Neuro‐immune markers, socioeconomic inequalities, and neurodegenerative disorders in older age

Abstract

AbstractBackgroundAccumulating evidence suggests that the neuro‐immune markers of inflammation may be involved in the onset of neurodegenerative disorders (Bostancıklıoğlu, 2019; Park et al., 2020). However, immune mechanisms linking socioeconomic adversities in later life and neurodegenerative disorders have yet to be fully explored. This study has used a large longitudinal study to investigate the mediating effects of neuro‐immune markers in the socioeconomic disparities of neurocognitive disorders in older adults.MethodData of 4815 participants aged 50 and above from the English Longitudinal Study of Ageing (ELSA) across three waves of data collection. Socioeconomic position was assessed in 2008/9 and neuro‐immune markers in 2012/2013. Neurocognitive disorders were ascertained using cognitive variables available in 2018/2019 using a well‐accepted consensus criterion (Richardson et al., 2019). It was categorised into no cognitive impairment, cognitive impairment, no dementia (CIND) and dementia. Mediation analysis was carried out to investigate the mediation effect of c‐reactive protein (CRP), fibrinogen and white blood cell (WBC) count in the association between socioeconomic position and different subtypes of neurocognitive disorders. All models were adjusted for age, sex, marital status and baseline cognitive status.ResultAfter accounting for potential confounders, CRP, fibrinogen, and WBC partly mediated the association of education, occupation, and wealth with cognitive impairment. Results on dementia were all non‐significant.ConclusionAdverse socioeconomic environment were related to early stages of neurocognitive disorders partly via elevated biomarker levels in later life. Neuroinflammation might be one of the immunobiological mechanisms underlying socioeconomic disparities in cognitive impairment. Further research should explore other plausible biological mechanisms to develop interventions to delay the onset of neurodegeneration.