In major dysmood disorder, physiosomatic, chronic fatigue and fibromyalgia symptoms are driven by immune activation and increased immune-associated neurotoxicity

Maes, Michael; Almulla, Abbas F.; Zhou, Bo; Algon, Ali Abbas Abo; Sodsai, Pimpayao

doi:10.1038/s41598-024-57350-1

Cited by 3 publications

References 82 publications

(102 reference statements)

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Do viral-associated pathways underlie the immune activation during the acute phase of severe major depression?

Maes,

Zhang,

Plaimas

et al. 2024

Preprint

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Background: Major depressive disorder (MDD) and its most severe phenotype, major dysmood disorder (MDMD), are distinguished by the activation of the immune-inflammatory response system, T cell activation, and a relative T regulatory cell suppression. Nevertheless, these immune data were not used to characterize the features of the immune protein-protein interaction (PPI) network of MDMD. Objectives: To identify the networks nodes and bottlenecks as well as the biological processes that are overrepresented in the PPI network, we conducted PPI network, annotation, and enrichment analyses. Results: The PPI network analysis has identified the following backbone genes: tumor necrosis factor945; (TNF), interleukin (IL)6, CXCL12, CXCL10, CCL5, cluster of differentiation (CD)4, CD8A, human leukocyte antigen (HLA)DR, and FOXP3. A cellular and defense response, an immune response system response, and a viral process that involves viral protein interaction with cytokines and cytokine receptors were all highly associated with the network. The chemokine network and TNF and nuclear factor-κB (NFKB) pathways are additional biological pathways that are enriched in the PPI network. Molecular complex detection extracted one component from the data, including viral protein interaction with cytokine and cytokine receptors and regulated by RELA (an NFKB subunit). Conclusions: Viral processes may underlie the activation of T cells and the cytokine and chemokine networks that are associated with MDMD. Future research on the pathogenesis of MDMD and MDD should examine whether and which viral infections are associated with the onset of these conditions, or whether viral reactivation is associated with the recurrence of illness.

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Do viral-associated pathways underlie the immune activation during the acute phase of severe major depression?

Maes,

Zhang,

Plaimas

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

Do viral-associated pathways underlie the immune activation during the acute phase of severe major depression?

Maes,

Zhang,

Plaimas

et al. 2024

Preprint

View full text Add to dashboard Cite

Background Major depressive disorder (MDD) and its most severe phenotype, major dysmood disorder (MDMD), are distinguished by the activation of the immune-inflammatory response system, T cell activation, and a relative T regulatory cell suppression. Nevertheless, these immune data were not used to characterize the features of the immune protein-protein interaction (PPI) network of MDMD. Objectives To identify the network's nodes and bottlenecks as well as the biological processes that are overrepresented in the PPI network, we conducted PPI network, annotation, and enrichment analyses. Results The PPI network analysis has identified the following backbone genes: tumor necrosis factor-α (TNF), interleukin (IL)6, CXCL12, CXCL10, CCL5, cluster of differentiation (CD)4, CD8A, human leukocyte antigen (HLA)-DR, and FOXP3. A “cellular and defense response”, an “immune response system response”, and “a viral process that involves viral protein interaction with cytokines and cytokine receptors” were all highly associated with the network. The chemokine network and TNF and nuclear factor-κB (NFKB) pathways are additional biological pathways that are enriched in the PPI network. Molecular complex detection extracted one component from the data, including viral protein interaction with cytokine and cytokine receptors and “regulated by RELA” (an NFKB subunit). Conclusions Viral processes may underlie the activation of T cells and the cytokine and chemokine networks that are associated with MDMD. Future research on the pathogenesis of MDMD and MDD should examine whether and which viral infections are associated with the onset of these conditions, or whether viral reactivation is associated with the recurrence of illness.

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Effects of Mental Disorders on Fibromyalgia Mediated by Insomnia: A Mendelian Randomization Study

Chang,

Sun,

Zeng

et al. 2024

JPR

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Background This study employed Mendelian randomization (MR) analysis to confirm the causal effects of mental disorders on fibromyalgia. Methods The summary data for exposures, mediator, and outcome were extracted from the GWAS catalog project, IEU openGWAS project, and Finn biobank database. Significantly associated and independent single-nucleotide polymorphisms (SNPs) meeting the criteria of p < 5×10−8, r2 < 0.001, and kb = 10,000 were selected for MR analysis. We used univariate and multivariate Mendelian randomization (i) to investigate the causal relationship between mental disorders/insomnia and fibromyalgia and (ii) to examine the mediating role of insomnia. The inverse variance weighted (IVW) method along with other MR methods was employed for analysis, while sensitivity analyses were conducted to assess reliability and stability. Results The results provided strong evidence to confirm the causal and positive associations between depression (OR = 6.749; 95% CI: 2.293–19.868, P = 0.001), irritability (OR: 1.873, 95% CI: 1.023−3.428, P = 0.042), insomnia (OR: 8.395, 95% CI: 1.384−50.931, P = 0.021), and fibromyalgia. Moreover, a positive causal relationship was detected between depression (OR = 1.230; 95% CI: 1.178–1.285; P < 0.001), irritability (OR = 1.084; 95% CI: 1.046–1.122; P < 0.001) and insomnia. Multivariate Mendelian randomization analysis showed that insomnia mediated the effects of depression and irritability on fibromyalgia, and the proportion of insomnia-mediated cases ranged from 25.2% to 26%. Conclusion This study showed a positive causal relationship between depression, irritability, insomnia, and fibromyalgia. Insomnia partly mediates this overall effect. Understanding the causal relationship between mental disorders and fibromyalgia and the mediating role of insomnia may provide more information for fibromyalgia intervention and prevention strategies.

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In major dysmood disorder, physiosomatic, chronic fatigue and fibromyalgia symptoms are driven by immune activation and increased immune-associated neurotoxicity

Cited by 3 publications

References 82 publications

Do viral-associated pathways underlie the immune activation during the acute phase of severe major depression?

Do viral-associated pathways underlie the immune activation during the acute phase of severe major depression?

Do viral-associated pathways underlie the immune activation during the acute phase of severe major depression?

Effects of Mental Disorders on Fibromyalgia Mediated by Insomnia: A Mendelian Randomization Study

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