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Behavior genetic methods are useful for examining mechanisms underlying the interaction between genetic and family environmental factors of internalizing problem behavior (INT). Previous twin studies, however, have shown little consistency in interaction patterns, depending on type and operationalization of measured environments. The aim of the current study was to explore different gene-by-environment interaction patterns among different family-level environmental risk factors and resources known to correlate with INT. Using an empirical-based approach, we combined various indicators of the family environment to derive four dimensions: "positive parenting," "negative parenting," "lack of parental resources," and "socioeconomic status." We then used a genetically informed design of twins raised in the same family to test whether interaction patterns followed a diathesis stress or vantage sensitivity model formulation. The sample consisted of 2,089 twin pairs and their families from two twin birth cohorts (ages 11 and 17) participating in Wave 1 of the German TwinLife study of social inequalities. In line with a vantage sensitivity pattern of interaction and with the bioecological model of development (Bronfenbrenner & Ceci, 1994), evidence for a general mechanism of gene-environment interaction with increasing nonshared environmental variance for more adverse and less propitious family conditions was found. In preadolescence, parenting behavior had a greater moderating influence on INT compared to general family conditions like socioeconomic status. Interventions for INT that directly involve parents, thus, may be more important in preadolescent populations whereas individual interventions for adolescents may be more successful if they are adapted to different levels of socioeconomic status.

Twins regularly score nearly a standard deviation below the population mean on standardized measures of cognitive development in infancy but recover to the population mean by early childhood, making rapid gains through the toddler years. To date, only polynomial growth models have been fit to model cognitive recovery across childhood, limiting the applicability of the growth parameters to later developmental periods. We fit a nonlinear asymptotic Gompertz growth model to prospective cognitive scores from 1,153 individual twins from 578 families (47.9% male, 91.5% White, 61.6% monozygotic) measured at 16 time points between 3 months and 15 years. Twins displayed a lower asymptote of 86.47 (0.90 SD below the population mean) and gained on average 17.01 points, achieving an upper asymptote of 103.48. Growth was observed to be most rapid at 3.26 years, highlighting the importance of the toddler years in cognitive development. Biometric analyses revealed that shared environmental factors accounted for the majority of the variance in initial cognitive ability as well as asymptotic growth in cognitive ability. Gestational age and family socioeconomic status (SES) were robust predictors of cognitive growth. Results from the present study provide insight into the growth processes underlying the recovery of cognitive ability to the population mean for children evincing slight delays in their initial cognitive ability. In particular, findings highlight prenatal factors and family economic resources as important aspects of the environment in the recovery of cognitive ability.

This study investigated the systematic rise in cognitive ability scores over generations, known as the "Flynn Effect," across middle childhood and early adolescence (7-15 years; 291 monozygotic pairs, 298 dizygotic pairs; 89% White). Leveraging the unique structure of the Louisville Twin Study (longitudinal data collected continuously from 1957 to 1999 using the Wechsler Intelligence Scale for Children [WISC], WISC-R, and WISC-III ed.), multilevel analyses revealed between-subjects Flynn Effects--as both decrease in mean scores upon test re-standardization and increase in mean scores across cohorts--as well as within-child Flynn Effects on cognitive growth across age. Overall gains equaled approximately three IQ points per decade. Novel genetically informed analyses suggested that individual sensitivity to the Flynn Effect was moderated by an interplay of genetic and environmental factors.

We examined whether attained socioeconomic status (SES) moderated genetic and environmental sources of individual differences in cognitive performance using pooled data from 9 adult twin studies. Prior work concerning SES moderation of cognitive performance has focused on rearing SES. The current adult sample of 12,196 individuals (aged 27-98 years) allowed for the examination of common sources of individual differences between attained SES and cognitive performance (signaling potential gene-environment correlation mechanisms, rGE), as well as sources of individual differences unique to cognitive performance (signaling potential gene-environment interaction mechanisms, G × E). Attained SES moderated sources of individual differences in 4 cognitive domains, assessed via performance on 5 cognitive tests ranging 2,149 to 8,722 participants. Attained SES moderated common sources of influences for 3 domains and influences unique to cognition in all 4 domains. The net effect was that genetic influences on the common pathway tended to be relatively more important at the upper end of attained SES indicating possible active rGE, whereas, genetic influences for the unique pathway were proportionally stable or less important at the upper end of attained SES. As a noted exception, at the upper end of attained SES, genetic influences unique to perceptual speed were amplified and genetic influences on the common pathway were dampened. Accounting for rearing SES did not alter attained SES moderation effects on cognitive performance, suggesting mechanisms germane to adulthood. Our findings suggest the importance of gene--environment mechanisms through which attained SES moderates sources of individual differences in cognitive performance.

This study tested phenotypic and biometric associations between physical and cognitive catch‐up growth in a community sample of twins (n = 1285, 51.8% female, 89.3% White). Height and weight were measured at up to 17 time points between birth and 15 years, and cognitive ability was assessed at up to 16 time points between 3 months and 15 years. Weight and length at birth were positively associated with cognitive abilities in infancy and adolescence (r's =.16–.51). More rapid weight catch‐up growth was associated with slower, steadier cognitive catch‐up growth. Shared and nonshared environmental factors accounted for positive associations between physical size at birth and cognitive outcomes. Findings highlight the role of prenatal environmental experiences in physical and cognitive co‐development. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Dementia predicts increased mortality. We used case‐control and co‐twin control models to investigate genetic and shared environmental influences on this association. METHODS: Case‐control design, including 987 twins with dementia and 2938 age‐ and sex‐matched controls in the Swedish Twin Registry. Co‐twin control design, including 90 monozygotic (MZ) and 288 dizygotic (DZ) twin pairs discordant for dementia. To test for genetic and environmental confounding, differences were examined in mortality risk between twins with dementia and their matched or co‐twin controls. RESULTS: Twins with dementia showed greater mortality risk than age‐ and sex‐matched controls (HR = 2.02 [1.86, 2.18]). Mortality risk is significantly elevated but attenuated substantially in discordant twin pairs, for example, comparing MZ twins with dementia to their co‐twin controls (HR = 1.48 [1.08, 2.04]). DISCUSSION: Findings suggest that genetic factors partially confound the association between dementia and mortality and provide an alternative hypothesis to increased mortality due to dementia itself. Highlights: We studied dementia and mortality in twin pairs discordant for dementia.People without dementia outlived people with dementia.Identical twins with dementia and their co‐twin controls had similar survival time.Findings suggest genotype may explain the link between dementia and mortality. [ABSTRACT FROM AUTHOR]

Objectives Loneliness may influence aging biomarkers related to cognitive functioning, for example, through accelerated DNA methylation (DNAm) aging. Methods In the present study, we tested whether six common DNAm age acceleration measures mediated the effects of baseline loneliness and five different longitudinal loneliness trajectories on general cognitive ability, immediate memory recall, delayed memory recall, and processing speed in 1,814 older adults in the Health and Retirement Study. Results We found that baseline loneliness and individuals who belong to the highest loneliness trajectories had poorer general cognitive ability and memory scores. Only DNAm age acceleration measures that index physiological comorbidities, unhealthy lifestyle factors (e.g. smoking), and mortality risk-mediated effects of baseline loneliness on general cognitive ability and memory functioning but not processing speed. These same DNAm measures mediated effects of the moderate-but-declining loneliness trajectory on cognitive functioning. Additionally, immediate and delayed memory scores were mediated by GrimAge Accel in the lowest and two highest loneliness trajectory groups. Total and mediated effects of loneliness on cognitive functioning outcomes were mainly accounted for by demographic, social, psychological, and physiological covariates, most notably self-rated health, depressive symptomatology, objective social isolation, and body mass index. Discussion Current findings suggest that DNAm biomarkers of aging, particularly GrimAge Accel, have promise for explaining the prospective association between loneliness and cognitive functioning outcomes. [ABSTRACT FROM AUTHOR]

The Spanish English Neuropsychological Assessment Scale (SENAS) is a cognitive battery with English and Spanish versions for use with persons for whom either language is predominant. Few studies have examined its utility outside the normative sample. The current study examined SENAS performance in samples of older adult Latines and Latines with or at risk for autosomal dominant Alzheimer's disease (ADAD) mutations. The SENAS was administered to 202 older adults from the Los Angeles Latino Eye Study (LALES) and 29 adults with (carriers) or without (non-carriers) mutations causing ADAD. We examined associations between SENAS, age, education, and language (LALES) and between SENAS, estimated years from familial age of dementia diagnosis, education, language, and acculturation (ADAD). Partial correlations were used to examine differences in correlational strength between estimated years from familial age of dementia diagnosis and SENAS scores among ADAD carriers compared to chronological age and SENAS in the LALES sample. Exploratory t-tests were performed to examine SENAS performance differences between ADAD carriers and non-carriers. In an older adult sample (LALES), increased age correlated with worse verbal delayed recall; English fluency and higher education correlated with better naming and visuospatial subtest performance. Among ADAD carriers, verbal and nonverbal delayed recall and object naming subtest performance worsened as they approached their familial age of dementia diagnosis. English fluency and higher U.S.-acculturation were related to better SENAS performance among carriers and non-carriers. Tests of verbal delayed recall and object naming best distinguished ADAD carriers from their familial non-carrier counterparts. Verbal delayed recall and object naming measures appear to be most sensitive to age-related changes in older adult samples and mutation-related changes in distinguishing ADAD carriers from non-carriers. Future research should examine the sensitivity of SENAS in other samples, such as larger samples of symptomatic ADAD carriers and other AD subtypes. [ABSTRACT FROM AUTHOR]

Behavior genetic methods are useful for examining mechanisms underlying the interaction between genetic and family environmental factors of internalizing problem behavior (INT). Previous twin studies, however, have shown little consistency in interaction patterns, depending on type and operationalization of measured environments. The aim of the current study was to explore different gene-by-environment interaction patterns among different family-level environmental risk factors and resources known to correlate with INT. Using an empirical-based approach, we combined various indicators of the family environment to derive four dimensions: positive parenting, negative parenting, lack of parental resources, and socioeconomic status. We then used a genetically informed design of twins raised in the same family to test whether interaction patterns followed a diathesis stress or vantage sensitivity model formulation. The sample consisted of 2,089 twin pairs and their families from two twin birth cohorts (ages 11 and 17) participating in Wave 1 of the German TwinLife study of social inequalities. In line with a vantage sensitivity pattern of interaction and with the bioecological model of development (Bronfenbrenner & Ceci, 1994), evidence for a general mechanism of gene–environment interaction with increasing nonshared environmental variance for more adverse and less propitious family conditions was found. In preadolescence, parenting behavior had a greater moderating influence on INT compared to general family conditions like socioeconomic status. Interventions for INT that directly involve parents, thus, may be more important in preadolescent populations whereas individual interventions for adolescents may be more successful if they are adapted to different levels of socioeconomic status. Public Significance Statement: The present study suggests that environmental influences outside the family may have a greater impact on internalizing problem behavior under less advantageous family conditions. In preadolescence, interventions for internalizing problem behavior should involve parents directly whereas in adolescence, interventions may be tailored individually that take into account adolescents' socioeconomic status. [ABSTRACT FROM AUTHOR]

Stress exposure and stress reactivity may be potent factors associated with increased risk of dementia. The 2017 Lancet Commission on Dementia and its 2020 update reviewed modifiable risk factors associated with dementia, but stress was not addressed directly. The present study provides a focused review of the association between stress and dementia across the lifespan, with measures of stress including stress exposure, psychological stress, posttraumatic stress disorder (PTSD), and biological markers of stress. Published research articles were identified in the American Psychological Association PsycINFO database (1887–2021), Web of Science database, and Google Scholar. A total of 53 samples from 40 studies published from 1985 to 2020 met inclusion criteria. Results suggest that stressful life events that occur earlier in the lifespan, such as loss of a parent, psychological stress experienced in midlife, and extreme stress responses, i.e., PTSD, correlate with higher risk of dementia. Although results generally are mixed, a consistent theme is that stress experienced earlier in the lifespan and chronic stress portend the greatest risk of dementia. Reducing stress exposure and improving stress management when stress exposure cannot be changed are thus relevant strategies in dementia risk reduction. [ABSTRACT FROM AUTHOR]

Latent variable models can create a latent dementia index (LDI) using cognitive and functional ability to approximate dementia likelihood. The LDI approach has been applied across diverse cohorts. It is unclear whether sex affects its measurement properties. We use Wave A (2001–2003) of the Aging, Demographics, and Memory Study (n = 856). Multiple group confirmatory factor analysis (CFA) was used to test measurement invariance (MI) using informant‐reported functional ability and cognitive performance tasks, which we group into verbal, nonverbal, and memory. Partial scalar invariance was found, allowing for testing sex differences in LDI means (MDiff = 0.38). The LDI correlated with consensus panel dementia diagnosis, Mini‐Mental State Examination (MMSE), and dementia risk factors (low education, advanced age, and apolipoprotein ε4 [APOE‐ε4] status) for men and women. The LDI validly captures dementia likelihood to permit estimation of sex differences. LDI sex differences indicate higher dementia likelihood in women, potentially due to social, environmental, and biological factors. [ABSTRACT FROM AUTHOR]

Background: Epidemiological research on dementia is hampered by differences across studies in how dementia is classified, especially where clinical diagnoses of dementia may not be available.Objective: We apply structural equation modeling to estimate dementia likelihood across heterogeneous samples within a multi-study consortium and use the twin design of the sample to validate the results.Methods: Using 10 twin studies, we implement a latent variable approach that aligns different tests available in each study to assess cognitive, memory, and functional ability. The model separates general cognitive ability from components indicative of dementia. We examine the validity of this continuous latent dementia index (LDI). We then identify cut-off points along the LDI distributions in each study and align them across studies to distinguish individuals with and without probable dementia. Finally, we validate the LDI by determining its heritability and estimating genetic and environmental correlations between the LDI and clinically diagnosed dementia where available.Results: Results indicate that coordinated estimation of LDI across 10 studies has validity against clinically diagnosed dementia. The LDI can be fit to heterogeneous sets of memory, other cognitive, and functional ability variables to extract a score reflective of likelihood of dementia that can be interpreted similarly across studies despite diverse study designs and sampling characteristics. Finally, the same genetic sources of variance strongly contribute to both the LDI and clinical diagnosis.Conclusion: This latent dementia indicator approach may serve as a model for other research consortia confronted with similar data integration challenges. [ABSTRACT FROM AUTHOR]

Background: A large literature demonstrates associations between socioeconomic status (SES) and health, including physiological health and well-being. Moreover, gender differences are often observed among measures of both SES and health. However, relationships between SES and health are sometimes questioned given the lack of true experiments, and the potential biological and SES mechanisms explaining gender differences in health are rarely examined simultaneously.Purpose: To use a national sample of twins to investigate lifetime socioeconomic adversity and a measure of physiological dysregulation separately by sex.Methods: Using the twin sample in the second wave of the Midlife in the United States survey (MIDUS II), biometric regression analysis was conducted to determine whether the established SES-physiological health association is observed among twins both before and after adjusting for potential familial-level confounds (additive genetic and shared environmental influences that may underly the SES-health link), and whether this association differs among men and women.Results: Although individuals with less socioeconomic adversity over the lifespan exhibited less physiological dysregulation among this sample of twins, this association only persisted among male twins after adjusting for familial influences.Conclusions: Findings from the present study suggest that, particularly for men, links between socioeconomic adversity and health are not spurious or better explained by additive genetic or early shared environmental influences. Furthermore, gender-specific role demands may create differential associations between SES and health. [ABSTRACT FROM AUTHOR]

Research demonstrates that psychological and physiological outcomes are impacted positively by spirituality. Yet, spirituality may also exacerbate the impact of stressors. In order to assess the relationships among spirituality, premenstrual [...]

Twins regularly score nearly a standard deviation below the population mean on standardized measures of cognitive development in infancy but recover to the population mean by early childhood, making rapid gains through the toddler years. To date, only polynomial growth models have been fit to model cognitive recovery across childhood, limiting the applicability of the growth parameters to later developmental periods. We fit a nonlinear asymptotic Gompertz growth model to prospective cognitive scores from 1,153 individual twins from 578 families (47.9% male, 91.5% White, 61.6% monozygotic) measured at 16 time points between 3 months and 15 years. Twins displayed a lower asymptote of 86.47 (.90 SD below the population mean) and gained on average 17.01 points, achieving an upper asymptote of 103.48. Growth was observed to be most rapid at 3.26 years, highlighting the importance of the toddler years in cognitive development. Biometric analyses revealed that shared environmental factors accounted for the majority of the variance in initial cognitive ability as well as asymptotic growth in cognitive ability. Gestational age and family socioeconomic status (SES) were robust predictors of cognitive growth. Results from the present study provide insight into the growth processes underlying the recovery of cognitive ability to the population mean for children evincing slight delays in their initial cognitive ability. In particular, findings highlight prenatal factors and family economic resources as important aspects of the environment in the recovery of cognitive ability. [ABSTRACT FROM AUTHOR]

Conventional longitudinal behavioral genetic models estimate the relative contribution of genetic and environmental factors to stability and change of traits and behaviors. Longitudinal models rarely explain the processes that generate observed differences between genetically and socially related individuals. We propose that exchanges between individuals and their environments (i.e., phenotype–environment effects) can explain the emergence of observed differences over time. Phenotype–environment models, however, would require violation of the independence assumption of standard behavioral genetic models; that is, uncorrelated genetic and environmental factors. We review how specification of phenotype–environment effects contributes to understanding observed changes in genetic variability over time and longitudinal correlations among nonshared environmental factors. We then provide an example using 30 days of positive and negative affect scores from an all-female sample of twins. Results demonstrate that the phenotype–environment effects explain how heritability estimates fluctuate as well as how nonshared environmental factors persist over time. We discuss possible mechanisms underlying change in gene–environment correlation over time, the advantages and challenges of including gene–environment correlation in longitudinal twin models, and recommendations for future research. [ABSTRACT FROM AUTHOR]

This study investigated the systematic rise in cognitive ability scores over generations, known as the Flynn Effect, across middle childhood and early adolescence (7–15 years; 291 monozygotic pairs, 298 dizygotic pairs; 89% White). Leveraging the unique structure of the Louisville Twin Study (longitudinal data collected continuously from 1957 to 1999 using the Wechsler Intelligence Scale for Children [WISC], WISC–R, and WISC–III ed.), multilevel analyses revealed between‐subjects Flynn Effects—as both decrease in mean scores upon test re‐standardization and increase in mean scores across cohorts—as well as within‐child Flynn Effects on cognitive growth across age. Overall gains equaled approximately three IQ points per decade. Novel genetically informed analyses suggested that individual sensitivity to the Flynn Effect was moderated by an interplay of genetic and environmental factors. [ABSTRACT FROM AUTHOR]

Background: Prior research among patients with autosomal dominant Alzheimer's Disease (ADAD) has identified early cognitive changes 10‐20 years before formal dementia diagnosis. ADAD provides a model of Alzheimer's disease (AD) with a relatively predictable onset and with fewer age‐related comorbidities, and as such, may aid in identifying presymptomatic stages of cognitive change for early AD detection. The CASI is a comprehensive screening tool for dementia with multilingual adaptations and may be useful in identifying early cognitive changes among those with or at risk of ADAD. Method: We examined whether subscales of the Cognitive Abilities Screening Instrument (CASI) could identify early cognitive changes in ADAD as well as the effects of test language (English or Spanish), education, and acculturation on CASI subscales. 141 persons (96 mutation carriers [MC], 45 noncarriers [NC]) with or at risk for inheriting PSEN1/2 or APP mutations completed the CASI. Linear mixed‐effect models were used to examine the effects of adjusted age, mutation status, mutation type (APP or PSEN), test language, education, and acculturation on the 9 CASI subscales. Result: MCs performed significantly worse on CASI subscales than NCs (ps<.001). Adjusted age (βs = ‐.29— ‐.09), mutation status (βs = ‐2.62—‐0.09), and adjusted age x mutation status (βs = ‐.29— ‐0.09) significantly predicted Attention (R2 = 0.36), Concentration (R2 = 0.40), Orientation (R2 = 0.53), Short‐Term Memory (R2 = 0.61), Long‐Term Memory (R2 = 0.27), Language (R2 = 0.39), Visuoconstruction (R2 = 0.53), Fluency (R2 = 0.34), and Abstraction/Judgment (R2 = 0.37), all ps <.001. Acculturation significantly predicted Long‐Term Memory (β =.34, p =.03). The effects of acculturation, test language, and education were not significant for any other CASI subscales. Conclusion: Adjusted age, mutation status, and an interactive effect between adjusted age and mutation status appear to be important predictors in CASI performance, such that MCs closer to their familial age of dementia diagnosis are more likely to perform worse on the CASI. No subtest emerged as the best predictor of early cognitive changes in MCs. Attention to potential cultural influences on the Long‐Term Memory subtest warrants further research. [ABSTRACT FROM AUTHOR]

Although several studies have shown small longitudinal associations between baseline loneliness and subsequent dementia risk, studies rarely test whether change in loneliness predicts dementia risk. Furthermore, as both increase with advancing age, genetic and environmental selection processes may confound the putative causal association between loneliness and dementia risk. We used a sample of 2,476 individual twins from three longitudinal twin studies of aging in the Swedish Twin Registry to test the hypothesis that greater positive change in loneliness predicts greater dementia risk. We then used a sample of 1,632 pairs of twins to evaluate the hypothesis that effects of change in loneliness on dementia risk would remain after adjusting for effects of genetic and environmental variance. Phenotypic model results suggest that mild levels of baseline loneliness predict greater dementia risk. Contrary to our hypothesis, change in loneliness did not correlate with dementia risk, regardless of whether genetic and environmental selection confounds were taken into account. Worsening loneliness with age may not confer greater dementia risk. [ABSTRACT FROM AUTHOR]

Family-of-origin aggression (FOA) exposure is a chronic childhood stressor that has been linked to altered stress reactivity of the hypothalamic-pituitary-adrenal (HPA) axis in adulthood. The effects of FOA also spill over between partners in romantic couples, such that one partner's FOA history influences the other's HPA reactivity during couple interactions. However, the direction of these effects is inconsistent, with both heightened and blunted HPA reactivity observed; this heterogeneity suggests the presence of moderators. This study measured HPA reactivity during emotionally vulnerable conversations between young adult romantic partners to assess whether romantic attachment avoidance accounts for this divergence by moderating actor and partner effects of FOA on HPA. A total of 112 opposite-sex couples (224 young adults) provided information on FOA and avoidance, completed dyadic interaction procedures, and provided saliva samples to assess HPA reactivity during interactions. Multilevel structural equation models revealed that FOA did not predict either the actor's or the partner's HPA reactivity. However, FOA and avoidance interacted to produce both actor and partner effects, such that greater FOA exposure heightened HPA reactivity when avoidance was high but blunted reactivity when avoidance was low. The results support the conjecture that proximal relationship-related characteristics, such as attachment avoidance, influence whether distal relationship-related stressors, such as FOA, amplify or attenuate physiological reactivity during emotionally vulnerable interactions. Because HPA reactivity has been linked to a variety of health outcomes, identifying relationship-related buffers of associations between FOA and HPA response may inform future interventions to protect health for FOA-exposed youth. (PsycInfo Database Record (c) 2020 APA, all rights reserved). [ABSTRACT FROM AUTHOR]

Puberty in girls represents a notable period of vulnerability for different psychological disorders. The research literature has primarily considered external and contextual factors that might explain these rises in symptomatology. In the present study, we investigate relations of pubertal status and timing with individual cognitive, emotional, and behavioral tendencies, commonly identified as transdiagnostic processes, in a sample of N = 228 girls (Mage = 11.75 years). We also test whether these transdiagnostic processes mediate associations of pubertal status and pubertal timing with depressive symptoms. Results support greater endorsement of rumination, co‐rumination, negative urgency, and both anxious and angry rejection sensitivity in girls with more advanced pubertal status, as well as in girls with early pubertal timing. Higher levels of transdiagnostic processes fully mediated associations of pubertal status and timing with depressive symptoms at significant and marginally significant levels, respectively. Although the data are cross‐sectional, these findings offer promising preliminary evidence that transdiagnostic processes represent an important mental health risk in early adolescent girls. [ABSTRACT FROM AUTHOR]

Objectives Education and cognition are closely associated, yet the role of spousal education is not well understood. We estimate the independent effects of own and spousal education on cognitive ability in late-life in Mexico, a developing country experiencing rapid aging. Method We analyzed 4,017 married dyads (age 50+) from the 2012 Mexican Health and Aging Study. Cognitive ability for married adults was a factor score from a single factor model. Using seemingly unrelated regression, we test whether spousal education influences older adults' cognitive ability, whether associations are explained by couple-level socioeconomic position, health and health behaviors, and social support, and whether associations differed by gender. Results Education and cognitive ability were correlated within couples. Higher spousal education was associated with better cognitive ability. Associations between spousal education and cognitive ability were independent of own education, did not differ by gender, and remained significant even after adjustment for couple-level socioeconomic position, health and health behaviors, and perceived social support. Discussion In addition to own education, spousal education was associated with better cognitive ability, even at relatively low levels of education. We discuss the possibility that spousal education may improve cognition via transmission of knowledge and mutually reinforcing cognitively stimulating environments. [ABSTRACT FROM AUTHOR]

Background: While sex differences in incidence of Alzheimer's disease (AD) and potential explanations have received considerable attention, less attention has been paid to possible sex differences in genetic risk for AD.Objective: We examined sex differences in genetic and environmental influences on disease risk and age at onset for All Dementia, AD Only, and Non-AD Dementia.Methods: Twin pairs were drawn from the Swedish Twin Registry. All Dementia analysis included 9,467 pairs; AD only, 8,696 pairs; and non-AD dementia, 8,195 pairs. APOE analyses included 1,740 individual twins with measured ɛ4 alleles. Dementia diagnoses were based on clinical workup and national health registry linkage.Results: Although within-pair correlations for All Dementia and AD Only were higher for women than for men, sex differences did not statistically differ for genetic or environmental etiology of All Dementia, AD Only, and Non-AD dementia. Similar results were observed when looking at specific genetic effects (APOEɛ4). Co-twin control analyses indicated that among twin pairs discordant for dementia, female twins without dementia had approximately 40% greater risk of developing dementia, compared with their male counterparts, in the 2-5 years following the first twin's diagnosis.Conclusion: For All Dementia, AD Only, and Non-AD Dementia, genetic influences could be equated across sex. Co-twin analyses, however, suggest greater risk to female than to male co-twins of dementia cases even though sex differences in either genetic or shared environmental influences on the risk of dementia could not be differentiated. [ABSTRACT FROM AUTHOR]

Objectives To examine whether neighborhood income and neighborhood safety concerns influence multisystem physiological risk after adjusting for genetic and environmental selection effects that may have biased previous tests of this association. Methods We used structural equation modeling with a genetically informed sample of 686 male and female twin pairs in the Midlife in the United States Study II (2004). Results Controlling for additive genetic and shared environmental processes that may have biased neighborhood–health links in previous examinations, higher neighborhood safety concerns were associated with less physiological risk among women but not men. Discussion Our findings suggest a possible causal role of neighborhood features for a measure of physiological risk that is associated with the development of disease. Efforts to increase neighborhood safety, perhaps through increased street lighting or neighborhood watch programs, may improve community-level health. [ABSTRACT FROM AUTHOR]

This study assessed change in self‐reported Big Five personality traits. We conducted a coordinated integrative data analysis using data from 16 longitudinal samples, comprising a total sample of over 60 000 participants. We coordinated models across multiple datasets and fit identical multi‐level growth models to assess and compare the extent of trait change over time. Quadratic change was assessed in a subset of samples with four or more measurement occasions. Across studies, the linear trajectory models revealed declines in conscientiousness, extraversion, and openness. Non‐linear models suggested late‐life increases in neuroticism. Meta‐analytic summaries indicated that the fixed effects of personality change are somewhat heterogeneous and that the variability in trait change is partially explained by sample age, country of origin, and personality measurement method. We also found mixed evidence for predictors of change, specifically for sex and baseline age. This study demonstrates the importance of coordinated conceptual replications for accelerating the accumulation of robust and reliable findings in the lifespan developmental psychological sciences. © 2020 European Association of Personality Psychology [ABSTRACT FROM AUTHOR]

Background: Poorer self‐rated health (SRH) is associated with increased dementia risk (Stephan et al., 2021). However, it is unclear whether genetic and/or environmental variance accounts for this risk. Although SRH declines with age (Finkel et al. 2020), it is unknown whether rates of change in SRH are independently associated with dementia outcomes. Using a validated latent dementia index (LDI) (Beam et al., 2022), we tested whether stability and change components of SRH predicted LDI via genetic and environmental pathways in two international cohorts of twins. Method: Our data consisted of two samples of monozygotic (MZ) and dizygotic (DZ) twins. We used data from the Swedish Adoption Twin Study of Aging (SATSA; Ntwins = 548, Npairs = 339) and the Longitudinal Study of Aging Danish Twins (LSADT; Ntwins = 3238, Npairs = 2561). Bivariate Cholesky decompositions and three‐level growth‐curve models with predictive intercepts and slopes were used for our cross‐sectional and longitudinal analyses respectively. All models were estimated in Mplus (Muthen & Muthen, 2017) using maximum likelihood with robust standard errors. Results: Cross‐sectional model results indicate that those with poorer SRH have lower LDI scores (b = ‐0.01, p =.008), even after adjusting for shared genetic covariance, age, sex, education, and depressive symptoms. Predictive growth models indicate that rates of change in SRH are negatively associated with LDI after adjusting for age, sex, education, and depressive symptoms (b = ‐0.17, p =.032). The degree of genetic confounding in the association between rates of change and LDI was inconclusive. Conclusion: Our study provides novel insights into the relationship between individual ratings of health and dementia risk. SRH predicted dementia likelihood after controlling for genetic confounding, opening up the possibility that subjective ratings of health account for unique variance in dementia risk. Additionally, changes in SRH also predicted dementia likelihood beyond their mean score. Taken together these results highlight the importance of subjective health measures in understanding dementia risk. [ABSTRACT FROM AUTHOR]

Background: DNA methylation may affect expression of genes that promote the accumulation of amyloid‐β (Aβ). Although prior studies suggest that DNA methylation correlates with Aβ in older adults (Levine et al. (2018). An epigenetic biomarker of aging for lifespan and healthspan. Aging, 10(4), 573.), Aβ begins to accumulate earlier than when clinical symptoms associated with Aβ are evident. The purpose of the current study is to present novel results on whether differentially methylated CpG sites (i.e., regions of DNA where methylation occurs) correlate with higher Aβ42/Aβ40 ratios across a sample of middle‐aged individuals. Method: Data from 193 individual twins from the Louisville Twin Study were used in the current analysis. Genomic DNA was extracted from venipuncture blood samples, and bisulfite‐converted DNA samples were assessed with the Illumina Infinium EpicArray BeadChip. Quality control and analyses were performed in R using the minfi package, and gene ontology analyses were performed using the MissMethyl package. Aβ42/Aβ40 was estimated using a capture sandwich immunoassay methodology that measures AD biomarkers in whole‐blood plasma. Differential DNA methylation was estimated using multivariable linear regression with an empirical Bayes estimator. Result: Estimation of differential DNA methylation was adequate (λ = 1.38), although some Type I inflation of p‐values was observed among CpG sites with higher p‐values. Although no CpG sites reached genome‐wide statistical significance, the top four CpG sites suggested differential methylation ranging between 2.8–4.8% per unit increase in the ratio of Aβ42/Aβ40. The top gene sets associated with differential methylation were response to glucocorticoids, response to corticosteroids, and response to Aβ. Conclusion: Despite no statistically significant CpG probes identified, likely due to the small sample size, the findings from the gene ontology analysis suggest that identification of epigenetic biomarkers may clarify the biological pathways through which the epigenome may regulate expression of Aβ proteins. As data collection is ongoing, we expect detected of genome‐wide significant probes with larger sample sizes. [ABSTRACT FROM AUTHOR]

Objectives: This article examines whether sexual minority men and women experience greater increases in depressive symptoms and loneliness with age compared to heterosexual men and women. Methods: Using three waves of data from sexual minority (nMen = 87 and nWomen = 62) and heterosexual (nMen = 1,297 and nWomen = 1,362) older adults in the National Social Life, Health, and Aging Project, we used latent growth curve modeling to test whether change in depressive symptoms and loneliness varies across sexual orientation and whether annual household income and family support accounted for this change. Results: Although differences in the growth trajectories of depressive symptoms and loneliness across sexual orientation were not observed, gender differences were. Annual household income and family support more strongly influenced initial depressive symptoms and loneliness in sexual minority men and women than in heterosexual men and women. Conclusions: Trajectories of depressive symptoms and loneliness in older adulthood do not vary by sexual orientation. Economic and family resources may allow sexual minorities to cope effectively with depressive symptoms and loneliness. Clinical Implications: Clinicians should be cautious about assuming that older sexual minority group members are more susceptible to depressive symptoms and loneliness than heterosexual groups by virtue of their sexual preference. [ABSTRACT FROM AUTHOR]

Openness to experience has been found to be a correlate of successful aging outcomes yet also has been found to decline from middle age onward. We hypothesized that decline in openness would be associated with death. Using longitudinal data from the Swedish Adoption/Twin Study of Aging (SATSA), the analytic sample encompassed 1954 individuals, approximately two-thirds of whom were deceased. We tested whether openness declines across late adulthood and, central to our hypothesis, whether the decline correlated with age at death. Multivariate modeling adjusted for age at study entry, sex, education, as well as the time-varying effects of physical illness, depressive symptoms, and cognitive ability. Correlations between change in neuroticism and extraversion and death were modeled for comparison. A follow-up cotwin control analysis adjusted for genetic and environmental familial confounders. Significant mean-level change was identified in all personality traits, but only for openness was change correlated with age at death, in support of our hypothesis. The findings were not explained by health factors or cognition. Cotwin control analyses indicated that the twin who died earlier showed a greater drop in openness prior to death, compared with their cotwin measured at the same time points. There was no cotwin finding for neuroticism or extraversion. We suggest that declines in openness may reflect a change in goal orientation due to the experience of a shortened time horizon, leading to an optimized selection of experiences as people approach the end of life. (PsycINFO Database Record (c) 2019 APA, all rights reserved). [ABSTRACT FROM AUTHOR]

We examined whether attained socioeconomic status (SES) moderated genetic and environmental sources of individual differences in cognitive performance using pooled data from 9 adult twin studies. Prior work concerning SES moderation of cognitive performance has focused on rearing SES. The current adult sample of 12,196 individuals (aged 27-98 years) allowed for the examination of common sources of individual differences between attained SES and cognitive performance (signaling potential gene-environment correlation mechanisms, rGE), as well as sources of individual differences unique to cognitive performance (signaling potential gene-environment interaction mechanisms, G x E). Attained SES moderated sources of individual differences in 4 cognitive domains, assessed via performance on 5 cognitive tests ranging 2,149 to 8,722 participants. Attained SES moderated common sources of influences for 3 domains and influences unique to cognition in all 4 domains. The net effect was that genetic influences on the common pathway tended to be relatively more important at the upper end of attained SES indicating possible active rGE, whereas, genetic influences for the unique pathway were proportionally stable or less important at the upper end of attained SES. As a noted exception, at the upper end of attained SES, genetic influences unique to perceptual speed were amplified and genetic influences on the common pathway were dampened. Accounting for rearing SES did not alter attained SES moderation effects on cognitive performance, suggesting mechanisms germane to adulthood. Our findings suggest the importance of gene-environment mechanisms through which attained SES moderates sources of individual differences in cognitive performance. [ABSTRACT FROM AUTHOR]