Social health (SH) markers, including marital status, contact frequency, network size, and social support, have been linked with increased cognitive capability. However, the underlying mechanisms remain poorly understood. We aim to investigate whether depression symptoms and inflammatory biomarkers mediate associations between SH and cognitive outcomes.

We used data from waves 1-9 of the English Longitudinal Study of Ageing, involving 7,136 participants aged 50 or older at baseline. First, we examined associations between SH (wave 1) and depression and inflammatory biomarkers (C-reactive protein (CRP) and fibrinogen) (wave 2) using linear regression models. Second, we tested associations between a) SH and b) depression and inflammation with subsequent standardised verbal fluency and memory in wave 3 and change between waves 3-9, indexed using slopes derived from multilevel models. We adjusted for age, sex, socio-economic position, cardiovascular disease, basic and instrumental activities of daily living, health behaviours, and baseline depression symptoms and cognition. We will also conduct causal mediation analysis.

All SH markers, except contact frequency, were associated with lower subsequent depression, but not inflammatory biomarkers. Greater contact frequency (e.g. once-twice a week vs <once per year: β=0.18 [0.01, 0.36]) and less negative support (β=0.02 [0.00, 0.03]) were associated with higher verbal fluency. Larger network size (>6 people vs none: β=0.007SD/year [0.001, 0.012]), less negative (β=0.001SD/year [0.001, 0.002]) and more positive support (β=0.001SD/year [0.000, 0.001]) were linked with slower memory decline, and more positive support predicted slower verbal fluency decline (β=0.001SD/year [0.000, 0.001]). Depression symptoms were associated with lower memory and verbal fluency, and faster memory decline (β=-0.001SD/year [-0.001, -0.000]) and verbal fluency (β=-0.001SD/year [-0.001, -0.000]). CRP was associated with lower verbal fluency (β=-0.02 [-0.04, 0.00]), whereas fibrinogen was linked with faster memory decline (β=-0.001SD/year [-0.003, -0.000]).

Depression symptoms and SH showed associations with subsequent cognitive capability and change. SH was linked with lower depression, but not inflammatory biomarkers. Findings highlight the potential for depression to underpin associations between SH and cognition, a pathway which we will test using causal mediation analysis. We will also examine whether findings replicate in the Swedish National Study of Aging and Care in Kungsholmen.