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Change in cognitive functioning is an important aspect of human aging and a key outcome in many medical conditions. However, cognitive change can rarely be measured directly, since prior cognitive data do not exist for most people. We examined the criterion validity and one-year stability of the difference between National Adult Reading Test (NART) and Raven's Standard Progressive Matrices Test (Raven) as an estimate of cognitive change. We followed up over 80 people whose cognitive ability (using the Moray House Test [MHT]) was measured at age 11 in the Scottish Mental Survey of 1932 (SMS 1932). At age 77 and again at 78 years, they took the NART, Raven, and two Wechsler Adult Intelligence Scale-Revised (WAIS-R) subtests. The difference between NART and Raven standardised scores ("estimated" cognitive change) correlated 0.638 (P less than 0.001) with the difference between MHT and Raven scores, and 0.658 (P less than 0.001) with the difference between MHT and WAIS scores (two measures of "actual" cognitive change). The stability of the NART-Raven difference across a one-year period was 0.643 (P less than 0.001). We have demonstrated the stability and criterion validity of an estimate of lifetime cognitive change that takes about half an hour to administer.

Examines the influence of apolipoprotein E gene states on three cognitive outcomes in 173 people at age 11 and in the same people at age 77 and examined the change in IQ between these ages. There was no significant main effect of gene status on IQ in youth or old age, nor in cognitive change across the lifespan. (SLD)

Tested the hypothesis that intelligence is related to the risk of mental illness by linking childhood mental ability data to registers of psychiatric contact in a stable population of 4,199 adults in Scotland. Findings show intelligence to be an independent predictor of psychiatric contact, with each standard deviation decrease in IQ resulting in a 12% increase in the risk of contact independent of gender and childhood resilience. (SLD)

Tested 101 adults, aged 77, who had completed psychometric intelligence testing in 1932, with the same test of mental ability. Results of this study, the longest follow-up study reported to date, show substantial stability in mental ability differences from childhood to late life. (SLD)

Understanding the determinants of healthy mental ageing is a priority for society today (1,2). So far, we know that intelligence differences show high stability from childhood to old age (3,4) and there are estimates of the genetic contribution to intelligence at different ages (5,6). However, attempts to discover whether genetic causes contribute to differences in cognitive ageing have been relatively uninformative (7-10). Here we provide an estimate of the genetic and environmental contributions to stability and change in intelligence across most of the human lifetime. We used genome-wide single nucleotide polymorphism (SNP) data from 1,940 unrelated individuals whose intelligence was measured in childhood (age 11 years) and again in old age (age 65, 70 or 79 years) (11,12). We use a statistical method that allows genetic (co)variance to be estimated from SNP data on unrelated individuals (13-17). We estimate that causal genetic variants in linkage disequilibrium with common SNPs account for 0.24 of the variation in cognitive ability change from childhood to old age. Using bivariate analysis, we estimate a genetic correlation between intelligence at age 11 years and in old age of 0.62. These estimates, derived from rarely available data on lifetime cognitive measures, warrant the search for genetic causes of cognitive stability and change., General cognitive ability (also known as general intelligence, or g (18)) is an important human trait. It shows consistent and strong associations with important life outcomes such as educational and [...]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.addbeh.2006.03.020 Byline: John M. Starr (a), Ian J. Deary (b), Helen C. Fox (c), Lawrence J. Whalley (c) Keywords: Smoking; Cognition; Memory; Respiratory function Abstract: Previously we reported that smoking is associated with a small relative decline in cognition from childhood to old age. In this study we perform confirmatory analyses on a further wave of data collected from 298 of the participants, all with age 11 IQ scores, at age 66years, 2years after the original observations. Non-smokers scored a mean 4.9 memory test and 2.6 information processing speed test points and ex-smokers 3.5 memory test and 1.9 information processing speed test points higher than current smokers respectively over the two waves of testing, equivalent to 4-8% of mean test scores, adjusted for the effects of childhood IQ. Across tests a 100l/min higher Peak Expiratory Flow Rate was associated with a 3-4% higher test score at ages 64 and 66years. These data confirm the adverse effect of smoking on information processing speed, and provide new evidence for a similar adverse effect on memory for people in their mid-sixties. Author Affiliation: (a) Department of Geriatric Medicine, University of Edinburgh, Scotland, UK (b) Department of Psychology, University of Edinburgh, Scotland, UK (c) Department of Mental Health, University of Aberdeen, Scotland, UK

The Scottish Mental Surveys of 1932 and 1947 collected valid IQ-type test scores for almost everyone born in 1921 and 1936 and attending school on June 1, 1932 (N = 89,498) and June 4, 1947 (N = 70,805). These surveys are described. This research, using the surveys' data, examined (a) the stability of intelligence differences across the life span, (b) the determinants of cognitive change from childhood to old age, and (e) the impact of childhood intelligence on survival and health in old age. Surviving participants of the Scottish Mental Surveys were tested, and the surveys' data were linked with public and health records. Novel findings on the stability of IQ scores from age 11 to age 80; sex differences in cognitive aging; the dedifferentiation hypothesis of cognitive aging; and the effect of childhood IQ on all-cause and specific mortality, morbidity, and frailty in old age are presented.

In 1932 a test was performed to study the cognitive ability distribution in 11 year old Scottish children, comprising almost everyone born in Scotland in 1921, in order to examine the difference in sexes with respect to their mean levels and variabilities in mental ability test scores. The findings went some distance in explaining the slight excess of men with learning difficulties and a similar level of excess of men achieving first class university degrees.

The Aberdeen birth cohorts of 1921 and 1936 (ABC21 and ABC36) were subjected to IQ tests in 1932 or 1947 when they were aged about 11y. They were recruited between 1997–2001 among cognitively healthy community residents and comprehensively phenotyped in a long-term study of brain aging and health up to 2017. Here, we report associations between baseline cognitive test scores and long-term cognitive outcomes. On recruitment, significant sex differences within and between the ABC21 and ABC36 cohorts supported advantages in verbal ability and learning among the ABC36 women that were not significant in ABC21. Comorbid physical disorders were self-reported in both ABC21 and ABC36 but did not contribute to differences in terms of performance in cognitive tests. When used alone without other criteria, cognitive tests scores which fell below the −1.5 SD criterion for tests of progressive matrices, namely verbal learning, digit symbol and block design, did not support the concept that Mild Cognitive Impairment (MCI) is a stable class of acquired loss of function with significant links to the later emergence of a clinical dementia syndrome. This is consistent with many previous reports. Furthermore, because childhood IQ-type data were available, we showed that a lower cognitive performance at about 64 or 78 y than that predicted by IQ at 11 ± 0.5 y did not improve the prediction of progress to MCI or greater cognitive loss. We used binary logistic regression to explore how MCI might contribute to the prediction of later progress to a clinical dementia syndrome. In a fully adjusted model using ABC21 data, we found that non-amnestic MCI, along with factors such as female sex and depressive symptoms, contributed to the prediction of later dementia. A comparable model using ABC36 data did not do so. We propose that (1) MCI criteria restricted to cognitive test scores do not improve the temporal stability of MCI classifications; (2) pathways towards dementia may differ according to age at dementia onset and (3) the concept of MCI may require measures (not captured here) that underly self-reported subjective age-related cognitive decline. [ABSTRACT FROM AUTHOR]