The long arm of childhood intelligence on terminal decline:Evidence from the Lothian Birth Cohort 1921

The current study investigates the heterogeneity of cognitive trajectories at the end of life by assigning individuals into groups according to their cognitive trajectories prior to death. It also examines the role of childhood intelligence and education on these trajectories and group membership. Participants were drawn from the Lothian Birth Cohort of 1921 (LBC1921), a longitudinal study of individuals with a mean age of 79 years at study entry, and observed up to a maximum of five times to their early 90s. Growth mixture modelling was employed to identify groups of individuals with similar trajectories of global cognitive function measured with the Mini-Mental State Examination (MMSE) in relation to time to death, accounting for childhood intelligence, education, the time to death from study entry, and health conditions (hypertension, diabetes and cardiovascular disease). Two distinct groups of individuals (classes) were identified: a smaller class (18% of the sample) of individuals whose MMSE scores dropped linearly with about 0.5 MMSE points per year closer to death, and a larger group (82% of the sample) with stable MMSE across the study period. Only childhood intelligence was found to be associated with an increased probability of belonging to the stable class of cognitive functioning prior to death (odds ratio=1.08, standard error=0.02, p≤.001). These findings support a protective role of childhood intelligence, a marker of cognitive reserve, against the loss of cognitive function prior to death. Our results also suggest that terminal decline is not necessarily a normative process

Lifecourse Activity Participation From Early, Mid, and Later Adulthood as Determinants of Cognitive Aging: The Lothian Birth Cohort 1921

OBJECTIVES: To examine potential sensitive periods for activity participation across adulthood to reduce cognitive decline and to determine whether associations persist after accounting for the lifetime stability of cognitive ability. METHOD: The Lothian Birth Cohort 1921 is a longitudinal study of cognitive aging. Participants were born in 1921 and most completed a mental ability test at the age of 11 years. Cognitive assessments were completed at mean ages 79 (N = 550), 83 (N = 321), 87 (N = 235), and 90 years (N = 129). Participants provided retrospective details of their activity participation for young (20–35 years), mid (40–55 years), and later adulthood (60–75 years), and contemporaneously at age 79. RESULTS: Associations between activity and the level of, and change in, cognitive ability in old age were examined with latent growth curve models. Accounting for demographics and childhood cognitive ability, engagement in leisure activities in midlife was positively associated with cognitive ability level (path coefficient = .32), whereas higher physical activity in later adulthood was associated with less cognitive decline (.27). DISCUSSION: The findings support a lifecourse approach in identifying determinants of cognitive aging; leisure and physical activity during different periods of adulthood may enhance cognitive abilities or reduce decline

Carotid disease at age 73 and cognitive change from age 70 to 76 years. A longitudinal cohort study

Cognitive decline and carotid artery atheroma are common at older ages. In community-dwelling subjects, we assessed cognition at ages 70, 73 and 76 and carotid Doppler ultrasound at age 73, to determine whether carotid stenosis was related to cognitive decline. We used latent growth curve models to examine associations between four carotid measures (internal carotid artery stenosis, velocity, pulsatility and resistivity indices) and four cognitive ability domains (memory, visuospatial function, crystallised intelligence, processing speed) adjusted for cognitive ability at age 11, current age, gender and vascular risk factors. Amongst 866 participants, carotid stenosis (median 12.96%) was not associated with cognitive abilities at age 70 or cognitive decline from age 70 to 76. Increased ICA pulsatility and resistivity indices were associated with slower processing speed (both P &lt; 0.001) and worse visuospatial function ( P = 0.036, 0.031, respectively) at age 70, and declining crystallised intelligence from ages 70 to 76 ( P = 0.008, 0.006, respectively). The findings suggest that vascular stiffening, rather than carotid luminal narrowing, adversely influences cognitive ageing and provides a potential target for ameliorating age-related cognitive decline. </jats:p

The epigenetic clock is correlated with physical and cognitive fitness in the Lothian Birth Cohort 1936

Background: The DNA methylation-based 'epigenetic clock' correlates strongly with chronological age, but it is currently unclear what drives individual differences. We examine cross-sectional and longitudinal associations between the epigenetic clock and four mortality-linked markers of physical and mental fitness: lung function, walking speed, grip strength and cognitive ability. Methods: DNA methylation-based age acceleration (residuals of the epigenetic clock estimate regressed on chronological age) were estimated in the Lothian Birth Cohort 1936 at ages 70 (n=920), 73 (n=299) and 76 (n=273) years. General cognitive ability, walking speed, lung function and grip strength were measured concurrently. Cross-sectional correlations between age acceleration and the fitness variables were calculated. Longitudinal change in the epigenetic clock estimates and the fitness variables were assessed via linear mixed models and latent growth curves. Epigenetic age acceleration at age 70 was used as a predictor of longitudinal change in fitness. Epigenome-wide association studies (EWASs) were conducted on the four fitness measures. Results: Cross-sectional correlations were significant between greater age acceleration and poorer performance on the lung function, cognition and grip strength measures (r range: -0.07 to -0.05, P range: 9.7 x 10 to 0.024). All of the fitness variables declined over time but age acceleration did not correlate with subsequent change over 6 years. There were no EWAS hits for the fitness traits. Conclusions: Markers of physical and mental fitness are associated with the epigenetic clock (lower abilities associated with age acceleration). However, age acceleration does not associate with decline in these measures, at least over a relatively short follow-up

Fluctuating asymmetry in brain structure and general intelligence in 73-Year-olds

SRC, MEB, JMW, IJD were supported by MRC grants MR/M013111/1 and MR/R024065/1. IJD is additionally supported by the Dementias Platform UK (MR/L015382/1), and he, SRC and SJR by the Age UK-funded Disconnected Mind project (http://www.disconnectedmind.ed.ac.uk). The work was done within the University of Edinburgh Centre for Cognitive Ageing and Cognitive Epidemiology; it was funded by the MRC and the BBSRC (MR/K026992/1) and supported SJR, IJD, and JMS. SRC, SJR, MEB and IJD were supported by a National Institutes of Health (NIH) research grant R01AG054628. JMW was supported by the Scottish Imaging Network: A Platform for Scientific Excellence (SINAPSE) collaboration (http://www.sinapse.ac.uk).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 (beta=-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.Publisher PDFPeer reviewe