C-reactive protein as a biomarker for major depressive disorder?

Publication type

Journal Article

Authors

Publication date

February 15, 2022

Summary:

The etiopathogenesis of depression is not entirely understood. Several studies have investigated the role of inflammation in major depressive disorder. The present work aims to review the literature on the association between C-Reactive Protein (CRP) and depression. A systematic review was performed for the topics of ‘CRP’ and ‘depression’ using the PubMed database from inception to December 2021. Fifty-six studies were identified and included in the review. Evidence suggested the presence of dysregulation in the inflammation system in individuals with depression. In most studies, higher blood CRP levels were associated with greater symptom severity, a specific pattern of depressive symptoms, and a worse response to treatment. Moreover, about one-third of depressed patients showed a low-grade inflammatory state, suggesting the presence of a different major depressive disorder (MDD) subgroup with a distinct etiopathogenesis, clinical course, treatment response, and prognosis, which could benefit from monitoring of CRP levels and might potentially respond to anti-inflammatory treatments. This work provides robust evidence about the potential role of CRP and its blood levels in depressive disorders. These findings can be relevant to developing new therapeutic strategies and better understanding if CRP may be considered a valuable biomarker for depression.

Published in

International Journal of Molecular Sciences

Volume

Volume: 23

DOI

https://doi.org/10.3390/ijms23031616

ISSN

16616596

Subjects

Notes

Open Access

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited

Reviewed studies include: Hughes, A. and Kumari, M. (2017) ‘Associations of C-reactive protein and psychological distress are modified by antidepressants, supporting an inflammatory depression subtype: findings from UKHLS’, Brain, Behavior, and Immunity, 66:89-93. doi: 10.1016/j.bbi.2017.07.009

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