Interferon-alpha–induced changes in tryptophan metabolism relationship to depression and paroxetine treatment

@article{Capuron2003InterferonalphainducedCI,
  title={Interferon-alpha–induced changes in tryptophan metabolism relationship to depression and paroxetine treatment},
  author={Lucile Capuron and Gabriele Neurauter and Dominique L. Musselman and David H. Lawson and Charles B. Nemeroff and Dietmar Fuchs and Andrew H. Miller},
  journal={Biological Psychiatry},
  year={2003},
  volume={54},
  pages={906-914}
}
IDO and interferon-α-induced depressive symptoms: a shift in hypothesis from tryptophan depletion to neurotoxicity
TLDR
A role for IDO activity in the pathophysiology of IFN-α-induced depressive symptoms is supported, through its induction of neurotoxic KYN metabolites.
ORIGINAL RESEARCH ARTICLE IDO and interferon-a-induced depressive symptoms: a shift in hypothesis from tryptophan depletion to neurotoxicity
TLDR
A role for IDO activity in the pathophysiology of IFN-a-induced depressive symptoms is supported, through its induction of neurotoxic KYN metabolites.
Interferon-α Influences Tryptophan Metabolism without Inducing Psychiatric Side Effects
TLDR
IFN-α was found to alter TRP metabolism without inducing psychiatric side effects, and a possible relationship between TRp metabolism and depression was not substantiated by this study.
CSF Concentrations of Brain Tryptophan and Kynurenines during Immune Stimulation with IFN-alpha: Relationship to CNS Immune Responses and Depression
TLDR
Peripheral administration of IFN-α activated IDO in concert with central cytokine responses, resulting in increased brain KYN and QUIN, which correlated with depressive symptoms.
Depressive symptoms following interferon-α therapy: mediated by immune-induced reductions in brain-derived neurotrophic factor?
TLDR
The 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.
Effect of immune activation on the kynurenine pathway and depression symptoms – A systematic review and meta-analysis
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References

SHOWING 1-10 OF 40 REFERENCES
Interferon-gamma-induced tryptophan degradation: neuropsychiatric and immunological consequences.
TLDR
Improved tryptophan degradation is observed in diseases and disorders concomitant with cellular immune activation, and IDO could represent a link between the immunological network and neuroendocrine functions with far reaching consequences regarding to the psychological status of patients.
Association between decreased serum tryptophan concentrations and depressive symptoms in cancer patients undergoing cytokine therapy
TLDR
Assessment of the relationship between serum concentrations of the amino acids tryptophan and tyrosine, major precursors of serotonin and norepinephrine respectively, and depression symptoms in cancer patients undergoing cytokine therapy indicates that the development of depressive symptoms in patients undergoing chemotherapy could be mediated by a reduced availability of the serotonin relevant amino acid precursor, tryptophile.
Paroxetine for the prevention of depression induced by high-dose interferon alfa.
TLDR
In patients with malignant melanoma, pretreatment with paroxetine appears to be an effective strategy for minimizing depression induced by interferon alfa.
Increased Depressive Ratings in Patients With Hepatitis C Receiving Interferon-α–Based Immunotherapy Are Related to Interferon-α–Induced Changes in the Serotonergic System
TLDR
It is suggested that theIFN-α–induced changes in the serotonergic turnover could play a role in the development of IFN- α–induced depressive symptoms.
Serotonin and the neurobiology of depression. Effects of tryptophan depletion in drug-free depressed patients.
TLDR
That tryptophan depletion did not rapidly worsen depression argues that serotonin function is not linearly related to the level of depression and if reduced serotonin function does cause depression, then it is either as predisposing factor or due to a postsynaptic deficit in the utilization of serotonin.
Clinical and Physiological Consequences of Rapid Tryptophan Depletion
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