Genetic variation in FKBP5 associated with the extent of stress hormone dysregulation in major depression

Menke, A.; Klengel, T.; Rubel, J.; Brückl, T.; Pfister, H.; Lucae, S.; Uhr, M.; Holsboer, F.; Binder, E. B.

doi:10.1111/gbb.12026

Cited by 151Stress Responses and CortisolGenetic Associations and EpidemiologyNeurotransmitter Receptor Influence on Behavior

Genetic variation in FKBP5 associated with the extent of stress hormone dysregulation in major depression

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Menke, A., Klengel, T., Rubel, J., Brückl, T., Pfister, H., Lucae, S., Uhr, M., Holsboer, F. +1 more·2013·Genes, Brain and Behavior

DOI 10.1111/gbb.12026

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Abstract

The FK 506 binding protein 51 or FKBP5 has been implicated in the regulation of glucocorticoid receptor (GR) sensitivity, and genetic variants in this gene have been associated with mood and anxiety disorders. GR resistance and associated stress hormone dysregulation are among the most robust biological findings in major depression, the extent of which may be moderated by FKBP5 polymorphisms. FKBP5 mRNA expression in peripheral blood cells (baseline and following in vivo GR stimulation with 1.5 mg dexamethasone p.o.) was analyzed together with plasma cortisol, ACTH, dexamethasone levels and the FKBP5 polymorphism rs1360780 in 68 depressed patients and 87 healthy controls. We observed a significant (P = 0.02) interaction between disease status and FKBP5 risk allele carrier status (minor allele T) on GR‐stimulated FKBP5 mRNA expression. Patients carrying the risk T allele, but not the CC genotype, showed a reduced induction of FKBP5 mRNA. This FKBP5 polymorphism by disease status interaction was paralleled by the extent of plasma cortisol and ACTH suppression following dexamethasone administration, with a reduced suppression only observed in depressed patients carrying the T allele. Only depressed patients carrying the FKBP5 rs1360780 risk allele showed significant GR resistance compared with healthy controls, as measured by dexamethasone‐induced FKBP5 mRNA induction in peripheral blood cells and suppression of plasma cortisol and ACTH concentrations. This finding suggests that endocrine alterations in depressed patients are determined by genetic variants and may allow identification of specific subgroups.

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FKBP5 gene expression has been shown to be altered in PTSD and major depression.
“FKBP5 gene expression has been shown to be altered in PTSD and major depression (32)(33)(34)(35).”
From Holocaust Exposure Induced Intergenerational Effects on FKBP5 Methylation (2016) · cites this paper as [32]

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FKBP5 gene expression as a biomarker for treatment outcome in depression
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Self-citation

Authors: Menke, A., Klengel, T., Rubel, J., Brückl, T., Pfister, H., Lucae, S., Uhr, M., Holsboer, F., & Binder, E. B.
Affiliations: Max Planck Institute of Psychiatry (DE)
Corresponding author: Menke, A.
ORCID: Menke, A.
Klengel, T.
Brückl, T.
Lucae, S.
Binder, E. B.
Venue: Genes, Brain and Behavior
Publisher: Wiley
Published: 2013-03-07
Volume: 12
Issue: 3
Pages: 289-296
ISSN: 1601-183X (ISSN-L)
1601-1848
DOI: 10.1111/gbb.12026
OpenAlex: W1593021244
Cited by: 151
References: 55
Citations by year: 2026: 4 · 2025: 7 · 2024: 8 · 2023: 7 · 2022: 5 · 2021: 10 · 2020: 6 · 2019: 9 · 2018: 15 · 2017: 11 · 2016: 15 · 2015: 24 · 2014: 20 · 2013: 10
FWCI: 10.43
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Genes Brain & Behavior (publishedVersion)
PubMed (publishedVersion)
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
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords: FKBP5, major depressive disorder, dexamethasone suppression, cortisol, ACTH, gene-disease interaction, genetic susceptibility
MeSH terms: Tacrolimus Binding Protein 5, Adolescent, Adrenocorticotropic Hormone, Adult, Aged, Alleles, Major Depressive Disorder, Dexamethasone, Female, Humans, Hydrocortisone, Male, Middle Aged, Receptors, Glucocorticoid, RNA, Messenger, Transcription, Genetic, Case-Control Studies, Polymorphism, Single Nucleotide, Tacrolimus Binding Proteins, Genetic Association Studies

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Genetic variation in FKBP5 associated with the extent of stress hormone dysregulation in major depression

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