Clinical variations modulate patterns of gene expression and define blood biomarkers in major depression

Belzeaux, Raoul; Formisano-Tréziny, Christine; Loundou, Anderson; Boyer, Laurent; Gabert, Jean; Samuelian, Jean-Claude; Féron, François; Naudin, Jean; Ibrahim, El Chérif

doi:10.1016/j.jpsychires.2010.04.011

Cited by 81 publications

(67 citation statements)

References 64 publications

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“…A greater increase in phosphorylated CREB in responders was confirmed by other studies using different pharmacological or psychotherapeutic treatments (Koch et al 2002(Koch et al , 2009, but no variation was reported after venlafaxine treat-ment (Rojas et al 2011). Inconsistent findings were reported in regard to CREB1 mRNA variations after antidepressant treatment (increased, Belzeaux et al 2010, or decreased, Lai et al 2003Iga et al 2007, levels).…”

Section: Peripheral Biomarkersmentioning

confidence: 65%

“…On the other hand, no difference in mRNA levels between patients and controls was demonstrated by other studies in small samples of MDD patients (Lai et al 2003;Belzeaux et al 2010;Iacob et al 2013). Another study focussed on mRNA levels in leukocytes demonstrated an opposite finding, i.e., higher CREB mRNA levels in MDD patients compared to controls (Iga et al 2007).…”

Section: Peripheral Biomarkersmentioning

confidence: 81%

“…SLC6A4 expression (mRNA level) in peripheral cells (lymphocytes) was also investigated, since lymphocytes are thought to potentially act as a neural probe for studying psychiatric dis-orders (Gladkevich et al 2004). Studies on small samples of depressed patients suggested a reduction of SERT expression after antidepressant treatment (Iga et al 2005;Tsao et al 2006) with a possible positive correlation with response (Belzeaux et al 2014), but opposite findings also exist (Pena et al 2005;Belzeaux et al 2010). The reduction of SERT expression in the rat brain was associated with antidepressant-like behaviours (Thakker et al 2005) and key markers of antidepressant action: reduced expression and function of 5-HT1A-autoreceptors, elevated extracellular 5-HT in the forebrain and increased neurogenesis and expression of plasticity-related genes (BDNF, VEGF, ARC)in the hippocampus (Ferres-Coy et al 2013).…”

Section: Peripheral Biomarkersmentioning

confidence: 99%

“…The reduction of SERT expression in the rat brain was associated with antidepressant-like behaviours (Thakker et al 2005) and key markers of antidepressant action: reduced expression and function of 5-HT1A-autoreceptors, elevated extracellular 5-HT in the forebrain and increased neurogenesis and expression of plasticity-related genes (BDNF, VEGF, ARC)in the hippocampus (Ferres-Coy et al 2013). No clear association between SLC6A4 expression and MDD risk was demonstrated, since the few studies reported either negative findings (Belzeaux et al 2010), higher expression of the gene in patients compared to controls (Iga et al 2005) or the opposite finding (Pena et al 2005).…”

Section: Peripheral Biomarkersmentioning

confidence: 99%

“…Despite increased receptor density, blunted receptor response was found in patients who have made high-lethality suicide attempts (Malone et al 2007). Preliminary evidence suggested that a trend of increased HTR2A mRNA levels in peripheral lymphocytes may be observed during the first 8 weeks of antidepressant treatment (Belzeaux et al 2010), suggesting that further studies should investigate this potential biomarker of antidepressant efficacy. Another preliminary study found that 5-HT2A receptor clustering in peripheral lymphocytes is altered in MDD and may be a bio-marker of therapeutic efficacy (Rivera-Baltanas et al 2014).…”

Section: Peripheral Biomarkersmentioning

confidence: 99%

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Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Fabbri

Hosák

Mößner

et al. 2016

The World Journal of Biological Psychiatry

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Major depressive disorder (MDD) is a heritable disease with a heavy personal and socio-economic burden. Antidepressants of different classes are prescribed to treat MDD, but reliable and reproducible markers of efficacy are not available for clinical use. Further complicating treatment, the diagnosis of MDD is not guided by objective criteria, resulting in the risk of under-or overtreatment. A number of markers of MDD and antidepressant response have been investigated at the genetic, epigenetic, gene expression and protein levels. Polymorphisms in genes involved in anti-depressant metabolism (cytochrome P450 isoenzymes), antidepressant transport (ABCB1), glucocorticoid signalling (FKBP5) and serotonin neurotransmission (SLC6A4 and HTR2A) were among those included in the first pharmacogenetic assays that have been tested for clinical applicability. The results of these investigations were encouraging when examining patient-outcome improvement. Furthermore, a nine-serum biomarker panel (including BDNF, cortisol and soluble TNF-a receptor type II) showed good sensitivity and specificity in differentiating between MDD and healthy controls. These first diagnostic and response-predictive tests for MDD provided a source of optimism for future clinical applications. However, such findings should be considered very carefully because their benefit/cost ratio and clinical indications were not clearly demonstrated. Future tests may include combinations of different types of biomarkers and be specific for MDD subtypes or pathological dimensions.

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Section: Peripheral Biomarkersmentioning

confidence: 65%

Section: Peripheral Biomarkersmentioning

confidence: 81%

Section: Peripheral Biomarkersmentioning

confidence: 99%

Section: Peripheral Biomarkersmentioning

confidence: 99%

Section: Peripheral Biomarkersmentioning

confidence: 99%

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Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Fabbri

Hosák

Mößner

et al. 2016

The World Journal of Biological Psychiatry

View full text Add to dashboard Cite

show abstract

Gene Expression Factor Analysis to Differentiate Pathways Linked to Fibromyalgia, Chronic Fatigue Syndrome, and Depression in a Diverse Patient Sample

Iacob

Light

Donaldson

et al. 2015

Arthritis Care & Research

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Objective To determine if independent candidate genes can be grouped into meaningful biological factors and if these factors are associated with the diagnosis of chronic fatigue syndrome (CFS) and fibromyalgia (FMS) while controlling for co-morbid depression, sex, and age. Methods We included leukocyte mRNA gene expression from a total of 261 individuals including healthy controls (n=61), patients with FMS only (n=15), CFS only (n=33), co-morbid CFS and FMS (n=79), and medication-resistant (n=42) or medication-responsive (n=31) depression. We used Exploratory Factor Analysis (EFA) on 34 candidate genes to determine factor scores and regression analysis to examine if these factors were associated with specific diagnoses. Results EFA resulted in four independent factors with minimal overlap of genes between factors explaining 51% of the variance. We labeled these factors by function as: 1) Purinergic and cellular modulators; 2) Neuronal growth and immune function; 3) Nociception and stress mediators; 4) Energy and mitochondrial function. Regression analysis predicting these biological factors using FMS, CFS, depression severity, age, and sex revealed that greater expression in Factors 1 and 3 was positively associated with CFS and negatively associated with depression severity (QIDS score), but not associated with FMS. Conclusion Expression of candidate genes can be grouped into meaningful clusters, and CFS and depression are associated with the same 2 clusters but in opposite directions when controlling for co-morbid FMS. Given high co-morbid disease and interrelationships between biomarkers, EFA may help determine patient subgroups in this population based on gene expression.

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Acute Effects of Psilocybin After Escitalopram or Placebo Pretreatment in a Randomized, Double‐Blind, Placebo‐Controlled, Crossover Study in Healthy Subjects

Becker

Holze

Grandinetti

et al. 2021

Clin Pharma and Therapeutics

105

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Trial registry: ClinicalTrials.gov (NCT03912974). Study HighlightsWHAT IS THE CURRENT KNOWLEDGE ON THE TOPIC? Case reports indicate that antidepressants generally reduce the response to psychedelics. Moreover, antidepressants are thought to increase the risks for adverse events when taken together with psychedelics. WHAT QUESTION DID THIS STUDY ADDRESS? Does an escitalopram pretreatment (10 mg for 7 days, followed by 20 mg for 7 days) interact with the acute response to psilocybin (25 mg), compared with a placebo pretreatment? WHAT DOES THIS STUDY ADD TO OUR KNOW-LEDGE? This study gives a first indication that psilocybin is not only safe to take during escitalopram treatment, moreover, it has no relevant effects on the positive drug effects of psilocybin. HOW MIGHT THIS CHANGE CLINICAL PHARMA-COLOGY OR TRANSLATIONAL SCIENCE? If the results are confirmed in subsequent studies, escitalopram pretreatment would no longer need to be stopped for psilocybin treatment in phase II trials and compassionate use. Thus, the risk for adverse effects due to escitalopram treatment interruption would be eliminated.

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Clinical variations modulate patterns of gene expression and define blood biomarkers in major depression

Cited by 81 publications

References 64 publications

Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Gene Expression Factor Analysis to Differentiate Pathways Linked to Fibromyalgia, Chronic Fatigue Syndrome, and Depression in a Diverse Patient Sample

Acute Effects of Psilocybin After Escitalopram or Placebo Pretreatment in a Randomized, Double‐Blind, Placebo‐Controlled, Crossover Study in Healthy Subjects

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