Cited by 58Tryptophan and brain disordersTreatment of Major DepressionStress Responses and Cortisol

Depressive symptoms following interferon-α therapy: mediated by immune-induced reductions in brain-derived neurotrophic factor?

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Kenis, Gunter, Prickaerts, Jos, van Os, Jim, Koek, Ger H., Robaeys, Geert, Steinbusch, Harry W. M., Wichers, Marieke·2011·The International Journal of Neuropsychopharmacology

Abstract

Interferon-α (IFN-α) therapy for the treatment of hepatitis C is known to induce depressive symptoms and major depression in a substantial proportion of patients. While immune activation and disturbances in peripheral tryptophan catabolism have been implicated, the exact underlying mechanism remains unknown. A role for brain-derived neurotrophic factor (BDNF) in the pathophysiology of mood disorders has recently emerged. This study examined whether depressive symptoms over time are associated with changes in serum BDNF concentration in hepatitis C patients treated with IFN-α, and whether BDNF mediates the effects of IFN-α-induced immune activation on depressive symptoms. For this purpose, 17 hepatitis C patients received IFN-α treatment with ribavirin. Patients were assessed before and at 1, 2, 4, 8, 12 and 24 wk after start of treatment. Depressive symptoms were assessed using the Montgomery-Asberg Depression Rating Scale (MADRS). In addition, cytokine concentrations and serum BDNF levels were measured at all time-points. Serum levels of BDNF decreased during the course of treatment, and were significantly and inversely associated with total MADRS score. Furthermore, pro-inflammatory cytokine levels predicted lower subsequent BDNF levels, whereas low BDNF levels, as well as increased cytokine levels, were independently associated with the development of depressive symptoms during IFN-α treatment. These findings suggest that the effect of IFN-α-induced immune activation on depression may be explained in part by alterations in neuroprotective capacity, reflected by decreases in serum BDNF following IFN-α treatment.

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Crossref · 10.1017/s1461145710000830

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Authors
Kenis, G., Prickaerts, J., van Os, J., Koek, G. H., Robaeys, G., Steinbusch, H. W. M., & Wichers, M.
Affiliations
  • Maastricht University (NL)
  • Maastricht University Medical Centre (NL)
  • Universitair Ziekenhuis Leuven (BE)
Corresponding author
Wichers, Marieke
Venue
The International Journal of Neuropsychopharmacology
Published
2010-07-29
Volume
14
Issue
02
Pages
247-253
ISSN
  • 1461-1457 (ISSN-L)
  • 1469-5111
OpenAlex
W2013693499
Cited by
58
References
51
Citations by year
2026: 2 · 2025: 1 · 2022: 2 · 2021: 2 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 4 · 2016: 7 · 2015: 3 · 2014: 8 · 2013: 8 · 2012: 7
FWCI
2.53
Type
journal article
Language
en
Licence
other-oa
Locations
  • The International Journal of Neuropsychopharmacology (publishedVersion)
  • PubMed (publishedVersion)
  • Research Publications (Maastricht University) (submittedVersion, other-oa)
  • Document Server@UHasselt (UHasselt) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
interferon-alpha, depressive symptoms, brain-derived neurotrophic factor, hepatitis C, immune activation, inflammatory cytokines, major depressive disorder, ribavirin, tryptophan catabolism, neuroprotection, mood disorders
MeSH terms
Antiviral Agents, Depression, Depressive Disorder, Major, Major Depressive Disorder, Female, Humans, Hydrocortisone, Immunologic Factors, Male, Psychiatric Status Rating Scales, Ribavirin, Time Factors, Cytokines, Interferon-alpha, Brain-Derived Neurotrophic Factor, Hepatitis C, Chronic

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