Cognitive functioning in anxiety and depression: results from the ALSPAC cohort

Steph Suddell*, Liam Mahedy, Caroline Skirrow, Ian s. Penton-Voak, Marcus r. Munafò, Robyn e. Wootton

*Corresponding author for this work

Research output: Contribution to journalArticle (Academic Journal)peer-review

Abstract

Anxiety and depression are associated with a range of impairments in cognitive functioning. Understanding the nature of these deficits may identify targets for intervention and prevent functional decline. We used observational and genetic methods to investigate the relationship of anxiety and depression with three cognitive domains: emotion recognition, response inhibition, and working memory, in the Avon Longitudinal Study of Parents and Children (ALSPAC). We examined: (i) cross-sectional associations between anxiety, depression, and cognition at age 24 (n = 2187), (ii) prospective associations between anxiety and depression at age 18 and cognition at age 24 (n = 1855), and (iii) the casual effect of anxiety and depression on cognition using Mendelian randomization (MR). Both disorders were associated with altered emotion recognition; anxiety with decreased happiness recognition (b = −0.27 [−0.54,0.01], p = 0.045), and depression with increased sadness recognition (b = 0.35 [0.07,0.64], p = 0.016). Anxiety was also associated with poorer working memory (b = −0.14 [−0.24,0.04], p = 0.005). There was no evidence for an association with response inhibition. MR provided no clear evidence of causal relationships between mental health and cognition, but these analyses were underpowered. Overall, there was little evidence for impairments in executive functioning, but moderate alterations in emotion recognition. This may inform the development of psychosocial interventions.
Original languageEnglish
Article number221161
JournalRoyal Society Open Science
Volume10
Issue number8
DOIs
Publication statusPublished - 9 Aug 2023

Bibliographical note

Funding Information:
The UK Medical Research Council and Wellcome (grant ref: 217065/Z/19/Z) and the University of Bristol provide core support for ALSPAC. A comprehensive list of grants funding is available on the ALSPAC website. GWAS data were generated by Sample Logistics and Genotyping Facilities at Wellcome Sanger Institute and LabCorp (Laboratory Corporation of America) using support from 23andMe. This work was undertaken with the support of the UK Medical Research Council Integrative Epidemiology Unit at the University of Bristol (grant no. MM_UU_00011/7). S.S., L.M., R.E.W., I.S.P.V. and M.R.M. are supported by the NIHR Biomedical Research Centre at University Hospitals Bristol and Weston NHS Foundation Trust and the University of Bristol (grant no. BRC-1215-20011). The views expressed are those of the author(s) and not necessarily those of the NIHR or the Department of Health and Social Care. R.E.W. is supported by a postdoctoral fellowship from the South-Eastern Regional Health Authority (grant no. 2020024). L.M. is supported by the Elizabeth Blackwell Institute for Health Research, University of Bristol and the Wellcome Trust Institutional Strategic Support Fund (grant ref: 204813/Z/16/Z). These funding sources had no involvement in the design of the study, data collection, data analysis or results interpretation, and were not involved in the decision to publish. Acknowledgements

Publisher Copyright:
© 2023 The Authors.

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