates in all models. Fasting status was included as a covariate in models of lipids. One standard deviation (SD) higher WHR in midlife was associated with 25% (95% CI 2-52%) higher dementia risk, with slight attenuation when adjusting for BMI. No evidence of mediation through CRP or lipid levels was present. After age 65, one SD higher BMI, but not WHR, was associated with 8% (95% CI 1-14%) lower dementia risk. The association was partly mediated by higher CRP, and suppressed when high-density lipoprotein levels were low. In conclusion, the negative effects of midlife adiposity on dementia risk were driven directly by factors associated with body fat distribution, with no evidence of mediation through inflammation or lipid levels. There was an inverse association between late-life adiposity and dementia risk, especially where the body's inflammatory response and lipid homeostasis is intact.

Place, publisher, year, edition, pages
Springer, 2022
Keywords
Adiposity, Obesity, Dementia, Mediation, Inflammation, Lipids
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:hj:diva-58661 (URN)10.1007/s10654-022-00918-w (DOI)000863551600001 ()36192662 (PubMedID)2-s2.0-85139204304 (Scopus ID)HOA;intsam;837880 (Local ID)HOA;intsam;837880 (Archive number)HOA;intsam;837880 (OAI)
Funder
Axel and Margaret Ax:son Johnson FoundationNIH (National Institutes of Health), R01 AG028555, R01 AG060470, R01 AG08724, R01 AG08861, R01 AG10175, U01 DK066134Vårdal FoundationSwedish Research Council, 2016-03081, 2017-00641Forte, Swedish Research Council for Health, Working Life and Welfare, 2018-01201
Available from: 2022-10-18 Created: 2022-10-18 Last updated: 2022-12-28Bibliographically approved
Ler, P., Li, X., Hassing, L. B., Reynolds, C. A., Finkel, D., Karlsson, I. K. & Dahl Aslan, A. K. (2022). Independent and joint effects of body mass index and metabolic health in mid- and late-life on all-cause mortality: a cohort study from the Swedish Twin Registry with a mean follow-up of 13 Years. BMC Public Health, 22(1), Article ID 718.
Open this publication in new window or tab >>Independent and joint effects of body mass index and metabolic health in mid- and late-life on all-cause mortality: a cohort study from the Swedish Twin Registry with a mean follow-up of 13 Years
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2022 (English)In: BMC Public Health, E-ISSN 1471-2458, Vol. 22, no 1, article id 718Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: There is robust evidence that in midlife, higher body mass index (BMI) and metabolic syndrome (MetS), which often co-exist, are associated with increased mortality risk. However, late-life findings are inconclusive, and few studies have examined how metabolic health status (MHS) affects the BMI-mortality association in different age categories. We, therefore, aimed to investigate how mid- and late-life BMI and MHS interact to affect the risk of mortality. METHODS: This cohort study included 12,467 participants from the Swedish Twin Registry, with height, weight, and MHS measures from 1958-2008 and mortality data linked through 2020. We applied Cox proportional hazard regression with age as a timescale to examine how BMI categories (normal weight, overweight, obesity) and MHS (identification of MetS determined by presence/absence of hypertension, hyperglycemia, low HDL, hypertriglyceridemia), independently and in interaction, are associated with the risk of all-cause mortality. Models were adjusted for sex, education, smoking, and cardiovascular disease. RESULTS: The midlife group included 6,252 participants with a mean age of 59.6 years (range = 44.9-65.0) and 44.1% women. The late-life group included 6,215 participants with mean age 73.1 years (65.1-95.3) and 46.6% women. In independent effect models, metabolically unhealthy status in midlife increased mortality risks by 31% [hazard ratio 1.31; 95% confidence interval 1.12-1.53] and in late-life, by 18% (1.18;1.10-1.26) relative to metabolically healthy individuals. Midlife obesity increased the mortality risks by 30% (1.30;1.06-1.60) and late-life obesity by 15% (1.15; 1.04-1.27) relative to normal weight. In joint models, the BMI estimates were attenuated while those of MHS were less affected. Models including BMI-MHS categories revealed that, compared to metabolically healthy normal weight, the metabolically unhealthy obesity group had increased mortality risks by 53% (1.53;1.19-1.96) in midlife, and across all BMI categories in late-life (normal weight 1.12; 1.01-1.25, overweight 1.10;1.01-1.21, obesity 1.31;1.15-1.49). Mortality risk was decreased by 9% (0.91; 0.83-0.99) among those with metabolically healthy overweight in late-life. CONCLUSIONS: MHS strongly influenced the BMI-mortality association, such that individuals who were metabolically healthy with overweight or obesity in mid- or late-life did not carry excess risks of mortality. Being metabolically unhealthy had a higher risk of mortality independent of their BMI. 

Place, publisher, year, edition, pages
Springer, 2022
Keywords
Body weight, Metabolic syndrome, Metabolically benign obesity, Metabolically healthy obesity, Mortality, Obesity, adult, aged, body mass, cohort analysis, complication, female, follow up, human, male, metabolic syndrome X, middle aged, register, risk factor, Sweden, Body Mass Index, Cohort Studies, Follow-Up Studies, Humans, Overweight, Registries, Risk Factors
National Category
Geriatrics
Identifiers
urn:nbn:se:hj:diva-56270 (URN)10.1186/s12889-022-13082-3 (DOI)000780938900003 ()35410261 (PubMedID)2-s2.0-85128008833 (Scopus ID)GOA;intsam;808345 (Local ID)GOA;intsam;808345 (Archive number)GOA;intsam;808345 (OAI)
Funder
Swedish Research Council, 2016-03081Forte, Swedish Research Council for Health, Working Life and Welfare, 2018-01201NIH (National Institute of Health), AG060470European Commission, 2017-00,641
Available from: 2022-04-25 Created: 2022-04-25 Last updated: 2023-08-28Bibliographically approved
Karlsson, I. K., Escott-Price, V., Gatz, M., Hardy, J., Pedersen, N. L., Shoai, M. & Reynolds, C. A. (2022). Measuring heritable contributions to Alzheimer's disease: polygenic risk score analysis with twins. Brain Communications, 4(1), Article ID fcab308.
Open this publication in new window or tab >>Measuring heritable contributions to Alzheimer's disease: polygenic risk score analysis with twins
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2022 (English)In: Brain Communications, E-ISSN 2632-1297, Vol. 4, no 1, article id fcab308Article in journal (Refereed) Published
Abstract [en]

The heritability of Alzheimer's disease estimated from twin studies is greater than the heritability derived from genome-based studies, for reasons that remain unclear. We apply both approaches to the same twin sample, considering both Alzheimer's disease polygenic risk scores and heritability from twin models, to provide insight into the role of measured genetic variants and to quantify uncaptured genetic risk. A population-based heritability and polygenic association study of Alzheimer's disease was conducted between 1986 and 2016 and is the first study to incorporate polygenic risk scores into biometrical twin models of Alzheimer's disease. The sample included 1586 twins drawn from the Swedish Twin Registry which were nested within 1137 twin pairs (449 complete pairs and 688 incomplete pairs) with clinically based diagnoses and registry follow-up (M-age = 85.28, SD = 7.02; 44% male; 431 cases and 1155 controls). We report contributions of polygenic risk scores at P < 1 x 10(-5), considering a full polygenic risk score (PRS), PRS without the APOE region (PRS.no.APOE) and PRS.no.APOE plus directly measured APOE alleles. Biometric twin models estimated the contribution of environmental influences and measured (PRS) and unmeasured genes to Alzheimer's disease risk. The full PRS and PRS.no.APOE contributed 10.1 and 2.4% to Alzheimer's disease risk, respectively. When APOE e4 alleles were added to the model with the PRS.no.APOE, the total contribution was 11.4% to Alzheimer's disease risk, where APOE e4 explained 9.3% and PRS.no.APOE dropped from 2.4 to 2.1%. The total genetic contribution to Alzheimer's disease risk, measured and unmeasured, was 71% while environmental influences unique to each twin accounted for 29% of the risk. The APOE region accounts for much of the measurable genetic contribution to Alzheimer's disease, with a smaller contribution from other measured polygenic influences. Importantly, substantial background genetic influences remain to be understood. Karlsson et al. report that measured polygenic scores from genome-based studies, including an outsized role for APOE, explain only a fraction of the heritability indicated by twin models of Alzheimer's disease, leaving most genetic risk for Alzheimer's disease unexplained. Sensitive designs are needed to capture all the genetic influences.

Place, publisher, year, edition, pages
Oxford University Press, 2022
Keywords
polygenic risk scores (PRSs), APOE, heritability, twins, Alzheimer's disease
National Category
Neurosciences
Identifiers
urn:nbn:se:hj:diva-57230 (URN)10.1093/braincomms/fcab308 (DOI)000804710200011 ()35169705 (PubMedID)HOA;intsam;818360 (Local ID)HOA;intsam;818360 (Archive number)HOA;intsam;818360 (OAI)
Funder
NIH (National Institute of Health)
Available from: 2022-06-16 Created: 2022-06-16 Last updated: 2022-10-31Bibliographically approved
Hou, J., Hess, J. L., Armstrong, N., Bis, J. C., Grenier-Boley, B., Karlsson, I. K., . . . Glatt, S. J. (2022). Polygenic resilience scores capture protective genetic effects for Alzheimer’s disease. Translational Psychiatry, 12(1), Article ID 296.
Open this publication in new window or tab >>Polygenic resilience scores capture protective genetic effects for Alzheimer’s disease
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2022 (English)In: Translational Psychiatry, E-ISSN 2158-3188, Vol. 12, no 1, article id 296Article in journal (Refereed) Published
Abstract [en]

Polygenic risk scores (PRSs) can boost risk prediction in late-onset Alzheimer’s disease (LOAD) beyond apolipoprotein E (APOE) but have not been leveraged to identify genetic resilience factors. Here, we sought to identify resilience-conferring common genetic variants in (1) unaffected individuals having high PRSs for LOAD, and (2) unaffected APOE-ε4 carriers also having high PRSs for LOAD. We used genome-wide association study (GWAS) to contrast “resilient” unaffected individuals at the highest genetic risk for LOAD with LOAD cases at comparable risk. From GWAS results, we constructed polygenic resilience scores to aggregate the addictive contributions of risk-orthogonal common variants that promote resilience to LOAD. Replication of resilience scores was undertaken in eight independent studies. We successfully replicated two polygenic resilience scores that reduce genetic risk penetrance for LOAD. We also showed that polygenic resilience scores positively correlate with polygenic risk scores in unaffected individuals, perhaps aiding in staving off disease. Our findings align with the hypothesis that a combination of risk-independent common variants mediates resilience to LOAD by moderating genetic disease risk.

Place, publisher, year, edition, pages
Springer, 2022
National Category
Geriatrics
Identifiers
urn:nbn:se:hj:diva-58139 (URN)10.1038/s41398-022-02055-0 (DOI)000829935000003 ()35879306 (PubMedID)2-s2.0-85134766683 (Scopus ID)HOA;intsam;824377 (Local ID)HOA;intsam;824377 (Archive number)HOA;intsam;824377 (OAI)
Funder
EU, Horizon 2020
Available from: 2022-08-09 Created: 2022-08-09 Last updated: 2024-01-17Bibliographically approved
Wightman, D. P., Jansen, I. E., Savage, J. E., Shadrin, A. A., Bahrami, S., Holland, D., . . . Team, 2. R. (2021). A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer’s disease. Nature Genetics, 53(9), 1276-1282
Open this publication in new window or tab >>A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer’s disease
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2021 (English)In: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 53, no 9, p. 1276-1282Article in journal (Refereed) Published
Abstract [en]

Late-onset Alzheimer’s disease is a prevalent age-related polygenic disease that accounts for 50–70% of dementia cases. Currently, only a fraction of the genetic variants underlying Alzheimer’s disease have been identified. Here we show that increased sample sizes allowed identification of seven previously unidentified genetic loci contributing to Alzheimer’s disease. This study highlights microglia, immune cells and protein catabolism as relevant to late-onset Alzheimer’s disease, while identifying and prioritizing previously unidentified genes of potential interest. We anticipate that these results can be included in larger meta-analyses of Alzheimer’s disease to identify further genetic variants that contribute to Alzheimer’s pathology.

Place, publisher, year, edition, pages
Springer Nature, 2021
National Category
Neurology
Identifiers
urn:nbn:se:hj:diva-54690 (URN)10.1038/s41588-021-00921-z (DOI)000694666000007 ()34493870 (PubMedID)2-s2.0-85114746630 (Scopus ID);intsam;766606 (Local ID);intsam;766606 (Archive number);intsam;766606 (OAI)
Funder
NIH (National Institute of Health)Wellcome trust, 082604/2/07/ZThe Research Council of Norway, 223273,248778,248980
Available from: 2021-09-20 Created: 2021-09-20 Last updated: 2022-10-31Bibliographically approved
Karlsson, I. K., Zhan, Y., Gatz, M., Reynolds, C. A. & Dahl Aslan, A. K. (2021). Change in cognition and body mass index in relation to preclinical dementia. Alzheimer’s & Dementia: Translational Research & Clinical Interventions, 7(1), Article ID e12176.
Open this publication in new window or tab >>Change in cognition and body mass index in relation to preclinical dementia
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2021 (English)In: Alzheimer’s & Dementia: Translational Research & Clinical Interventions, E-ISSN 2352-8737, Vol. 7, no 1, article id e12176Article in journal (Refereed) Published
Abstract [en]

Introduction To study if declining cognition drives weight loss in preclinical dementia, we examined the longitudinal association between body mass index (BMI) and cognitive abilities in individuals who did or did not later develop dementia. Methods Using data from individuals spanning age 50 to 89, we applied dual change score models separately in individuals who remained cognitively intact (n = 1498) and those who were diagnosed with dementia within 5 years of last assessment (n = 459). Results Among the cognitively intact, there was a bidirectional association: Stable BMI predicted stable cognition and vice versa. Among individuals who were subsequently diagnosed with dementia, the association was unidirectional: Higher BMI predicted declining cognition but cognition did not predict change in BMI. Discussion Although BMI and cognition stabilized each other when cognitive functioning was intact, this buffering effect was missing in the preclinical dementia phase. This finding indicates that weight loss in preclinical dementia is not driven by declining cognition.

Place, publisher, year, edition, pages
John Wiley & Sons, 2021
Keywords
body mass index, cognition, longitudinal, preclinical dementia, weight change
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:hj:diva-55909 (URN)10.1002/trc2.12176 (DOI)000750546300073 ()34027026 (PubMedID)2-s2.0-85124384254 (Scopus ID)HOA;intsam;796586 (Local ID)HOA;intsam;796586 (Archive number)HOA;intsam;796586 (OAI)
Funder
Forte, Swedish Research Council for Health, Working Life and Welfare, 2018-01201Swedish Research Council, 2016-03081, 2017-00641European Commission, 825-2007-7460, 825-2009-6141NIH (National Institutes of Health), NIH AG060470, AG04563, AG10175, R01AG08861
Available from: 2022-02-17 Created: 2022-02-17 Last updated: 2023-03-13Bibliographically approved
de Rojas, I., Moreno-Grau, S., Tesi, N., Grenier-Boley, B., Andrade, V., Jansen, I. E., . . . consortia, P.-A. (2021). Common variants in Alzheimer’s disease and risk stratification by polygenic risk scores. Nature Communications, 12(1), Article ID 3417.
Open this publication in new window or tab >>Common variants in Alzheimer’s disease and risk stratification by polygenic risk scores
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2021 (English)In: Nature Communications, E-ISSN 2041-1723, Vol. 12, no 1, article id 3417Article in journal (Refereed) Published
Abstract [en]

Genetic discoveries of Alzheimer’s disease are the drivers of our understanding, and together with polygenetic risk stratification can contribute towards planning of feasible and efficient preventive and curative clinical trials. We first perform a large genetic association study by merging all available case-control datasets and by-proxy study results (discovery n = 409,435 and validation size n = 58,190). Here, we add six variants associated with Alzheimer’s disease risk (near APP, CHRNE, PRKD3/NDUFAF7, PLCG2 and two exonic variants in the SHARPIN gene). Assessment of the polygenic risk score and stratifying by APOE reveal a 4 to 5.5 years difference in median age at onset of Alzheimer’s disease patients in APOE ɛ4 carriers. Because of this study, the underlying mechanisms of APP can be studied to refine the amyloid cascade and the polygenic risk score provides a tool to select individuals at high risk of Alzheimer’s disease.

Place, publisher, year, edition, pages
Springer Nature, 2021
Keywords
detection method, genetic analysis, nervous system disorder, public health, risk assessment, risk factor, stratification, amyloid precursor protein, apolipoprotein E, APP protein, human, aged, Alzheimer disease, case control study, cohort analysis, female, follow up, genetic predisposition, genetics, genome-wide association study, heterozygote, human, information processing, male, metabolism, middle aged, multifactorial inheritance, onset age, pathology, procedures, single nucleotide polymorphism, very elderly, Age of Onset, Aged, 80 and over, Amyloid beta-Protein Precursor, Apolipoproteins E, Case-Control Studies, Cohort Studies, Datasets as Topic, Follow-Up Studies, Genetic Predisposition to Disease, Humans, Polymorphism, Single Nucleotide, Risk Factors
National Category
Neurosciences
Identifiers
urn:nbn:se:hj:diva-54089 (URN)10.1038/s41467-021-22491-8 (DOI)000667727200071 ()34099642 (PubMedID)2-s2.0-85107895788 (Scopus ID)GOA;intsam;54089 (Local ID)GOA;intsam;54089 (Archive number)GOA;intsam;54089 (OAI)
Available from: 2021-07-15 Created: 2021-07-15 Last updated: 2023-03-28Bibliographically approved
Karlsson, I. K., Arpawong, T. E., Zhan, Y. & Lehto, K. (2021). Editorial: Genetics of Age-Related Diseases and Their Risk and Protective Factors. Frontiers in Genetics, 12, Article ID 771109.
Open this publication in new window or tab >>Editorial: Genetics of Age-Related Diseases and Their Risk and Protective Factors
2021 (English)In: Frontiers in Genetics, E-ISSN 1664-8021, Vol. 12, article id 771109Article in journal, Editorial material (Other academic) Published
Place, publisher, year, edition, pages
Frontiers Media S.A., 2021
Keywords
age-related disease, aging, editorial, genetic epidemiology, protective factor, risk factor
National Category
Geriatrics
Identifiers
urn:nbn:se:hj:diva-54939 (URN)10.3389/fgene.2021.771109 (DOI)000717384400001 ()34646315 (PubMedID)2-s2.0-85116885173 (Scopus ID)
Available from: 2021-10-25 Created: 2021-10-25 Last updated: 2023-02-23Bibliographically approved
Karlsson, I. K., Ericsson, M., Wang, Y., Jylhävä, J., Hägg, S., Dahl Aslan, A. K., . . . Pedersen, N. L. (2021). Epigenome-wide association study of level and change in cognitive abilities from midlife through late life. Clinical Epigenetics, 13(1), Article ID 85.
Open this publication in new window or tab >>Epigenome-wide association study of level and change in cognitive abilities from midlife through late life
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2021 (English)In: Clinical Epigenetics, ISSN 1868-7075, Vol. 13, no 1, article id 85Article in journal (Refereed) Published
Abstract [en]

Background: Epigenetic mechanisms are important in aging and may be involved in late-life changes in cognitive abilities. We conducted an epigenome-wide association study of leukocyte DNA methylation in relation to level and change in cognitive abilities, from midlife through late life in 535 Swedish twins. Results: Methylation levels were measured with the Infinium Human Methylation 450 K or Infinium MethylationEPIC array, and all sites passing quality control on both arrays were selected for analysis (n = 250,816). Empirical Bayes estimates of individual intercept (age 65), linear, and quadratic change were obtained from latent growth curve models of cognitive traits and used as outcomes in linear regression models. Significant sites (p &lt; 2.4 × 10–7) were followed up in between-within twin pair models adjusting for familial confounding and full-growth modeling. We identified six significant associations between DNA methylation and level of cognitive abilities at age 65: cg18064256 (PPP1R13L) with processing speed and spatial ability; cg04549090 (NRXN3) with spatial ability; cg09988380 (POGZ), cg25651129 (-), and cg08011941 (ENTPD8) with working memory. The genes are involved in neuroinflammation, neuropsychiatric disorders, and ATP metabolism. Within-pair associations were approximately half that of between-pair associations across all sites. In full-growth curve models, associations between DNA methylation and cognitive level at age 65 were of small effect sizes, and associations between DNA methylation and longitudinal change in cognitive abilities of very small effect sizes. Conclusions: Leukocyte DNA methylation was associated with level, but not change in cognitive abilities. The associations were substantially attenuated in within-pair analyses, indicating they are influenced in part by genetic factors.

Place, publisher, year, edition, pages
BioMed Central, 2021
Keywords
Aging, Cognition, DNA methylation, EWAS, Longitudinal
National Category
Gerontology, specialising in Medical and Health Sciences
Identifiers
urn:nbn:se:hj:diva-52430 (URN)10.1186/s13148-021-01075-9 (DOI)000643777400003 ()33883019 (PubMedID)2-s2.0-85104700219 (Scopus ID)GOA;intsam;739769 (Local ID)GOA;intsam;739769 (Archive number)GOA;intsam;739769 (OAI)
Funder
Swedish Research Council, 2017-00641, 2019-01272, 2013-08689, 2015-03255, 2015-06796Knut and Alice Wallenberg FoundationNIH (National Institute of Health), AG10175, AG04563Forte, Swedish Research Council for Health, Working Life and Welfare, 2018-01201, 2013-02292
Available from: 2021-05-10 Created: 2021-05-10 Last updated: 2022-10-31Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0003-3605-7829

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