Lack of association of indoleamine 2,3-dioxygenase polymorphisms with interferon-alpha-related depression in hepatitis C

Almeida, Amanda Cristina Galvão Oliveira de; Quarantini, Lucas de Castro; Sampaio, Aline Santos; Lyra, André Castro; Parise, Carmen Lívia; Paraná, Raymundo; Oliveira, Irismar Reis de; Koenen, Karestan C.; Miranda-Scippa, Ângela; Guindalini, Camila

doi:10.1016/j.bbi.2011.06.001

Cited by 22 publications

(11 citation statements)

References 56 publications

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“…In presented paper the both studied polymorphisms of IDO1, i.e., c.-1849C > A (rs3824259) and c.-1493G > C (rs10089084), are localized in 5 region of the gene. A previous study showed no association between the two polymorphisms and IFN-α-related depression [61]. Similarly, our team found no correlation between the frequency of the c.-1849C > A (rs3824259) polymorphism and the risk of stroke occurrence.…”

Section: Discussionsupporting

confidence: 51%

Variation of Genes Encoding Tryptophan Catabolites Pathway Enzymes in Stroke

Wigner

Saluk‐Bijak

Synowiec

et al. 2019

JCM

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The abnormal activation of the tryptophan catabolites pathway (TRYCATs) is observed in patients suffering from cerebrovascular disease, including stroke. A previous study confirmed that lower bioavailability of tryptophan for serotonin synthesis was characterized in the patients during the acute stroke phase. Interestingly, according to various studies, polymorphisms of the genes involved in the TRYCATs pathway may modulate the risk of stroke occurrence. Therefore, this study aimed to investigate the association between the occurrence of TPH1, TPH2, KAT1, KAT2 and IDO1 polymorphisms and the risk of stroke development.The following 10 polymorphisms of the genes encoding enzymes of the TRYCATs pathway were selected: c.804-7C > A (rs10488682), c.-1668T > A (rs623580), c.803+221C > A (rs1800532), c.-173A > T (rs1799913) – TPH1, c.-1449C > A (rs7963803), and c.-844G > T (rs4570625) – TPH2. c.*456G > A of KAT1 (rs10988134), c.975-7T > C of KAT2 (rs1480544), c.-1849C > A (rs3824259) and c. -1493G > C (rs10089084) of IDO1. The study was carried out on DNA isolated from the peripheral blood taken from 107 patients after a stroke and 107 healthy volunteers. All DNA samples were genotyped using TaqMan probes. The genotypes of eight studied polymorphisms modulated the risk of stroke. No significant difference in genotype and allele frequencies of the c.804-7C > A –TPH1 (rs10488682) and c.*456G > A – KAT1 (rs10988134) polymorphisms were found between patients and controls. Having performed haplotype and gen-gen analyses, it was possible to determine that patients after a stroke and controls differed in terms of the frequency of selected genotypes and haplotypes. Among the studied polymorphisms, eight SNPs were linked with stroke risk modulation. The results obtained confirmed our hypothesis regarding the involvement of the TRYCATs pathway in the pathogenesis of stroke.

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Section: Discussionsupporting

confidence: 51%

Variation of Genes Encoding Tryptophan Catabolites Pathway Enzymes in Stroke

Wigner

Saluk‐Bijak

Synowiec

et al. 2019

JCM

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“…Patients who carried the C/C genotype were more likely to exhibit moderate or severe depression at week 12 of IFN-α treatment compared with those with either the C/T or T/T genotypes (Smith et al , 2011). However, a second cross-sectional study, conducted in a Brazilian population, found no associations (Galvao-de Almeida et al , 2011). Utilizing the STAR*D cohort, Cutler et al (2012) discovered two IDO SNPs (rs2929115 and rs2929116) that were associated with response to treatment with citalopram.…”

Section: Resultsmentioning

confidence: 98%

Genetic Contributions of Inflammation to Depression

Barnes

Mondelli

Pariante

2016

Neuropsychopharmacol

197

114

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This paper describes the effects of immune genes genetic variants and mRNA expression on depression's risk, severity, and response to antidepressant treatment, through a systematic review on all papers published between 2000 and 2016. Our results, based largely on case–control studies, suggest that common genetic variants and gene-expression pathways are involved in both immune activation and depression. The most replicated and relevant genetic variants include polymorphisms in the genes for interleukin (IL)-1β, IL-6, IL-10, monocyte chemoattractant protein-1, tumor necrosis factor-alpha, C-reactive protein, and phospholipase A2. Moreover, increased blood cytokines mRNA expression (especially of IL-1β) identifies patients that are less likely to respond to conventional antidepressants. However, even for the most replicated findings there are inconsistent results, not only between studies, but also between the immune effects of the genetic variants and the resulting effects on depression. We find evidence that these discrepant findings may be explained, at least in part, by the heterogeneity of the depression immunophenotype, by environmental influences and gene × environment interactions, and by the complex interfacing of genetic variants with gene expression. Indeed, some of the most robust findings have been obtained in patients developing depression in the context of treatment with interferon-alpha, a widely used model to mimic depression in the context of inflammation. Further ‘omics' approaches, through GWAS and transcriptomics, will finally shed light on the interaction between immune genes, their expression, and the influence of the environment, in the pathogenesis of depression.

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“…Thus, the genes involved with KYN pathway may play an important role in both pathogenesis and treatment of mood disorders. However, in patients with IFN-α therapy depression and anxiety the symptoms were not linked to variants in the IDO gene (Galvao de Almeida et al, 2011), though these discrepancies could be related to the cross-sectional study design.…”

Section: Resultsmentioning

confidence: 99%

Kynurenine pathway dysfunction in the pathophysiology and treatment of depression: Evidences from animal and human studies

Réus¹,

Jansen

Titus³

et al. 2015

Journal of Psychiatric Research

198

113

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Treatment-resistant depression affects up to 20% of individuals suffering from major depressive disorder (MDD). The medications currently available to treat depression, including serotonin re-uptake inhibitors (SSRIs), monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants (TCAs), fail to produce adequate remission of depressive symptoms for a large number of patients. The monoamine hypothesis upon which these medications are predicated should be expanded and revised as research elucidates alternative mechanisms of depression and effective methods to treat the underlying pathologic consequences. Research into the role of tryptophan degradation and the kynurenine pathway in the setting of inflammation has brought new insight into potential etiologies of MDD. Further investigation into the connection between inflammatory mediators, tryptophan degradation, and MDD can provide many targets for novel antidepressant therapies. Thus, this review will highlight the role of the kynurenine pathway in the pathophysiology of depression, as well as a novel therapeutic target to classic and new modulators to treat depression based on findings from preclinical and clinical studies.

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Lack of association of indoleamine 2,3-dioxygenase polymorphisms with interferon-alpha-related depression in hepatitis C

Cited by 22 publications

References 56 publications

Variation of Genes Encoding Tryptophan Catabolites Pathway Enzymes in Stroke

Variation of Genes Encoding Tryptophan Catabolites Pathway Enzymes in Stroke

Genetic Contributions of Inflammation to Depression

Kynurenine pathway dysfunction in the pathophysiology and treatment of depression: Evidences from animal and human studies

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