PreprintArticleVersion 1Preserved in Portico This version is not peer-reviewed
In Schizophrenia, Chronic Fatigue Syndrome- and Fibromyalgia-Like Symptoms are Driven by Breakdown of the Paracellular Pathway with Increased Zonulin and Immune Activation-Associated Neurotoxicity
Version 1
: Received: 9 May 2021 / Approved: 10 May 2021 / Online: 10 May 2021 (12:27:45 CEST)
How to cite:
Maes, M.; Andrés-Rodríguez, L.; Vojdani, A.; Sirivichayakul, S.; Barbosa, D.; Kanchanatawan, B. In Schizophrenia, Chronic Fatigue Syndrome- and Fibromyalgia-Like Symptoms are Driven by Breakdown of the Paracellular Pathway with Increased Zonulin and Immune Activation-Associated Neurotoxicity. Preprints2021, 2021050182. https://doi.org/10.20944/preprints202105.0182.v1
Maes, M.; Andrés-Rodríguez, L.; Vojdani, A.; Sirivichayakul, S.; Barbosa, D.; Kanchanatawan, B. In Schizophrenia, Chronic Fatigue Syndrome- and Fibromyalgia-Like Symptoms are Driven by Breakdown of the Paracellular Pathway with Increased Zonulin and Immune Activation-Associated Neurotoxicity. Preprints 2021, 2021050182. https://doi.org/10.20944/preprints202105.0182.v1
Maes, M.; Andrés-Rodríguez, L.; Vojdani, A.; Sirivichayakul, S.; Barbosa, D.; Kanchanatawan, B. In Schizophrenia, Chronic Fatigue Syndrome- and Fibromyalgia-Like Symptoms are Driven by Breakdown of the Paracellular Pathway with Increased Zonulin and Immune Activation-Associated Neurotoxicity. Preprints2021, 2021050182. https://doi.org/10.20944/preprints202105.0182.v1
APA Style
Maes, M., Andrés-Rodríguez, L., Vojdani, A., Sirivichayakul, S., Barbosa, D., & Kanchanatawan, B. (2021). In Schizophrenia, Chronic Fatigue Syndrome- and Fibromyalgia-Like Symptoms are Driven by Breakdown of the Paracellular Pathway with Increased Zonulin and Immune Activation-Associated Neurotoxicity. Preprints. https://doi.org/10.20944/preprints202105.0182.v1
Chicago/Turabian Style
Maes, M., Décio Barbosa and Buranee Kanchanatawan. 2021 "In Schizophrenia, Chronic Fatigue Syndrome- and Fibromyalgia-Like Symptoms are Driven by Breakdown of the Paracellular Pathway with Increased Zonulin and Immune Activation-Associated Neurotoxicity" Preprints. https://doi.org/10.20944/preprints202105.0182.v1
Abstract
Background: A meaningful part of schizophrenia patients suffer from physiosomatic symptoms (formerly named psychosomatic) which are reminiscent of chronic fatigue syndrome and fibromyalgia (FF) and are associated with signs of immune activation and increased levels of tryptophan catabolites (TRYCATs). Aims: To examine whether FF symptoms in schizophrenia are associated with breakdown of the paracellular pathway, zonulin, lowered natural IgM responses to oxidative specific epitopes (OSEs); and whether FF symptoms belong to the behavioral-cognitive-physical-psychosocial-(BCPS)-worsening index consisting of indices of a general cognitive decline (G-CoDe), symptomatome of schizophrenia, and quality of life (QoL)-phenomenome. Methods: FF symptoms were assessed using the Fibromyalgia and Chronic Fatigue Rating scale in 80 schizophrenia patients and 40 healthy controls and serum cytokines/chemokines, IgA levels to TRYCATs, IgM to OSEs, zonulin and transcellular/paracellular (TRANS/PARA) molecules were assayed using ELISA methods. Results: A large part (42.3%) of the variance in the total FF score was explained by the regression on the PARA/TRANS ratio, pro-inflammatory cytokines, IgM to zonulin, IgA to TRYCATs (all positively) and IgM to OSEs (inversely). There were highly significant correlations between the total FF score and G-CoDe, symtopmatome, QoL phenomenome and BCPS-worsening score. FF symptoms belong to a common core shared by G-CoDe, symtopmatome, and QoL phenomenome. Discussion: The physio-somatic symptoms of schizophrenia are driven by various pathways including increased zonulin, breakdown of the paracellular tight-junctions pathway, immune activation with induction of the TRYCAT pathway, and consequent neurotoxicity. It is concluded that FF symptoms are part of the phenome of schizophrenia and BCPS-worsening as well.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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