Which factors through the course of life promote and protect cognitive capability and which increase vulnerability to decline?
Research programme: Mental Ageing
Programme leader: Professor Marcus Richards
UCL studentships: Gemma Archer (completed), Alison Sizer
This programme brings a life course approach to bear on maintaining quality of later life through promoting cognitive capability and reducing risk of depression. The essence of this approach is to map life course determinants and consequences of cognition and affect; their associations with each other, and their associations with other aspects of health and function through common and sequential causes. In most parts of the world older people account for the fastest-growing proportion of the population, with huge corresponding increases in the absolute prevalence of dementia - a trend that is projected to continue well into the future. In addition the World Health Organization has identified depression as the leading cause of disease burden in middle and high income countries. The long-term priorities of this programme are therefore to reduce the risk of these outcomes using a life course approach across all levels of explanation: from societal opportunities and barriers, through behavioural choices, to underlying biological regulation from genes, endocrine systems, inflammatory mechanisms, and autonomic control.
The fundamental goals of the Mental Ageing programme, over 2013-2018 and in the much longer term, are to identify how to optimise cognitive function and reduce risk of depression in later life through a life course approach; and to study how abnormal mental ageing impacts on other aspects of health and function. This will be done within three closely inter-related Themes:
- Capturing mental ageing, focusing on life course trajectories of cognitive function and mental health and the ascertainment of clinically significant cognitive decline, neurodegeneration, and affective disorder;
- Maintaining mental capability in early old age, emphasising education, work and retirement, and self-management of health;
- Integration of mental and physical ageing, investigating links between cognitive capability and common mental disorder, and between these entities and aspects of physical health: cardio-respiratory, metabolic, musculoskeletal; and ultimately survival.
Byford M, Kuh D, Richards M. Parenting practices and intergenerational associations in cognitive ability. Evidence from two generations of a British birth cohort. International Journal of Epidemiology 2012, 41, 263-72.
This study exploits the rare availability of data based on three generations and provides evidence that parenting styles have effects on cognitive development that are independent of grandparental SEP, parental cognitive capability and mental health, parental educational attainment and SEP, and offspring behavioural characteristics.
Richards M, Brayne C. What do we mean by Alzheimer’s disease? British Medical Journal 2010, 341(no. 7778), 865-867.
This invited analysis paper challenges the pathology-led model of Alzheimer’s disease, and argues that, in older age groups, this disease is a diffuse clinical syndrome representing the gradual accumulation of multiple pathologies, arising from multiple interlocking risk factors over the life course.
Hatch SL, Feinstein L, Link B, Wadsworth MEJ, Richards M. The continuing benefits of education: adult education and midlife cognitive ability in the British 1946 birth cohort. Journal of Gerontology Series B 2007, 62, S404-S414.
This study suggests an important choice of an activity that maintains cognitive capability. It also reinforces our previous evidence that education has a causal effect on cognitive capability, since the association between the two was independent of prior cognition and education, and of any social mobility that may have arisen as a result of continuing education.
Richards M, Power C, Sacker A. Paths to literacy and numeracy problems: evidence from two British birth cohorts. Journal of Epidemiology and Community Health 2009, 63, 239-244.
Extending the path model of Richards & Sacker, linking paternal SEP to midlife cognitive capability in NSHD, the above study shows a stronger protective path from education to functional literacy and numeracy in the British 1958 cohort than in NSHD, almost certainly resulting from raising the school leaving age by one year in the intervening 12 years.
Murray GK, Jones PB, Kuh D, Richards M. Infant developmental milestones and subsequent cognitive function. Annals of Neurology 2007, 62, 128-136.
This paper was one of the first studies to show an inverse association between postnatal neurodevelopment, indicated by age at motor milestone attainment, and cognitive development.
Richards M, Deary IJ. A life course approach to cognitive reserve: a model for cognitive aging and development? Annals of Neurology 2005, 58, 617-622.
This position piece challenges the conventional model of cognitive reserve, which holds that brain structure or function buffer the clinical expression of neuropathology but do not influence the risk of that neuropathology occurring. On the contrary, a life course approach suggests that factors influencing cognitive reserve, such as cognitive development and education, are on the causal path to that risk. The piece also suggests that reserve may be represented by mature crystallised cognitive ability.
Richards M, Sacker A. Lifetime antecedents of cognitive reserve. Journal of Clinical and Experimental Neuropsychology, 2003, 25, 614-24.
This is a path model linking early circumstances (represented by father’s occupational social class) to midlife cognitive function in the same respondents, via cognitive development, educational attainment, and adult occupational social class. The modelling technique allows all direct and indirect paths between these variables to be estimated, and provides a useful basic framework for a life course approach to cognitive ageing.
Richards M, Maughan B, Hardy R, Hall I, Strydom A, Wadsworth M. Long-term affective disorder in people with mild learning disability. British Journal of Psychiatry 2001, 179, 523-527.
In the context of links between cognition and affect, this study showed that mild learning disability was associated with a fourfold increase in risk of affective disorder, not accounted for by social and material disadvantage or by medical disorder.
Richards M, Hardy R, Kuh D, Wadsworth M. Birthweight and cognitive function in the British 1946 birth cohort. British Medical Journal 2001, 322, 199-202.
At this time there was a strong international interest in whether birth weight is associated with cognitive development, in the context of the developmental origins of health model. This was our contribution, which showed a graded positive association between increasing birth weight and childhood function until the heaviest birth weight quintile, which may reflect macrosomy arising from gestational diabetes. The positive association probably reflects early physiological common cause; however, there was no evidence that the association extended into midlife cognition.
Richards M, Kuh D, Hardy R, Wadsworth M. Lifetime cognitive function and timing of the natural menopause. Neurology, 1999, 52, 308-14.
This study began as an investigation into whether menopause was associated with loss of cognitive function because of oestrogen depletion. However, it became one of the first to show that, in fact, higher childhood cognition predicts later menopause. This association was robust to numerous potential confounders, and was stronger the earlier cognition was measured.
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