Biological mechanisms of depression following treatment with interferon for chronic hepatitis C: A critical systematic review

Machado, Myrela O.; Oriolo, Giovanni; Bortolato, Beatrice; Köhler, Cristiano A.; Maes, Michaël; Solmi, Marco; Grande, Iría; Martín‐Santos, Rocío; Vieta, Eduard; Carvalho, André F.

doi:10.1016/j.jad.2016.11.039

Cited by 50 publications

(22 citation statements)

References 65 publications

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“…Exclusion criteria for patients were (1) other axis‐1 DSM‐IV‐TR diagnoses besides BD/MDD/tobacco use disorder (TUD) and anxiety disorders, (2) a current (hypo)manic episode, and (3) mood disorders due to a general medical condition or substance/drug use . Controls were excluded if any major axis‐1 psychiatric disorder was evident.…”

Section: Methodsmentioning

confidence: 99%

Lowered quality of life in mood disorders is associated with increased neuro‐oxidative stress and basal thyroid‐stimulating hormone levels and use of anticonvulsant mood stabilizers

Nunes

Maes

Roomruangwong

et al. 2018

Evaluation Clinical Practice

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Section: Methodsmentioning

confidence: 99%

Lowered quality of life in mood disorders is associated with increased neuro‐oxidative stress and basal thyroid‐stimulating hormone levels and use of anticonvulsant mood stabilizers

Nunes

Maes

Roomruangwong

et al. 2018

Evaluation Clinical Practice

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“…In the present study, we examine peripherally induced systemic inflammation and brain TSPO binding in healthy humans using interferon (IFN)-α 24,25 . IFN-α is a proinflammatory cytokine with antiviral, anticancer, and immunomodulatory effects, approved for treatment of cancer and chronic hepatitis C 26,27 . IFN-α induces a systemic immune response associated with sickness behaviour, and, when administered over weeks or months as a treatment for patients with cancer or hepatitis C, is associated with a diagnosis of major depression in up to 30-50% of patients, and is thus considered the most validated clinical model of inflammation-induced depression 28 .…”

Section: Introductionmentioning

confidence: 99%

PET imaging shows no changes in TSPO brain density after IFN-α immune challenge in healthy human volunteers

et al. 2020

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Depression is associated with peripheral inflammation, but its link with brain microglial activity remains unclear. In seven healthy males, we used repeated translocator protein-Positron Emission Tomography (TSPO-PET) dynamic scans with [ 11 C]PBR28 to image brain microglial activation before and 24 h after the immune challenge interferon (IFN)-α. We also investigated the association between changes in peripheral inflammation, changes in microglial activity, and changes in mood. IFN-α administration decreased [ 11 C]PBR28 PET tissue volume of distribution (Vt) across the brain (−20 ± 4%; t 6 = 4.1, p = 0.01), but after correction for radioligand free-plasma fraction there were no longer any changes (+23 ± 31%; t = 0.1, p = 0.91). IFN-α increased serum IL-6 (1826 ± 513%, t 6 = −7.5, p < 0.001), IL-7 (39 ± 12%, t 6 = −3.6, p = 0.01), IL-10 (328 ± 48%, t 6 = −12.8, p < 0.001), and IFN-γ (272 ± 64%, t 6 = −7.0, p < 0.001) at 4-6 h, and increased serum TNF-α (49 ± 7.6%, t 6 = −7.5, p < 0.001), IL-8 (39 ± 12%, t 6 = −3.5, p = 0.013), and C-reactive protein (1320 ± 459%, t 6 = −7.2, p < 0.001) at 24 h. IFN-α induced temporary mood changes and sickness symptoms after 4-6 h, measured as an increase in POMS-2 total mood score, confusion and fatigue, and a decrease in vigor and friendliness (all p ≤ 0.04). No association was found between changes in peripheral inflammation and changes in PET or mood measures. Our work suggests that brain TSPO-PET signal is highly dependent of inflammation-induced changes in ligand binding to plasma proteins. This limits its usefulness as a sensitive marker of neuroinflammation and consequently, data interpretation. Thus, our results can be interpreted as showing either that [ 11 C]PBR28 is not sensitive enough under these conditions, or that there is simply no microglial activation in this model.

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“…In light of such evidence, omega‐3 PUFA supplementation continues to be tested as augmentation therapy in neuropsychiatric disease with mixed results. In hepatitis C patients receiving interferon alpha (INFα) therapy, depression is a common adverse effect (Machado et al, ). EPA but not DHA supplementation reduced the percentage of patients (n = 154) developing depression while on INFα therapy (Su et al, ).…”

Section: Resultsmentioning

confidence: 99%

Putative neuroprotective pharmacotherapies to target the staged progression of mental illness

Robertson

Coronado

Sethi

et al. 2019

Early Intervention Psych

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Aim: Neuropsychiatric disorders including depression, bipolar and schizophrenia frequently exhibit a neuroprogressive course from prodrome to chronicity. There are a range of agents exhibiting capacity to attenuate biological mechanisms associated with neuroprogression. This review will update the evidence for putative neuroprotective agents including clinical efficacy, mechanisms of action and limitations in current assessment tools, and identify novel agents with neuroprotective potential.Method: Data for this review were sourced from online databases PUBMED, Embase and Web of Science. Only data published since 2012 were included in this review, no data were excluded based on language or publication origin.Results: Each of the agents reviewed inhibit one or multiple pathways of neuroprogression including: inflammatory gene expression and cytokine release, oxidative and nitrosative stress, mitochondrial dysfunction, neurotrophin dysregulation and apoptotic signalling. Some demonstrate clinical efficacy in preventing neural damage or loss, relapse or cognitive/functional decline. Agents include: the psychotropic medications lithium, second generation antipsychotics and antidepressants; other pharmacological agents such as minocycline, aspirin, cyclooxygenase-2 inhibitors, statins, ketamine and alpha-2-delta ligands; and others such as erythropoietin, oestrogen, leptin, N-acetylcysteine, curcumin, melatonin and ebselen.Conclusions: Signals of evidence of clinical neuroprotection are evident for a number of candidate agents. Adjunctive use of multiple agents may present a viable avenue to clinical realization of neuroprotection. Definitive prospective studies of neuroprotection with multimodal assessment tools are required.

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Biological mechanisms of depression following treatment with interferon for chronic hepatitis C: A critical systematic review

Cited by 50 publications

References 65 publications

Lowered quality of life in mood disorders is associated with increased neuro‐oxidative stress and basal thyroid‐stimulating hormone levels and use of anticonvulsant mood stabilizers

Lowered quality of life in mood disorders is associated with increased neuro‐oxidative stress and basal thyroid‐stimulating hormone levels and use of anticonvulsant mood stabilizers

PET imaging shows no changes in TSPO brain density after IFN-α immune challenge in healthy human volunteers

Putative neuroprotective pharmacotherapies to target the staged progression of mental illness

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