Trial reportBrain, behavior, and immunity2013
Transcriptional signatures related to glucose and lipid metabolism predict treatment response to the tumor necrosis factor antagonist infliximab in patients with treatment-resistant depression.
Trial report in Brain, behavior, and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00463580 (An Evaluation of the Efficacy of the Tumor Necrosis Factor-alpha Antagonist Infliximab in Treatment Resistant Major Depression), which is not on this map. Cited by 40 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
An Evaluation of the Efficacy of the Tumor Necrosis Factor-alpha Antagonist Infliximab in Treatment Resistant Major Depression: Mechanisms and Mediators
Who cites it
40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.
- Genetic Contributions of Inflammation to Depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Pooled it
- Pathogenetic and Therapeutic Applications of Tumor Necrosis Factor-α (TNF-α) in Major Depressive Disorder: A Systematic Review.International journal of molecular sciences · 2016Pooled it
- Peripheral inflammatory biomarkers define biotypes of bipolar depression.Molecular psychiatry · 2021Trial
- Trial
- Inhibition of tumor necrosis factor improves sleep continuity in patients with treatment resistant depression and high inflammation.Brain, behavior, and immunity · 2015Trial
- Molecular and Cellular Mechanisms Linking Mood Disorders, HPA Axis Dysregulation, and Neurocognitive Inflammation to Perioperative Neurocognitive Disorders.Biomolecules · 2026Review
- Depression remodels tumor microenvironment to drive tumor progression: Bio-behavioural signalling pathways and clinical interventions.Journal of advanced research · 2026Review
- Monocyte abundance and glycolytic reprogramming associate with motivational impairment in depression.Brain, behavior, and immunity · 2026Article
- Insights into the interplay between stroke and depression through lipid metabolism-related diagnostic genes.Molecular brain · 2026Article
- Advancing an Inflammatory Subtype of Major Depression.The American journal of psychiatry · 2025Review
- 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
- Lipids and C-reactive protein predict anhedonia and reward circuit functional connectivity responses to anti-cytokine and dopaminergic therapies in patients with depression.Comprehensive psychoneuroendocrinology · 2025Article
- Glycolytic metabolism: Food for immune cells, fuel for depression?Brain, behavior, & immunity - health · 2024Article
- Immune-Targeted Therapies for Depression: Current Evidence for Antidepressant Effects of Monoclonal Antibodies.The Journal of clinical psychiatry · 2024Review
- Annual Research Review: Neuroimmune network model of depression: a developmental perspective.Journal of child psychology and psychiatry, and allied disciplines · 2024Review
- Cellular and immunometabolic mechanisms of inflammation in depression: Preliminary findings from single cell RNA sequencing and a tribute to Bruce McEwen.Neurobiology of stress · 2022Article
- Metabolomic and inflammatory signatures of symptom dimensions in major depression.Brain, behavior, and immunity · 2022Article
- Transcriptomic signatures of psychomotor slowing in peripheral blood of depressed patients: evidence for immunometabolic reprogramming.Molecular psychiatry · 2021Article
- The interaction of lipids and inflammatory markers predict negative symptom severity in patients with schizophrenia.NPJ schizophrenia · 2021Article
- Aiding and Abetting Anhedonia: Impact of Inflammation on the Brain and Pharmacological Implications.Pharmacological reviews · 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
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The tumor necrosis factor (TNF) antagonist infliximab was recently found to reduce depressive symptoms in patients with increased baseline inflammation as reflected by a plasma C-reactive protein concentration >5 mg/L. To further explore predictors and targets of response to infliximab, differential gene expression was examined in peripheral blood mononuclear cells from infliximab responders (n=13) versus non-responders (n=14) compared to placebo at baseline and 6 h, 24 h, and 2 weeks after the first infliximab infusion. Treatment response was defined as 50% reduction in depressive symptoms at any point during the 12-week trial. One-hundred-forty-eight gene transcripts were significantly associated (1.2-fold, adjusted p≤0.01) with response to infliximab and were distinct from placebo responders. Transcripts predictive of infliximab response were associated with gluconeogenesis and cholesterol transport, and were enriched in a network regulated by hepatocyte nuclear factor (HNF)4-alpha, a transcription factor involved in gluconeogenesis and cholesterol and lipid homeostasis. Of the 148 transcripts differentially expressed at baseline, 48% were significantly regulated over time in infliximab responders, including genes related to gluconeogenesis and the HNF4-alpha network, indicating that these predictive genes were responsive to infliximab. Responders also demonstrated inhibition of genes related to apoptosis through TNF signaling at 6 h and 24 h after infusion. Transcripts down-regulated in responders 2 weeks after infliximab were related to innate immune signaling and nuclear factor-kappa B. Thus, baseline transcriptional signatures reflective of alterations in glucose and lipid metabolism predicted antidepressant response to infliximab, and infliximab response involved regulation of metabolic genes and inhibition of genes related to innate immune activation.
Indexed as
Identifiers
What Socratic 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 Socratic graph.