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Depression pathogenesis and treatment: what can we learn from blood mRNA expression?
Open accessAbstract
Alterations in several biological systems, including the neuroendocrine and immune systems, have been consistently demonstrated in patients with major depressive disorder. These alterations have been predominantly studied using easily accessible systems such as blood and saliva. In recent years there has been an increasing body of evidence supporting the use of peripheral blood gene expression to investigate the pathogenesis of depression, and to identify relevant biomarkers. In this paper we review the current literature on gene expression alterations in depression, focusing in particular on three important and interlinked biological domains: inflammation, glucocorticoid receptor functionality and neuroplasticity. We also briefly review the few existing transcriptomics studies. Our review summarizes data showing that patients with major depressive disorder exhibit an altered pattern of expression in several genes belonging to these three biological domains when compared with healthy controls. In particular, we show evidence for a pattern of 'state-related' gene expression changes that are normalized either by remission or by antidepressant treatment. Taken together, these findings highlight the use of peripheral blood gene expression as a clinically relevant biomarker approach.
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“have established the measurement of blood mRNA immune genes as a reliable and clinically significant biomarker in the context of psychoneuroimmunology, to complement (and at times surpass) the routine measurement of serum/plasma cytokines (Hepgul et al., 2013).”
From Why are depressed patients inflamed? A reflection on 20 years of research on depression, glucocorticoid resistance and inflammation (2017) · cites this paper as Hepgul et al., 2013
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Metadata
- Authors
- Hepgul, N., Cattaneo, A., Zunszain, P. A., & Pariante, C. M.
- Affiliations
- King's College London (GB)
- Corresponding author
- Pariante, Carmine M
- Venue
- BMC Medicine
- Published
- 2013-02-05
- Volume
- 11
- Issue
- 1
- Pages
- 28-28
- ISSN
- 1741-7015 (ISSN-L)
- PMC
- PMC3606439
- OpenAlex
- W2030900581
- Cited by
- 127
- References
- 86
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 10 · 2023: 10 · 2022: 8 · 2021: 13 · 2020: 8 · 2019: 7 · 2018: 7 · 2017: 11 · 2016: 17 · 2015: 12 · 2014: 11 · 2013: 5
- FWCI
- 1.89
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- BMC Medicine (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion, other-oa)
- Funders
- South London and Maudsley NHS Foundation Trust (MR/J002739/1)
- National Alliance for Research on Schizophrenia and Depression
- Psychiatry Research Trust
- National Institute for Health and Care Research (MR/J002739/1)
- King's College London
- Medical Research Council (MR/J002739/1)
- Topics
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- major depressive disorder, depression pathogenesis, peripheral blood gene expression, biomarkers, inflammation, glucocorticoid receptor, neuroplasticity, transcriptomics, antidepressant response, remission, neuroendocrine system, immune system
- MeSH terms
- Depression, Humans, Inflammation, Neuronal Plasticity, Receptors, Glucocorticoid, Microarray Analysis, Transcriptome
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