The Importance of the Structural Similarity of Drugs Used for Depression and Inflammation, Two Comorbid Diseases

Bayram, F Esra Önen; Reıs, Rengin; Tunçer, Barış; Sipahi, Hande

doi:10.2174/1568026618666180821144704

Cited by 14 publications

(10 citation statements)

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“…The anti-diabetic drug, metformin, also has neuroprotective effects via activation of antioxidant and anti-inflammatory pathways [81]. Since antidepressants share common molecular mechanisms with anti-inflammatory drugs [82], these common mechanisms appear to be the basis for the ability of antidepressants to protect against neurodegeneration [83]. Given that TBI is a risk factor for depression [84] and TBI patients with depression are treated with antidepressant drugs, we speculate that the recovery of the TBI patients treated with antidepressants may be attributed, in part, to the anti-inflammatory effects of these drugs [85].…”

Section: Discussionmentioning

confidence: 99%

Traumatic brain injury induces long-lasting changes in immune and regenerative signaling

et al. 2019

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There are no existing treatments for the long-term degenerative effects of traumatic brain injury (TBI). This is due, in part, to our limited understanding of chronic TBI and uncertainty about which proposed mechanisms for long-term neurodegeneration are amenable to treatment with existing or novel drugs. Here, we used microarray and pathway analyses to interrogate TBI-induced gene expression in the rat hippocampus and cortex at several acute, subchronic and chronic intervals (24 hours, 2 weeks, 1, 2, 3, 6 and 12 months) after parasagittal fluid percussion injury. We used Ingenuity pathway analysis (IPA) and Gene Ontology enrichment analysis to identify significantly expressed genes and prominent cell signaling pathways that are dysregulated weeks to months after TBI and potentially amenable to therapeutic modulation. We noted long-term, coordinated changes in expression of genes belonging to canonical pathways associated with the innate immune response (i.e., NF-κB signaling, NFAT signaling, Complement System, Acute Phase Response, Toll-like receptor signaling, and Neuroinflammatory signaling). Bioinformatic analysis suggested that dysregulation of these immune mediators—many are key hub genes—would compromise multiple cell signaling pathways essential for homeostatic brain function, particularly those involved in cell survival and neuroplasticity. Importantly, the temporal profile of beneficial and maladaptive immunoregulatory genes in the weeks to months after the initial TBI suggests wider therapeutic windows than previously indicated.

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Section: Discussionmentioning

confidence: 99%

Traumatic brain injury induces long-lasting changes in immune and regenerative signaling

et al. 2019

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“…The potential for anti-inflammatory drugs to have antidepressant effects is part of the evidence put forward by proponents of immunopsychiatry: “Randomized controlled studies using anti-inflammatories for depression have shown therapeutic effects [105]” [2] (p. 198). Finally, structural similarities between antidepressants affecting serotonin signaling (agomelatine, duloxetine and vortioxetine) and non-steroidal anti-inflammatory drugs (NSAIDs: Diclofenac, ketoprofen, naproxen and nabumetone) have recently been pointed out [106]. This thus would provide a structural basis for the claims that NSAIDS have antidepressant effects and antidepressants anti-inflammatory effects.…”

Section: Antidepressants and Anti-inflammatory Drugs May Not Be “Smentioning

confidence: 99%

Inflammation and Depression: A Nervous Plea for Psychiatry to Not Become Immune to Interpretation

Konsman

2019

Pharmaceuticals

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The possibility that inflammation plays a causal role in major depression is an important claim in the emerging field of immunopsychiatry and has generated hope for new treatments. The aims of the present review are first to provide some historical background and to consider the evidence in favor of the claim that inflammation is causally involved in major depression. The second part discusses some of the possibilities allowed for by the use of broad ‘umbrella’ concepts, such as inflammation and stress, in terms of proposing new working hypotheses and potential mechanisms. The third part reviews proposed biomarkers of inflammation and depression and the final part addresses how elements discussed in the preceding sections are used in immunopsychiatry. The ‘umbrella’ concepts of inflammation and stress, as well as insufficiently-met criteria based inferences and reverse inferences are being used to some extent in immunopsychiatry. The field is therefore encouraged to specify concepts and constructs, as well as to consider potential alternative interpretations and explanations for findings obtained. The hope is that pointing out some of the potential problems will allow for a clearer picture of immunopsychiatry’s current strengths and limitations and help the field mature.

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“…Recent studies have shown the role of inflammatory mechanisms [1][2][3][4] and autoimmune mechanisms in the onset of psychiatric symptoms, such as depression [5][6][7]. In this sense, structural similarities have been identified between anti-inflammatory drugs and some antidepressants [8].…”

Section: Introductionmentioning

confidence: 99%

Assessment of Subclinical Psychotic Symptoms in Patients with Rheumatoid Arthritis and Spondyloarthritis

Prados-Ojeda

Luque-Luque

Gordillo-Urbano

et al. 2021

JCM

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Inflammatory and autoimmune processes have been associated with the onset of depressive and psychotic symptoms. Rheumatoid arthritis (RA) and spondyloarthritis (SpA) are rheumatic diseases with an inflammatory etiology. A high prevalence of depressive and anxiety-related comorbidity has been reported for both diseases, with no evidence of a greater prevalence of psychosis. The objective of the present study was to evaluate for the first time subclinical psychotic symptoms in patients with RA and SpA. This is a cross-sectional, single-center study including RA and SpA patients, as well as healthy controls. Abnormal psychotic experiences (positive, negative, and depressive symptoms) were evaluated using the Community Assessment of Psychic Experiences (CAPE-42). Functional capacity was evaluated using the Short-Form Health Survey SF-12. We compared the CAPE and SF-12 scores between the three groups. We recruited 385 individuals: 218 with RA, 100 with SpA, and 67 healthy controls. According to the CAPE scale, the frequency of subclinical psychotic symptoms was greater in patients than in healthy controls (RA, 1.90 vs. 1.63, p < 0.001; SpA, 1.88 vs. 1.63, p = 0.001). Distress was also greater in patients than in controls owing to the presence of symptoms. No differences were observed between the three groups for the mental dimension scores in the SF-12 Health Survey (43.75 in RA, 45.54 in SpA, and 43.19 in healthy controls). Our findings point to a greater prevalence of subclinical psychotic symptoms in patients with RA and patients with SpA than in the general population. The results suggest an association between inflammation and depression/subclinical psychotic symptoms.

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The Importance of the Structural Similarity of Drugs Used for Depression and Inflammation, Two Comorbid Diseases

Cited by 14 publications

References 0 publications

Traumatic brain injury induces long-lasting changes in immune and regenerative signaling

Traumatic brain injury induces long-lasting changes in immune and regenerative signaling

Inflammation and Depression: A Nervous Plea for Psychiatry to Not Become Immune to Interpretation

Assessment of Subclinical Psychotic Symptoms in Patients with Rheumatoid Arthritis and Spondyloarthritis

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