Inflammation in Schizophrenia: Pathogenetic Aspects and Therapeutic Considerations.
TLDR
Support for the relevance of a low-level neuroinflammatory process in schizophrenia is provided by the loss of central nervous system volume and microglial activation demonstrated in neuroimaging studies, and the benefit of anti-inflammatory medications found in some studies and the intrinsic anti- inflammatory and immunomodulatory effects of antipsychotics provide further support for the role of inflammation in this debilitating disease.Abstract:
This paper discusses the current evidence from animal and human studies for a central role of inflammation in schizophrenia. In animal models, pre- or perinatal elicitation of the immune response may increase immune reactivity throughout life, and similar findings have been described in humans. Levels of pro-inflammatory markers, such as cytokines, have been found to be increased in the blood and cerebrospinal fluid of patients with schizophrenia. Numerous epidemiological and clinical studies have provided evidence that various infectious agents are risk factors for schizophrenia and other psychoses. For example, a large-scale epidemiological study performed in Denmark clearly showed that severe infections and autoimmune disorders are such risk factors. The vulnerability-stress-inflammation model may help to explain the role of inflammation in schizophrenia because stress can increase pro-inflammatory cytokines and may even contribute to a chronic pro-inflammatory state. Schizophrenia is characterized by risk genes that promote inflammation and by environmental stress factors and alterations of the immune system. Typical alterations of dopaminergic, serotonergic, noradrenergic, and glutamatergic neurotransmission described in schizophrenia have also been found in low-level neuroinflammation and consequently may be key factors in the generation of schizophrenia symptoms. Further support for the relevance of a low-level neuroinflammatory process in schizophrenia is provided by the loss of central nervous system volume and microglial activation demonstrated in neuroimaging studies. Last but not least, the benefit of anti-inflammatory medications found in some studies and the intrinsic anti-inflammatory and immunomodulatory effects of antipsychotics provide further support for the role of inflammation in this debilitating disease.read more
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Increased risk of COVID-19 infection and mortality in people with mental disorders: analysis from electronic health records in the United States
TL;DR: Individuals with a recent diagnosis of a mental disorder are identified as being at increased risk for COVID‐19 infection, which is further exacerbated among African Americans and women, and as having a higher frequency of some adverse outcomes of the infection.
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Association of Psychiatric Disorders With Mortality Among Patients With COVID-19.
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TL;DR: It is suggested that schizophrenia spectrum disorders may be a risk factor for mortality in patients with COVID-19 and adults with a schizophrenia spectrum disorder diagnosis were associated with an increased risk for mortality, but those with mood and anxiety disorders were not associated with a risk of mortality.
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Inflammation-related biomarkers in major psychiatric disorders: a cross-disorder assessment of reproducibility and specificity in 43 meta-analyses.
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Cytokine Alterations in Schizophrenia: An Updated Review.
Sara Momtazmanesh,Sara Momtazmanesh,Ameneh Zare-Shahabadi,Ameneh Zare-Shahabadi,Nima Rezaei,Nima Rezaei +5 more
TL;DR: There is a substantial need for studies investigating the levels of cytokines before disease development and delineating the therapeutic implications of the disrupted cytokine levels in schizophrenia, and the available evidence shows a potential causative role for cytokines in schizophrenia development.
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COVID-19 vaccination for people with severe mental illness: why, what, and how?
TL;DR: In this article, the authors discuss the risk for worse COVID-19 outcomes in this vulnerable group, the effect of severe mental illnesses and psychotropic medications on vaccination response, the attitudes of people with severe mental illness towards vaccination, and, the potential barriers to, and possible solutions for, an efficient vaccination programme in this population.
References
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Book
Janeway's immunobiology
TL;DR: The Evolution of the Immune System Appendix I Immunologists' Toolbox Appendix II CD Antigens Appendix III Cytokines and their Receptors Appendix IV Chemokinesand their Receptionors Appendix V Immunological Constants.
Vulnerability—A New View of Schizophrenia
Joseph Zubin,Bonnie Spring +1 more
TL;DR: A second-order model, vulnerability, is proposed as the common denominator, and methods for finding markers of vulnerability are suggested in the hope of revitalizing the field.
Journal ArticleDOI
Vulnerability--a new view of schizophrenia.
Joseph Zubin,Bonnie Spring +1 more
TL;DR: In this article, a second-order model, vulnerability, is proposed as the common denominator, and methods for finding markers of vulnerability are suggested in the hope of revitalizing the field.
Journal ArticleDOI
Cortical demyelination and diffuse white matter injury in multiple sclerosis
Alexandra Kutzelnigg,Claudia F. Lucchinetti,Christine Stadelmann,Wolfgang Brück,Helmut Rauschka,Markus Bergmann,Manfred Schmidbauer,Joseph E. Parisi,Hans Lassmann +8 more
TL;DR: Global brain pathology in multiple sclerosis is analysed, focusing on the normal-appearing white matter (NAWM) and the cortex, to suggest that multiple sclerosis starts as a focal inflammatory disease of the CNS, which gives rise to circumscribed demyelinated plaques in the white matter.
Journal ArticleDOI
Maternal Immune Activation Alters Fetal Brain Development through Interleukin-6
Stephen E. P. Smith,Jennifer S. Li,Jennifer S. Li,Krassimira A. Garbett,Karoly Mirnics,Paul H. Patterson +5 more
TL;DR: It is shown that the cytokine interleukin-6 (IL-6) is critical for mediating the behavioral and transcriptional changes in the offspring and should be identified as a key intermediary in the molecular dissection of the pathways whereby MIA alters fetal brain development.
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