The Tryptophan System in Cocaine-Induced Depression

Fonseca, Francina; Mestre-Pintó, Joan Ignasi; Gómez-Gómez, Álex; Martinez-Sanvisens, Diana; Rodríguez-Minguela, Rocío; Papaseit, Esther; Pérez‐Mañá, Clara; Langohr, Klaus; Valverde, Olga; Pozo, Óscar J.; Farré, Magı́; Torrens, Marta

doi:10.3390/jcm9124103

Cited by 14 publications

(15 citation statements)

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“…As the diagnosis of depression is based on clinical criteria, sometimes with suboptimal rates of validity and accuracy, the detection of measurable biomarkers has implications in the study of the pathophysiology of depression and the introduction of effective treatments. As previously reported, the monoamine theory of depression cannot completely explain the pathogenesis of induced depressions (32), and other physiological systems should be studied. Stress is related to both MDD (41,42) and SUD (43,44), and in turn, cortisol is associated with stress.…”

Section: Discussionmentioning

confidence: 93%

“…At present, it is crucial to perform accurate diagnoses of CUD-primary-MDD and CUD-induced-MDD. As the monoamine hypothesis of depression is proven insufficient to explain differences between both types of MDD ( 32 ), it is essential to investigate the involvement of different systems in dual depression. We, therefore, carried out this study aimed at investigating differences in BDNF and cortisol plasmatic levels in patients diagnosed with CUD-primary-MDD and CUD-induced-MDD and also to compare them with a sample of MDD patients (without cocaine use), a sample of CUD (without MDD), and a group of healthy controls (HC) before and after a stress challenge.…”

Section: Introductionmentioning

confidence: 99%

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BDNF and Cortisol in the Diagnosis of Cocaine-Induced Depression

et al. 2022

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BackgroundMajor depressive disorder (MDD) and cocaine use disorder (CUD) are related with disability and high mortality rates. The assessment and treatment of psychiatric comorbidity is challenging due to its high prevalence and its clinical severity, mostly due to suicide rates and the presence of medical comorbidities. The aim of this study is to investigate differences in brain derived neurotrophic factor (BDNF) and cortisol plasmatic levels in patients diagnosed with CUD-primary-MDD and CUD-induced-MDD and also to compare them to a sample of MDD patients (without cocaine use), a sample of CUD (without MDD), and a group of healthy controls (HC) after a stress challenge.MethodsA total of 46 subjects were included: MDD (n = 6), CUD (n = 15), CUD-primary-MDD (n = 16), CUD-induced-MDD (n = 9), and 21 HC. Psychiatric comorbidity was assessed with the Spanish version of the Psychiatric Research Interview for Substance and Mental Disorders IV (PRISM-IV), and depression severity was measured with the Hamilton Depression Rating Scale (HDRS). Patients were administered the Trier Social Stress Test (TSST) before and after the biological measures, including BDNF, and cortisol levels were obtained.ResultsAfter the TSST, Cohen's d values between CUD-primary-MDD and CUD-induced-MDD increased in each assessment from 0.19 post-TSST to 2.04 post-90-TSST. Pairwise differences among CUD-induced-MDD and both MDD and HC groups had also a large effect size value in post-30-TSST and post-90-TSST. In the case of the BDNF concentrations, CUD-primary-MDD and CUD-induced-MDD in post-90-TSST (12,627.27 ± 5488.09 vs.17,144.84 ± 6581.06, respectively) had a large effect size (0.77).ConclusionResults suggest a different pathogenesis for CUD-induced-MDD with higher levels of cortisol and BDNF compared with CUD-primary-MDD. Such variations should imply different approaches in treatment.

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Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

BDNF and Cortisol in the Diagnosis of Cocaine-Induced Depression

et al. 2022

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“…The plasma 5-hydroxytryptamine (5-HT) concentration was significantly higher and the KYN/5-HT ratio was significantly lower in patients with CUD-induced MDD than those with MDD, while there were no differences between CUD-primary MDD and MDD. It suggests that the TRP-KYN pathway participates less in CUD-induced MDD and the presence of other mechanisms of the development of depression [156] (Table 2).…”

Section: Substance Use Disordermentioning

confidence: 99%

Immune Influencers in Action: Metabolites and Enzymes of the Tryptophan-Kynurenine Metabolic Pathway

et al. 2021

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The tryptophan (TRP)-kynurenine (KYN) metabolic pathway is a main player of TRP metabolism through which more than 95% of TRP is catabolized. The pathway is activated by acute and chronic immune responses leading to a wide range of illnesses including cancer, immune diseases, neurodegenerative diseases and psychiatric disorders. The presence of positive feedback loops facilitates amplifying the immune responses vice versa. The TRP-KYN pathway synthesizes multifarious metabolites including oxidants, antioxidants, neurotoxins, neuroprotectants and immunomodulators. The immunomodulators are known to facilitate the immune system towards a tolerogenic state, resulting in chronic low-grade inflammation (LGI) that is commonly present in obesity, poor nutrition, exposer to chemicals or allergens, prodromal stage of various illnesses and chronic diseases. KYN, kynurenic acid, xanthurenic acid and cinnabarinic acid are aryl hydrocarbon receptor ligands that serve as immunomodulators. Furthermore, TRP-KYN pathway enzymes are known to be activated by the stress hormone cortisol and inflammatory cytokines, and genotypic variants were observed to contribute to inflammation and thus various diseases. The tryptophan 2,3-dioxygenase, the indoleamine 2,3-dioxygenases and the kynurenine-3-monooxygenase are main enzymes in the pathway. This review article discusses the TRP-KYN pathway with special emphasis on its interaction with the immune system and the tolerogenic shift towards chronic LGI and overviews the major symptoms, pro- and anti-inflammatory cytokines and toxic and protective KYNs to explore the linkage between chronic LGI, KYNs, and major psychiatric disorders, including depressive disorder, bipolar disorder, substance use disorder, post-traumatic stress disorder, schizophrenia and autism spectrum disorder.

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Section: Substance Use Disordermentioning

confidence: 99%

Immune Influencers in Action: Metabolites and Enzymes of the Tryptophan-Kynurenine Metabolic Pathway

Tanaka¹,

Tóth²,

Polyák³

et al. 2021

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The tryptophan (TRP)-kynurenine (KYN) metabolic pathway is a main player of TRP metabolism through which more than 95% of TRP is catabolized. The pathway is activated by acute and chronic immune responses leading to a wide range of illnesses including cancer, immune diseases, neurodegenerative diseases, and psychiatric disorders. The TRP-KYN pathway synthesizes multifarious metabolites including oxidants, antioxidants, neurotoxins, neuroprotectants, and immunomodulators. The immunomodulators are known to facilitate the immune system towards a tolerogenic state, resulting in chronic low-grade inflammation (LGI) that is commonly present in obesity, poor nutrition, exposer to chemicals or allergens, prodromal stage of various illnesses, and chronic diseases. KYN, kynurenic acid, xanthurenic acid, and cinnabarinic acid are aryl hydrocarbon receptor ligands that serve as immunomodulators. Furthermore, TRP-KYN pathway enzymes are known to be activated by the stress hormone cortisol and inflammatory cytokines, and genotypic variants were observed to contribute to inflammation and thus various diseases. The tryptophan 2,3-dioxygenase, the indoleamine 2, 3-oxygenases, and the kynurenine-3-monooxygenase are main enzymes in the pathway. This review article discusses the TRP-KYN pathway with special emphasis on its interaction with the immune system and the tolerogenic shift towards chronic LGI and overviews the major symptoms, pro- and anti-inflammatory cytokines, and toxic and protective KYNs to explore the linkage between chronic LGI, KYNs, and major psychiatric, including depressive disorder, bipolar disorder, substance use disorder, post-traumatic stress disorder, schizophrenia, and autism spectrum disorder.

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The Tryptophan System in Cocaine-Induced Depression

Cited by 14 publications

References 55 publications

BDNF and Cortisol in the Diagnosis of Cocaine-Induced Depression

BDNF and Cortisol in the Diagnosis of Cocaine-Induced Depression

Immune Influencers in Action: Metabolites and Enzymes of the Tryptophan-Kynurenine Metabolic Pathway

Immune Influencers in Action: Metabolites and Enzymes of the Tryptophan-Kynurenine Metabolic Pathway

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