Cargando…

Adverse childhood experiences and cognitive function in adulthood: examining the roles of depressive symptoms and inflammation in a prospective cohort study

PURPOSE: Adverse childhood experiences (ACEs) have been associated with cognitive decline in adulthood. However, the underlying mechanisms implicated remain unclear. This study investigated depressive symptoms and systemic inflammation as potential mediators of the association between ACEs and later...

Descripción completa

Detalles Bibliográficos
Autores principales: Lowry, Elaine, McInerney, Amy, Schmitz, Norbert, Deschênes, Sonya S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9244111/
https://www.ncbi.nlm.nih.gov/pubmed/35753000
http://dx.doi.org/10.1007/s00127-022-02315-w
Descripción
Sumario:PURPOSE: Adverse childhood experiences (ACEs) have been associated with cognitive decline in adulthood. However, the underlying mechanisms implicated remain unclear. This study investigated depressive symptoms and systemic inflammation as potential mediators of the association between ACEs and later cognitive function. METHODS: Participants were adults aged 50 + from the English Longitudinal Study of Ageing (N = 3029; 54.8% female). Measures included self-reported ACEs at wave 3 (2006–2007), C-reactive protein (CRP) and depressive symptoms at wave 4 (2008–2009), and cognitive function at waves 3 and 7 (2014–2015). Mediation analyses examined the direct associations between ACEs and cognitive function at wave 7 and the indirect associations via depressive symptoms and CRP at wave 4. In a first set of analyses, models were adjusted for sociodemographic factors and baseline cognitive function. In a second set of analyses, models were additionally adjusted for BMI and health behaviours (n = 1915). RESULTS: Cumulative ACEs exposure positively predicted depressive symptoms (b = 0.184, s.e. = 0.034, p < .001), which in turn predicted poorer cognitive function at wave 7 (b =  − 0.035, s.e. = 0.008, p < .001). ACEs also positively predicted systemic inflammation as measured by CRP (b = 0.031, s.e. = 0.01, p = 0.0016). However, CRP did not mediate the association between ACEs and later cognitive function (b =  − 0.0002, 95% CI: − 0.002, 0.002). CONCLUSION: These findings suggest that ACEs may be related to cognitive decline partly via depressive symptoms and corroborate prior research linking ACEs with systemic inflammation in adulthood. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00127-022-02315-w.