Association Study of the Interleukin-1beta (C-511T) Genetic Polymorphism with Major Depressive Disorder, Associated Symptomatology, and Antidepressant Response

Yu, Younger W.‐Y.; Chen, Tai‐Jui; Hong, Chen‐Jee; Chen, Hung-Mei; Tsai, Shih-Jen

doi:10.1038/sj.npp.1300172

Cited by 135 publications

(85 citation statements)

References 24 publications

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“…The G allele of the rs16944 polymorphism (located within the promoter of the IL-1b gene) has been associated with SSRI non-response (Yu et al 2003;Tadic et al 2008;Baune et al 2010) and with recurrent major depression (Borkowska et al 2011). In addition, IL-1b promoter polymorphism rs1143627 was also associated with recurrent major depression (Borkowska et al 2011).…”

Section: Genetic Polymorphismsmentioning

confidence: 99%

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: Genetic Polymorphismsmentioning

confidence: 99%

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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show abstract

“…Furthermore, a recent study among 74 depressed patients found that expression of genes related to inflammation predicted non-response to a 8-week treatment with escitalopram or nortriptyline (Cattaneo et al, 2013). Lastly, the IL-1b gene (C-511T, rs19644 and rs1143643) has been shown to predict antidepressant non-response (Baune et al, 2010;Yu et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Inflammatory and Metabolic Dysregulation and the 2-Year Course of Depressive Disorders in Antidepressant Users

Vogelzangs

Beekman

Dortland

et al. 2014

Neuropsychopharmacol

116

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Scarce evidence suggests that inflammatory and metabolic dysregulation predicts poor response to antidepressants, which could result in worse depression outcome. This study prospectively examined whether inflammatory and metabolic dysregulation predicted the 2-year course of depressive disorders among antidepressant users. Data were from the Netherlands Study of Depression and Anxiety, including 315 persons (18-65 years) with a current depressive disorder (major depressive disorder, dysthymia) at baseline according to the DSM-IV criteria and using antidepressants. Inflammatory (C-reactive protein, interleukin-6 (IL-6), tumor-necrosis factor-a) and metabolic (waist circumference, triglycerides, high-density lipoprotein (HDL) cholesterol, blood pressure, fasting glucose) factors were measured at baseline. Primary outcome for course of depression was indicated by whether or not a DSM-IV depressive disorder diagnosis was still/ again present at 2-year follow-up, indicating chronicity of depression. Elevated IL-6, low HDL cholesterol, hypertriglyceridemia, and hyperglycemia were associated with chronicity of depression in antidepressant users. Persons showing X4 inflammatory or metabolic dysregulations had a 1.90 increased odds of depression chronicity (95% CI ¼ 1.12-3.23). Among persons who recently (ie, at most 3 months) started antidepressant medication (N ¼ 103), having X4 dysregulations was associated with a 6.85 increased odds of depression chronicity (95% CI ¼ 1.95-24.06). In conclusion, inflammatory and metabolic dysregulations were found to predict a more chronic course of depressive disorders among patients using antidepressants. This could suggest that inflammatory and metabolic dysregulation worsens depression course owing to reduced antidepressant treatment response and that alternative intervention treatments may be needed for depressed persons with inflammatory and metabolic dysregulation.

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“…10,11 (4) Genetic association between genes of inflammatory factors, including polymorphisms in IL-1 family genes, and severity of depression and its responsiveness to antidepressant treatment. 12 (5) Cytokine-related induction of depressed mood in normal subjects following experimental exposure to immune challenges. [13][14][15] (6) Studies in experimental animals, showing that exposure to various immune challenges, as well as exogenous administration of IL-1, either peripherally or directly into the brain, produce depressive-like symptoms, which can be attenuated by chronic treatment with antidepressant drugs, 1,[16][17][18][19] as well as by pretreatment with cytokine antagonists, particularly IL-1ra, and by manipulations in IL-1 family genes.…”

Section: Introductionmentioning

confidence: 99%

Brain interleukin-1 mediates chronic stress-induced depression in mice via adrenocortical activation and hippocampal neurogenesis suppression

et al. 2007

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Several lines of evidence implicate the pro-inflammatory cytokine interleukin-1 (IL-1) in the etiology and pathophysiology of major depression. To explore the role of IL-1 in chronic stress-induced depression and some of its underlying biological mechanisms, we used the chronic mild stress (CMS) model of depression. Mice subjected to CMS for 5 weeks exhibited depressive-like symptoms, including decreased sucrose preference, reduced social exploration and adrenocortical activation, concomitantly with increased IL-1b levels in the hippocampus. In contrast, mice with deletion of the IL-1 receptor type I (IL-1rKO) or mice with transgenic, brain-restricted overexpression of IL-1 receptor antagonist did not display CMS-induced behavioral or neuroendocrine changes. Similarly, whereas in wild-type (WT) mice CMS significantly reduced hippocampal neurogenesis, measured by incorporation of bromodeoxyuridine (BrdU) and by doublecortin immunohistochemistry, no such decrease was observed IL-1rKO mice. The blunting of the adrenocortical activation in IL-1rKO mice may play a causal role in their resistance to depression, because removal of endogenous glucocorticoids by adrenalectomy also abolished the depressive-like effects of CMS, whereas chronic administration of corticosterone for 4 weeks produced depressive symptoms and reduced neurogenesis in both WT and IL-1rKO mice. The effects of CMS on both behavioral depression and neurogenesis could be mimicked by exogenous subcutaneous administration of IL-1b via osmotic minipumps for 4 weeks. These findings indicate that elevation in brain IL-1 levels, which characterizes many medical conditions, is both necessary and sufficient for producing the high incidence of depression found in these conditions. Thus, procedures aimed at reducing brain IL-1 levels may have potent antidepressive actions.

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Association Study of the Interleukin-1beta (C-511T) Genetic Polymorphism with Major Depressive Disorder, Associated Symptomatology, and Antidepressant Response

Cited by 135 publications

References 24 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

Inflammatory and Metabolic Dysregulation and the 2-Year Course of Depressive Disorders in Antidepressant Users

Brain interleukin-1 mediates chronic stress-induced depression in mice via adrenocortical activation and hippocampal neurogenesis suppression

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