All-cause mortality in the Aberdeen 1921 birth cohort: Effects of socio-demographic, physical and cognitive factors

<p>Abstract</p> <p>Background</p> <p>Childhood intelligence predicts mortality throughout most of the life span. However, it is unknown whether its effect persists into advanced old age.</p> <p>Methods</p> <p>The Aberdeen Birth Cohort born in 1921 (n = 354) and that had an IQ test as part of the national Scottish Mental Survey of 1932 were seen in 1997 at age 76 years when childhood and adult socio-environmental, medical and cognitive data were collected. Participants were followed until May 2007 and vital status determined from the General Register for Scotland records. Univariate associations between baseline variables and mortality were determined and multivariable survival analysis performed with Cox's proportional hazards modelling.</p> <p>Results</p> <p>One hundred and fifty-eight (44.6%) of the 354 cohort members had died by the census date. Significantly more men (n = 102) died during follow-up than women (n = 56, χ²= 5.27, p = .022). Lower scores on four of the six cognitive tests at age 76 years were associated with increased mortality, but not IQ age 11. Survival was associated with gender (H.R. 0.32, 95% C.I. 0.11–0.89 for women versus men), peak expiratory flow rate (H.R. 0.997, 95% C.I. 0.992–1.001 per l/min) and the Uses of Common Objects test (H.R. 0.91, 95% C.I. 0.82–1.01)</p> <p>Conclusion</p> <p>Both physical and psychological variables independently predicted survival in old age: respiratory function and executive function in particular. Male gender conferred increased risk of mortality and this was not explained by the broad range of socio-environmental, mental ability and health status variables examined in the study.</p

Structural brain complexity and cognitive decline in late life : A longitudinal study in the Aberdeen 1936 Birth Cohort

Copyright © 2014 Elsevier Inc. All rights reserved.Peer reviewedPostprin

Cognitive function in childhood and lifetime cognitive change in relation to mental wellbeing in four cohorts of older people

Background: poorer cognitive ability in youth is a risk factor for later mental health problems but it is largely unknown whether cognitive ability, in youth or in later life, is predictive of mental wellbeing. The purpose of this study was to investigate whether cognitive ability at age 11 years, cognitive ability in later life, or lifetime cognitive change are associated with mental wellbeing in older people.Methods: we used data on 8191 men and women aged 50 to 87 years from four cohorts in the HALCyon collaborative research programme into healthy ageing: the Aberdeen Birth Cohort 1936, the Lothian Birth Cohort 1921, the National Child Development Survey, and the MRC National Survey for Health and Development. We used linear regression to examine associations between cognitive ability at age 11, cognitive ability in later life, and lifetime change in cognitive ability and mean score on the Warwick Edinburgh Mental Wellbeing Scale and meta-analysis to obtain an overall estimate of the effect of each.Results: people whose cognitive ability at age 11 was a standard deviation above the mean scored 0.53 points higher on the mental wellbeing scale (95% confidence interval 0.36, 0.71). The equivalent value for cognitive ability in later life was 0.89 points (0.72, 1.07). A standard deviation improvement in cognitive ability in later life relative to childhood ability was associated with 0.66 points (0.39, 0.93) advantage in wellbeing score. These effect sizes equate to around 0.1 of a standard deviation in mental wellbeing score. Adjustment for potential confounding and mediating variables, primarily the personality trait neuroticism, substantially attenuated these associations.Conclusion: associations between cognitive ability in childhood or lifetime cognitive change and mental wellbeing in older people are slight and may be confounded by personality trait difference

Childhood IQ and marriage by mid-life: the Scottish Mental Survey 1932 and the Midspan Studies

The study examined the influence of IQ at age 11 years on marital status by mid-adulthood. The combined databases of the Scottish Mental Survey 1932 and the Midspan studies provided data from 883 subjects. With regard to IQ at age 11, there was an interaction between sex and marital status by mid-adulthood (p &#61; 0.0001). Women who had ever-married achieved mean lower childhood IQ scores than women who had never-married (p &#60; 0.001). Conversely, there was a trend for men who had ever-married to achieve higher childhood IQ scores than men who had never-married (p &#61; 0.07). In men, the odds ratio of ever marrying was 1.35 (95&#37; CI 0.98–1.86&#59; p &#61; 0.07) for each standard deviation increase in childhood IQ. Among women, the odds ratio of ever marrying by mid-life was 0.42 (95&#37; CI 0.27–0.64; p &#61; 0.0001) for each standard deviation increase in childhood IQ. Mid-life social class had a similar association with marriage, with women in more professional jobs and men in more manual jobs being less likely to have ever-married by mid-life. Adjustment for the effects of mid-life social class and height on the association between childhood IQ and later marriage, and vice versa, attenuated the effects somewhat, but suggested that IQ, height and social class acted partly independently

Increased diastolic blood pressure is associated with MRI biomarkers of dementia-related brain pathology in normative ageing

Background hypertension is a risk for brain ageing, but the mechanisms underlying this effect remain unclear. Magnetic resonance imaging (MRI) detected biomarkers of brain ageing include white matter hyperintensities (WMHs), a marker of cerebrovascular disease, and hippocampal volume, a marker of Alzheimer’s disease pathology. Objective to examine relationships between blood pressure (BP) components and brain pathology in older adults. Subjects two hundred and twenty-seven members of the Aberdeen 1936 Birth Cohort between ages 64 and 68 years. Methods BP was assessed biennially between 64 and 68 years and brain MRI performed at 68 years. The risk factors of interest were diastolic and systolic BP and their visit-to-visit variability. Outcomes were WMH abundance and hippocampal volume. Regression models, controlling for confounding factors, examined their relationships. Results higher diastolic BP predicted increased WMH (β = 0.13, P = 0.044) and smaller hippocampi (β = −0.25, P = 0.006). In contrast, increased systolic BP predicted larger hippocampi (β = 0.22, P = 0.013). Variability of diastolic BP predicted lower hippocampal volume (β = −0.15, P = 0.033). These relationships were independent of confounding life-course risk factors. Anti-hypertensive medication did not modify these relationships, but was independently associated with increased WMH (β = 0.17, P = 0.011). Conclusion increased diastolic BP is associated with biomarkers of both cerebrovascular and Alzheimer’s diseases, whereas the role of systolic BP is less clear, with evidence for a protective effect on hippocampal volume. These differing relationships emphasise the importance of considering individual BP components with regard to brain ageing and pathology. Interventions targeting diastolic hypertension and its chronic variability may provide new strategies able to slow the accumulation of these harmful pathologies

Cognitive Test Scores and Progressive Cognitive Decline in the Aberdeen 1921 and 1936 Birth Cohorts

Acknowledgments: We remain grateful to the kindness of the staff at the Scottish Council for Research in Education who allowed us access to their archive and remained supportive and gracious throughout our collaboration. We thank the many people of Aberdeen who volunteered generously and committed to the long-term success of this program. We thank Victoria Bourne, who made substantial contributions to study design, data collection, data analysis and hypothesis generation. Jen Herbert (deceased) recruited the ABC36 participants, collected data (sessions I and II) and, through her encouragement and professionalism, ensured the continued involvement of many participants. She was much loved by participants and the study team. Funding: The Aberdeen Birth Cohort 1921 and 1936 research program was established in 1997 with funding from the Henry Smith (Kensington Estates) Charity and continued by The UK Biotechnology and Biological Sciences Research Council (1999–2002), The Wellcome Trust (2001–2006), The Scottish Government (2000–2002), the Medical Research Council (2003), Alzheimer Research UK (2002–2005) and the University of Aberdeen Development Trust (2007–2010, 2014).Peer reviewedPublisher PD

A genetic association analysis of cognitive ability and cognitive ageing using 325 markers for 109 genes associated with oxidative stress or cognition

<p>Abstract</p> <p>Background</p> <p>Non-pathological cognitive ageing is a distressing condition affecting an increasing number of people in our 'ageing society'. Oxidative stress is hypothesised to have a major role in cellular ageing, including brain ageing.</p> <p>Results</p> <p>Associations between cognitive ageing and 325 single nucleotide polymorphisms (SNPs), located in 109 genes implicated in oxidative stress and/or cognition, were examined in a unique cohort of relatively healthy older people, on whom we have cognitive ability scores at ages 11 and 79 years (LBC1921). SNPs showing a significant positive association were then genotyped in a second cohort for whom we have cognitive ability scores at the ages of 11 and 64 years (ABC1936). An intronic SNP in the <it>APP </it>gene (rs2830102) was significantly associated with cognitive ageing in both LBC1921 and a combined LBC1921/ABC1936 analysis (<it>p </it>< 0.01), but not in ABC1936 alone.</p> <p>Conclusion</p> <p>This study suggests a possible role for APP in normal cognitive ageing, in addition to its role in Alzheimer's disease.</p

Aspirin moderates the association between cardiovascular risk, brain white matter hyperintensity total lesion volume and processing speed in normal ageing

ABC1936 was funded (1999-2009) by the Biotechnology and Biological Sciences Research Council, Scottish Health Department, Wellcome Trust, Medical Research Council, Alzheimer Research UK, Alzheimer Society and University of Aberdeen Development Trust. This work was supported by the Elphinstone Scholarship, Roland Sutton Academic Trust, the Morningfield Association and the Rabin Ezra Scholarship Trust, which provides salary cost and consumables to MK.Peer reviewedPostprin

The NART as an index of prior intellectual functioning: a retrospective validity study covering a 66-year interval

Background. The National Adult Reading Test (NART) is widely used in research and clinical practice as an estimate of pre-morbid or prior ability. However, most of the evidence on the NART's validity as a measure of prior intellectual ability is based on concurrent administration of the NART and an IQ measure. Method. We followed up 179 individuals who had taken an IQ test (the Moray House Test) at age 11 and administered the NART and the Mini-Mental State Examination (MMSE) at age 77. A subset (N=97) were also re-administered the original IQ test. Results. The correlation between NART performance at age 77 and IQ age 11 was high and statistically significant (r=0·73; P<0·001). This correlation was comparable to the correlation between NART and current IQ, and childhood IQ and current IQ, despite the shared influences on the latter variable pairings. The NART had a significant correlation with the MMSE but this correlation fell to near zero (r=0·02) after partialling out the influence of childhood IQ. Discussion. The pattern of results provides strong support for the claim that the NART primarily indexes prior (rather than current) intellectual ability

Pollution, particles, and dementia: A hypothetical causative pathway

© 2020 The Authors. Published by MDPI. This is an open access article available under a Creative Commons licence. The published version can be accessed at the following link on the publisher’s website: https://doi.org/10.3390/ijerph17030862© 2020 by the authors. Licensee MDPI, Basel, Switzerland. Epidemiological studies of air pollution have shown associations between exposure to particles and dementia. The mechanism of this is unclear. As these seem unlikely in terms of the very small dose likely to reach the brain in usual Western urban circumstances, we extend our 1995 hypothetical explanation of the association of air pollution with cardiac deaths as a plausible alternative explanation of its associations with dementia. Since our original proposal, it has become apparent that inflammation may be carried by blood from organ to organ by biologic microparticles derived from cell membranes. These transmit inflammatory messages to endothelial cells throughout the body as part of a general defensive response to assumed bacterial infection; particulate air pollution has recently been shown to be associated with their release into the blood. We propose that episodic release of biologic microparticles from pollution-induced lung inflammation causes secondary inflammation in the blood-brain barrier and cerebral microbleeds, culminating over time in cognitive impairment. Ultimately, by incomplete repair and accumulation of amyloid, this increases the risk of Alzheimer’s disease. Importantly, this mechanism may also explain the relationships of other inflammatory conditions and environmental factors with cognitive decline, and point to new opportunities to understand and prevent dementia.Published versio