Background Previous research has often shown that morbidity and disability are hinged to negative events and exposures that can accumulate over the life course, but less clear is their impact on late-life cognitive health. We assessed the biopsychosocial mechanisms influencing the associations between adverse childhood experiences and cognitive impairment at advanced ages.

Methods Data were from 3,130 dementia-free adults aged 50+ from the English Longitudinal Study of Ageing (ELSA) with data available from wave 3 (2006/07) to wave 8 (2016/17). ELSA provides a wide variety of psychosocial data collected via face-to-face computer-assisted personal interviews (CAPI) and self-completion questionnaires. All participants provided informed consent prior to their participation in the study. We used structural equation modelling to estimate direct and indirect associations between adverse childhood experiences (ACEs) and cognitive impairment (measured with 1.5 SD below the mean on the modified Telephone Cognitive Screening Interview scale range 0 to 35) via markers of SES (education and wealth), inflammation (serum fibrinogen and C-reactive protein [CRP]), physician-diagnosed chronic conditions (diabetes, hypertension, stroke and Coronary heart disease) and depressive symptoms ascertained with the Center for Epidemiologic Studies Depression Scale range 0 to 8. We controlled for age, sex and Apolipoprotein E (APOE).

Results Our findings suggest that experiencing financial hardship in childhood (20% of the sample) was associated with a higher risk of cognitive impairment (OR=1.55, 95% CI 1.15 – 2.09) in later life. A similar pattern was observed for having parents unemployed (7% of the sample) (OR=1.63, 95% CI 1.09 – 2.46) or physically abusive parents (3%) (OR=3.21, 95% CI 1.82–5.66). We also found that increased depressive symptoms were interlinked with higher cognitive impairment, while APOEe4 and inflammatory markers were not directly associated. However, inflammation was indirectly associated with cognitive impairment, via depressive symptoms (β=0.08, SE=0.03, p=0.020) and chronic conditions (β=0.39, SE=0.19, p=0.042).

Conclusion These findings support the psychosocial paradigm. They suggest that those from disadvantaged family backgrounds are more likely to have lower levels of education and be less wealthy, which in turn lead to poorer health, such as higher overall inflammation and increased depressive symptoms. These findings provide a plausible explanation for inequalities in late-life cognitive health.