Search

Regional cortical brain volume is the product of surface area and thickness. These measures exhibit partially distinct trajectories of change across the brain's cortex in older age, but it is unclear which cortical characteristics at which loci are sensitive to cognitive ageing differences. We examine associations between change in intelligence from age 11 to 73 years and regional cortical volume, surface area, and thickness measured at age 73 years in 568 community-dwelling older adults, all born in 1936. A relative positive change in intelligence from 11 to 73 was associated with larger volume and surface area in selective frontal, temporal, parietal, and occipital regions ( r < 0.180, FDR-corrected q < 0.05). There were no significant associations between cognitive ageing and a thinner cortex for any region. Interestingly, thickness and surface area were phenotypically independent across bilateral lateral temporal loci, whose surface area was significantly related to change in intelligence. These findings suggest that associations between regional cortical volume and cognitive ageing differences are predominantly driven by surface area rather than thickness among healthy older adults. Regional brain surface area has been relatively underexplored, and is a potentially informative biomarker for identifying determinants of cognitive ageing differences. [ABSTRACT FROM AUTHOR]

We examined whether apolipoprotein E ( APOE ) status interacts with vascular risk factors (VRFs) to predict the progression of white matter hyperintensities (WMHs) on brain MRI scans over a specific period of life in older age when the risk of dementia increases. At age 73 years, baseline VRFs were assessed via self-reported history of diabetes, hypertension, smoking, and hypercholesterolemia, and via objective measures of blood HbA1c, body mass index, diastolic and systolic blood pressure, and blood high-density lipoprotein to total cholesterol (HDL) ratio. APOE e4 allele was coded as either present or absent. WMH progression was measured on MRI over 3 years in 434 older adults, in a same-year-of-birth cohort. APOE e4 carriers with either a self-reported diagnosis of diabetes ( β = 0.160, p = 0.002) or higher glycated hemoglobin levels ( β = 0.114, p = 0.014) exhibited greater WMH progression, and the former survived correction for multiple testing. All other APOE -VRF interactions were nonsignificant ( β interaction < 0.056, p > 0.228). The results suggest that carrying the APOE “risk” e4 allele increases the risk of greater age-related WMH progression over the early part of the eighth decade of life, when combined with poorer glycemic control. The interaction effect was robust to co-occurring VRFs, suggesting a possible target for mitigating brain and cognitive aging at this age. [ABSTRACT FROM AUTHOR]

Background: Poorer self-rated health (SRH) predicts worse health outcomes, even when adjusted for objective measures of disease at time of rating. Twin studies indicate SRH has a heritability of up to 60% and that its genetic architecture may overlap with that of personality and cognition.Methods: We carried out a genome-wide association study (GWAS) of SRH on 111 749 members of the UK Biobank sample. Univariate genome-wide complex trait analysis (GCTA)-GREML analyses were used to estimate the proportion of variance explained by all common autosomal single nucleotide polymorphisms (SNPs) for SRH. Linkage disequilibrium (LD) score regression and polygenic risk scoring, two complementary methods, were used to investigate pleiotropy between SRH in the UK Biobank and up to 21 health-related and personality and cognitive traits from published GWAS consortia.Results: The GWAS identified 13 independent signals associated with SRH, including several in regions previously associated with diseases or disease-related traits. The strongest signal was on chromosome 2 (rs2360675, P = 1.77 x 10 -10 ) close to KLF7 . A second strong peak was identified on chromosome 6 in the major histocompatibility region (rs76380179, P = 6.15 x 10 -10 ). The proportion of variance in SRH that was explained by all common genetic variants was 13%. Polygenic scores for the following traits and disorders were associated with SRH: cognitive ability, education, neuroticism, body mass index (BMI), longevity, attention-deficit hyperactivity disorder (ADHD), major depressive disorder, schizophrenia, lung function, blood pressure, coronary artery disease, large vessel disease stroke and type 2 diabetes.Conclusions: Individual differences in how people respond to a single item on SRH are partly explained by their genetic propensity to many common psychiatric and physical disorders and psychological traits. [ABSTRACT FROM AUTHOR]

Maintaining good cognitive function is important for successful aging, and it has been suggested recently that having and optimistic outlook may also be valuable. However few have studied the relationship between cognitive ability and dispositional optimism and pessimism in older age. It is unclear whether associations found previously between cognitive ability and pessimism in older age, are evident across the life course, and are consistent at different points in older age. In the present study we examined associations between dispositional optimism and pessimism measured in the eighth and ninth decade of life and childhood and older age cognitive ability, and lifetime change in cognitive ability. Participants were two independent narrow-age samples of older individuals with mean ages about 73 ( n = 847) and 87 ( n = 220) years from the Lothian Birth Cohorts of 1936 (LBC1936) and 1921 (LBC1921), respectively. Higher cognitive ability in childhood and older-age, and healthier cognitive change across the lifetime were associated with lower pessimism in older age: age-11 IQ (LBC1936: β = − 0.17, p < 0.001; LBC1921: β = − 0.29, p = 0.001), older-age IQ (LBC1936: β = − 0.18, p < 0.001; LBC1921: β = − 0.27, p < 0.001), cognitive change (LBC1936: β = − 0.06, p < 0.04; LBC1921: β = − 0.15, p = 0.05). Cognitive ability was not significantly associated with optimism in bivariate analyses, and after adjustment for covariates had only small associations with optimism and only in the LBC1936. The results are consistent with differential associations between cognitive functions and optimism and pessimism, and indicate that their associations with cognitive ability are similar in the eighth and ninth decades of life. [ABSTRACT FROM AUTHOR]

Educational attainment is associated with many health outcomes, including longevity. It is also known to be substantially heritable. Here, we used data from three large genetic epidemiology cohort studies (Generation Scotland, n = ~17,000; UK Biobank, n = ~115,000; and the Estonian Biobank, n = ~6,000) to test whether education-linked genetic variants can predict lifespan length. We did so by using cohort members' polygenic profile score for education to predict their parents' longevity. Across the three cohorts, meta-analysis showed that a 1 SD higher polygenic education score was associated with ~2.7% lower mortality risk for both mothers (total ndeaths= 79,702) and ~2.4% lower risk for fathers (total ndeaths = 97,630). On average, the parents of offspring in the upper third of the polygenic score distribution lived 0.55 y longer compared with those of offspring in the lower third. Overall, these results indicate that the genetic contributions to educational attainment are useful in the prediction of human longevity. [ABSTRACT FROM AUTHOR]

It is critical to discover why some people's cognitive abilities age better than others'. We applied multivariate growth curve models to data from a narrow-age cohort measured on a multi-domain IQ measure at age 11 years and a comprehensive battery of thirteen measures of visuospatial, memory, crystallized, and processing speed abilities at ages 70, 73, and 76 years ( n = 1091 at age 70). We found that 48% of the variance in change in performance on the thirteen cognitive measures was shared across all measures, an additional 26% was specific to the four ability domains, and 26% was test-specific. We tested the association of a wide variety of sociodemographic, fitness, health, and genetic variables with each of these cognitive change factors. Models that simultaneously included all covariates accounted for appreciable proportions of variance in the cognitive change factors (e.g. approximately one third of the variance in general cognitive change). However, beyond physical fitness and possession of the APOE e4 allele, very few predictors were incrementally associated with cognitive change at statistically significant levels. The results highlight a small number of factors that predict differences in cognitive ageing, and underscore that correlates of cognitive level are not necessarily predictors of decline. Even larger samples will likely be required to identify additional variables with more modest associations with normal-range heterogeneity in aging-related cognitive declines. [ABSTRACT FROM AUTHOR]

Fluctuating body asymmetry is theorized to indicate developmental instability, and to have small positive associations with low socioeconomic status (SES). Previous studies have reported small negative associations between fluctuating body asymmetry and cognitive functioning, but relationships between fluctuating brain asymmetry and cognitive functioning remain unclear. The present study investigated the association between general intelligence (a latent factor derived from a factor analysis on 13 cognitive tests) and the fluctuating asymmetry of four structural measures of brain hemispheric asymmetry: cortical surface area, cortical volume, cortical thickness, and white matter fractional anisotropy. The sample comprised members of the Lothian Birth Cohort 1936 (LBC1936, N = 636, mean age = 72.9 years). Two methods were used to calculate structural hemispheric asymmetry: in the first method, regions contributed equally to the overall asymmetry score; in the second method, regions contributed proportionally to their size. When regions contributed equally, cortical thickness asymmetry was negatively associated with general intelligence (β = −0.18, p <.001). There was no association between cortical thickness asymmetry and childhood SES, suggesting that other mechanisms are involved in the thickness asymmetry-intelligence association. Across all cortical metrics, asymmetry of regions identified by the parieto-frontal integration theory (P-FIT) was not more strongly associated with general intelligence than non-P-FIT asymmetry. When regions contributed proportionally, there were no associations between general intelligence and any of the asymmetry measures. The implications of these findings, and of different methods of calculating structural hemispheric asymmetry, are discussed. • Previous work has shown links between cortical asymmetry and intelligence. • In the current study, two methods of calculating global cortical hemispheric asymmetry were compared. • Equal region contribution: the association between cortical thickness asymmetry and general intelligence was β = −0.18. • Proportional region contribution: no associations between three measures of cortical asymmetry and general intelligence. [ABSTRACT FROM AUTHOR]