ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2016
Transcriptomics in Interferon-α-Treated Patients Identifies Inflammation-, Neuroplasticity- and Oxidative Stress-Related Signatures as Predictors and Correlates of Depression.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 39 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Inflammatory Control of Antidepressant Efficacy: a Pharmaco-epigenetic Approach
Adjusting Immune Activation to Reinstate Neural Plasticity and Promote the Beneficial Effect of Non-pharmacological Interventions
Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Genetic Contributions of Inflammation to Depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Pooled it
- The interaction between the immune system and the autonomic nervous system in the pathophysiology of major depressive disorder: a scoping review.Brain, behavior, & immunity - health · 2026Review
- Parallel Pathways, Divergent Outcomes: Adipose Tissue-Neural Crosstalk in Depression and Obesity.Journal of clinical medicine · 2025Review
- The dietary ligands, omega-3 fatty acid endocannabinoids and short-chain fatty acids prevent cytokine-induced reduction of human hippocampal neurogenesis and alter the expression of genes involved in neuroinflammation and neuroplasticity.Molecular psychiatry · 2025Article
- A comparative computational analysis of IFN-alpha pharmacokinetics and its induced cellular response in mice and humans.PLoS computational biology · 2025Article
- Transcriptomic profiles in major depressive disorder: the role of immunometabolic and cell-cycle-related pathways in depression with different levels of inflammation.Molecular psychiatry · 2025Observational
- Identifying behavior regulatory leverage over mental disorders transcriptomic network hubs toward lifestyle-dependent psychiatric drugs repurposing.Human genomics · 2025Article
- Neurotransmitter and metabolic effects of interferon-alpha in association with decreased striatal dopamine in a non-human primate model of cytokine-Induced depression.Brain, behavior, and immunity · 2025Article
- Ketamine Prevents Inflammation-Induced Reduction of Human Hippocampal Neurogenesis via Inhibiting the Production of Neurotoxic Metabolites of the Kynurenine Pathway.The international journal of neuropsychopharmacology · 2024Article
- Inflammation and immune system pathways as biological signatures of adolescent depression-the IDEA-RiSCo study.Translational psychiatry · 2024Article
- Higher immune-related gene expression in major depression is independent of CRP levels: results from the BIODEP study.Translational psychiatry · 2023Article
- Interferon therapy and its association with depressive disorders - A review.Frontiers in immunology · 2023Review
- Neurogenesis is disrupted in human hippocampal progenitor cells upon exposure to serum samples from hospitalized COVID-19 patients with neurological symptoms.Molecular psychiatry · 2022Article
- SARS-Cov-2 Damage on the Nervous System and Mental Health.Current neuropharmacology · 2022Review
- Transcriptomic signatures of psychomotor slowing in peripheral blood of depressed patients: evidence for immunometabolic reprogramming.Molecular psychiatry · 2021Article
- In(s) and out(s) of adolescent depression - Trajectories of development and recovery.Brain, behavior, & immunity - health · 2021Article
- Article
- Gene expression studies in Depression development and treatment: an overview of the underlying molecular mechanisms and biological processes to identify biomarkers.Translational psychiatry · 2021Review
- Canonical TGF-β signaling regulates the relationship between prenatal maternal depression and amygdala development in early life.Translational psychiatry · 2021Article
- The neuropsychiatric manifestations of COVID-19: Interactions with psychiatric illness and pharmacological treatment.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
Owing to the unique opportunity to assess individuals before and after they develop depression within a short timeframe, interferon-α (IFN-α) treatment for chronic hepatitis C virus (HCV) infection is an ideal model to identify molecular mechanisms relevant to major depression, especially in the context of enhanced inflammation. Fifty-eight patients were assessed prospectively, at baseline and monthly over 24 weeks of IFN-α treatment. New-onset cases of depression were determined using the Mini International Neuropsychiatric Interview (MINI). Whole-blood transcriptomic analyses were conducted to investigate the following: (1) baseline gene expression differences associated with future development of IFN-α-induced depression, before IFN-α, and (2) longitudinal gene expression changes from baseline to weeks 4 or 24 of IFN-α treatment, separately in those who did and did not develop depression. Transcriptomics data were analyzed using Partek Genomics Suite (1.4-fold, FDR adjusted p⩽0.05) and Ingenuity Pathway Analysis Software. Twenty patients (34%) developed IFN-α-induced depression. At baseline, 73 genes were differentially expressed in patients who later developed depression compared with those who did not. After 4 weeks of IFN-α treatment, 592 genes were modulated in the whole sample, representing primarily IFN-α-responsive genes. Substantially more genes were modulated only in patients who developed depression (n=506, compared with n=70 in patients who did not), with enrichment in inflammation-, neuroplasticity- and oxidative stress-related pathways. A similar picture was observed at week 24. Our data indicate that patients who develop IFN-α-induced depression have an increased biological sensitivity to IFN-α, as shown by larger gene expression changes, and specific signatures both as predictors and as correlates.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.