Evidence map›Paper›PMID 32457424›Full record

ArticleMolecular psychiatry2021

Interferon and anti-TNF therapies differentially modulate amygdala reactivity which predicts associated bidirectional changes in depressive symptoms.

Kevin A Davies, Ella Cooper, Valerie Voon, Jeremy Tibble, Mara Cercignani, Neil A Harrison

Open access · hybridAbstract read
In one paragraph

Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from 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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Neural processes linking joint hypermobility and anxiety: key roles for the amygdala and insular cortex.The British journal of psychiatry : the journal of mental science · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Advancing an Inflammatory Subtype of Major Depression.The American journal of psychiatry · 2025
    Review
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  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Kevin A DaviesDepartment of Neuroscience, Brighton and Sussex Medical School, University of Sussex Campus, Brighton, BN1 9RY, UK.
Ella CooperDepartment of Neuroscience, Brighton and Sussex Medical School, University of Sussex Campus, Brighton, BN1 9RY, UK.
Valerie VoonDepartment of Psychiatry, University of Cambridge, Cambridge, CB2 0QQ, UK.
Jeremy TibbleDepartment of Hepatology, Brighton & Sussex University Hospitals, Brighton, UK.
Mara CercignaniDepartment of Neuroscience, Brighton and Sussex Medical School, University of Sussex Campus, Brighton, BN1 9RY, UK.ORCID http://orcid.org/0000-0002-4550-2456
Neil A HarrisonDepartment of Neuroscience, Brighton and Sussex Medical School, University of Sussex Campus, Brighton, BN1 9RY, UK. HarrisonN4@cardiff.ac.uk.
Brighton and Sussex Medical School · GBUniversity of Cambridge · GB

Funding

Medical Research Council MR/P008747/1Wellcome TrustWellcome Trust 093881/Z/10/Z
6 · The paper itself

Abstract

A third of patients receiving Interferon-α (IFN-α) treatment for Hepatitis-C develop major depressive disorder (MDD). Conversely, anti-Tumor Necrosis Factor (TNF) therapies improve depression providing key empirical support for the "inflammatory theory" of depression. Heightened amygdala reactivity (particularly to negatively valanced stimuli) is a consistent finding within MDD; can predict treatment efficacy and reverses following successful treatment. However, whether IFN-α and anti-TNF enhance/attenuate depressive symptoms through modulation of amygdala emotional reactivity is unknown. Utilizing a prospective study design, we recruited 30 patients (mean 48.0 ± 10.5 years, 21 male) initiating IFN-α treatment for Hepatitis-C and 30 (mean 50.4 ± 15.7 years, 10 male) anti-TNF therapy for inflammatory arthritis. All completed an emotional face-processing task during fMRI and blood sampling before and after their first IFN-α (4-h) or anti-TNF (24-h) injection and follow-up psychiatric assessments for 3 months of treatment. IFN-α significantly increased depression symptoms (Hamilton Depression Rating Scale HAM-D) at 4 weeks (p < 0.001) but not 4-h after first dose (p > 0.1). Conversely, anti-TNF significantly improved depressive symptoms (Hospital Anxiety and Depression Rating Scale HADS) at both 24-h (P = 0.015) and 12 weeks (p = 0.018). In support of our a-priori hypothesis, both IFN-α and anti-TNF significantly modulated amygdala reactivity with IFN-α acutely enhancing right amygdala responses to sad (compared with neutral) faces (p = 0.032) and anti-TNF conversely decreasing right amygdala reactivity (across emotional valence) (p = 0.033). Furthermore, these changes predicted IFN-induced increases in HAM-D 4 weeks later (R

Indexed as

DepressionMajor Depressive DisorderAmygdalaHumansInterferon-alphaMaleProspective StudiesTumor Necrosis Factor InhibitorsInterferon-alphaTumor Necrosis Factor Inhibitors

Identifiers

PMID32457424
PMCPMC8589643
OpenAlexW3029231620

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Registered trials

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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.