ArticleJournal of psychiatry & neuroscience : JPN2021
The role of anthranilic acid in the increase of depressive symptoms and major depressive disorder during treatment for hepatitis C with pegylated interferon-α2a and oral ribavirin.
Article in Journal of psychiatry & neuroscience : JPN, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Cell Signaling by Tryptophan Catabolism.Biochemistry · 2026Review
- Interleukin 13 (IL-13) Signalling as a Potential Target for Cell Therapies in Liver Fibrosis.International journal of molecular sciences · 2026Review
- Contextual Regulation of the Kynurenine Pathway and Its Relevance for Personalized Psychiatry.Journal of personalized medicine · 2026Review
- Tryptophan metabolite atlas uncovers organ, age, and sex-specific variations.FEBS open bio · 2026Article
- Neurochemical Insights into the Role of Tryptophan Metabolites and Kynurenine Pathway in Insomnia and its Psychological and Neurological Comorbidities.Molecular neurobiology · 2025Review
- Procognitive effects of methyl 2-amino-3-methoxybenzoate (or daopine) may involve the dorsal striatal anthranilic acid pathway and mutimetabolite-multitarget pharmacology.Behavioural pharmacology · 2025Article
- High Baseline Plasma Anthranilic Acid Predicts Remission Upon Acute-Series Ketamine Infusion for Treatment-Resistant Depression.Biological psychiatry global open science · 2025Article
- Stir-bakedFrontiers in microbiology · 2025Article
- Direct-acting antivirals (DAA) positively affect depression and cognitive function in patients with chronic hepatitis C.PloS one · 2025Article
- Anthranilic Acid-G-Protein Coupled Receptor109A-Cytosolic Phospholipase A2-Myelin-Cognition Cascade: A New Target for the Treatment/Prevention of Cognitive Impairment in Schizophrenia, Dementia, and Aging.International journal of molecular sciences · 2024Review
- Neuroactive Kynurenines as Pharmacological Targets: New Experimental Tools and Exciting Therapeutic Opportunities.Pharmacological reviews · 2024Review
- Review
- Anthranilic Acid, a GPR109A Agonist, and Schizophrenia.International journal of tryptophan research : IJTR · 2024Article
- Frontostriatal circuitry and the tryptophan kynurenine pathway in major psychiatric disorders.Psychopharmacology · 2024Article
- Microbial-Derived Tryptophan Metabolites and Their Role in Neurological Disease: Anthranilic Acid and Anthranilic Acid Derivatives.Microorganisms · 2023Review
- Tryptophan Metabolism in Central Nervous System Diseases: Pathophysiology and Potential Therapeutic Strategies.Aging and disease · 2023Review
- Extension of life span by down-regulation of enzymes catalyzing tryptophan conversion into kynurenine: Possible implications for mechanisms of aging.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Article
- Why Are Some People with Lower Urinary Tract Symptoms (LUTS) Depressed? New Evidence That Peripheral Inflammation in the Bladder Causes Central Inflammation and Mood Disorders.International journal of molecular sciences · 2023Review
- Amino acid profile in overweight and obese prepubertal children - can simple biochemical tests help in the early prevention of associated comorbidities?Frontiers in endocrinology · 2023Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Tryptophan metabolism via the kynurenine pathway is considered the link between the immune and endocrine systems. Dysregulation of serotonergic transmission can stem from the direct influence of interferon-α on the activity of serotonergic receptors 5-HT1A and 5-HT2A, and from its indirect effect on tryptophan metabolism. Induction of the kynurenine pathway increases the concentration of neurotoxic kynurenine metabolites, and the activity of kynurenine derivatives is linked to the onset of depression. The aim of our study was to evaluate the relationships between depressive symptoms and kynurenine, tryptophan, anthranilic acid and kynurenic acid concentrations, indolamine 2,3-dioxygenase (IDO) activity and tryptophan availability to the brain. Methods: The study followed a prospective longitudinal cohort design. We evaluated 101 patients with chronic hepatitis C who were treated with pegylated interferon-α2a, and 40 controls who were awaiting treatment. We evaluated the relationships between total score on the Montgomery-Åsberg Depression Rating Scale and kynurenine, tryptophan, anthranilic acid and kynurenic acid concentrations, IDO activity and tryptophan availability to the brain. A logistic regression model was adapted for the diagnosis of major depressive disorder at each time point, taking into account changes in parameters of the kynurenine pathway between a given time point and the baseline measurement. Results: Of the treated patients, 44% fulfilled the criteria for major depressive disorder at least once during the 24 weeks of treatment. Anthranilic acid concentrations were significantly increased compared to baseline for all time points except week 2. Tryptophan availability showed a significant decrease (β = -0.09, p = 0.01) only in week 12 of treatment. Over time, kynurenine, tryptophan and anthranilic acid concentrations, as well as IDO activity and tryptophan availability to the brain, were significantly associated with total score on the Montgomery-Åsberg Depression Rating Scale. A logistic regression model revealed that participants with decreased tryptophan availability to the brain at 12 weeks of treatment and participants with increased anthranilic acid concentrations at week 24 of treatment were at increased risk for diagnosis of major depressive disorder (odds ratios 2.92 and 3.59, respectively). Limitations: This study had an open-label design in a population receiving naturalistic treatment. Conclusion: The present study provides the first direct evidence of the role of anthranilic acid in the pathogenesis of inflammation-induced major depressive disorder during treatment for hepatitis C with pegylated interferon-α2a.
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