Dexamethasone stimulated gene expression in peripheral blood is a sensitive marker for glucocorticoid receptor resistance in depressed patients
Open accessAbstract
Although gene expression profiles in peripheral blood in major depression are not likely to identify genes directly involved in the pathomechanism of affective disorders, they may serve as biomarkers for this disorder. As previous studies using baseline gene expression profiles have provided mixed results, our approach was to use an in vivo dexamethasone challenge test and to compare glucocorticoid receptor (GR)-mediated changes in gene expression between depressed patients and healthy controls. Whole genome gene expression data (baseline and following GR-stimulation with 1.5 mg dexamethasone p.o.) from two independent cohorts were analyzed to identify gene expression pattern that would predict case and control status using a training (N=18 cases/18 controls) and a test cohort (N=11/13). Dexamethasone led to reproducible regulation of 2670 genes in controls and 1151 transcripts in cases. Several genes, including FKBP5 and DUSP1, previously associated with the pathophysiology of major depression, were found to be reliable markers of GR-activation. Using random forest analyses for classification, GR-stimulated gene expression outperformed baseline gene expression as a classifier for case and control status with a correct classification of 79.1 vs 41.6% in the test cohort. GR-stimulated gene expression performed best in dexamethasone non-suppressor patients (88.7% correctly classified with 100% sensitivity), but also correctly classified 77.3% of the suppressor patients (76.7% sensitivity), when using a refined set of 19 genes. Our study suggests that in vivo stimulated gene expression in peripheral blood cells could be a promising molecular marker of altered GR-functioning, an important component of the underlying pathology, in patients suffering from depressive episodes.
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In BD, methylation variations in FKBP5 expression are observed which suggests a role in mood regulation and stress response mechanisms.
“With BD, methylation variations in FKBP5 expression are observed which suggests a role in mood regulation and stress response mechanisms”
From The clinical use of epigenetics in psychiatry: a narrative review of epigenetic mechanisms, key candidate genes, and precision psychiatry (2025) · cites this paper as [90]
The GR-resistance and Validation of Differentially Regulated Transcripts sections report differences in FKBP5 expression responses between depressed patients and controls; Table 1 shows that some patients had bipolar disorder. The Discussion also links FKBP5 to mood disorders. None of these passages reports FKBP5 methylation variations or establishes a finding specific to bipolar disorder. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe mDST was able to identify HPA axis alterations in MDD, job-related exhaustion, anxious depression and childhood trauma, chronic stress, and healthy females compared to healthy men.
“The mDST was able to identify HPA axis alterations in MDD [67], job-related exhaustion [69], anxious depression and childhood trauma [70], chronic stress [31], and healthy females compared to healthy men [71].”
From The HPA Axis as Target for Depression (2024) · cites this paper as [67]
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Self-citation
- Authors
- Menke, A., Arloth, J., Pütz, B., Weber, P., Klengel, T., Mehta, D., Gonik, M., Rex-Haffner, M., Rubel, J., Uhr, M., Lucae, S., Deussing, J. M., Müller-Myhsok, B., Holsboer, F., & Binder, E. B.
- Affiliations
- Max Planck Institute of Psychiatry (DE)
- Helmholtz Munich (DE)
- Corresponding author
- Menke, Andreas
- ORCID
- Venue
- Neuropsychopharmacology
- Published
- 2012-01-11
- Volume
- 37
- Issue
- 6
- Pages
- 1455-1464
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC3327850
- OpenAlex
- W2037815828
- Cited by
- 177
- References
- 57
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 8 · 2023: 8 · 2022: 23 · 2021: 14 · 2020: 12 · 2019: 12 · 2018: 20 · 2017: 12 · 2016: 13 · 2015: 14 · 2014: 16 · 2013: 5 · 2012: 8
- FWCI
- 5.71
- Type
- journal article
- Language
- en
- Update notices
- erratum (2012-06-15)
- Open access
- bronze
- doi.org
- Locations
- Neuropsychopharmacology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- QUT ePrints (Queensland University of Technology) (submittedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- Site cant be reached (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- Bundesministerium für Bildung und Forschung (01GS0481)
- Max-Planck-Gesellschaft
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- major depressive disorder, peripheral blood gene expression, biomarkers, FKBP5, MKP-1, random forest classification
- MeSH terms
- Tacrolimus Binding Protein 5, Adolescent, Adrenocorticotropic Hormone, Adult, Aged, Blood Cell Count, Depression, Dexamethasone, Gene Expression Regulation, Humans, Hydrocortisone, Male, Middle Aged, Receptors, Glucocorticoid, RNA, Messenger, Reproducibility of Results, Cohort Studies, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Tacrolimus Binding Proteins, Dual Specificity Phosphatase 1, Young Adult
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