Interleukin 1 beta gene and risk of schizophrenia: detailed case–control and family‐based studies and an updated meta‐analysis

Shibuya, Masako; Watanabe, Yuichiro; Nunokawa, Ayako; Egawa, Jun; Kaneko, Naoshi; Igeta, Hirofumi; Someya, Toshiyuki

doi:10.1002/hup.2365

Cited by 19 publications

(5 citation statements)

References 28 publications

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“…Allelic or genotypic association between the IL-1β C-511T polymorphism and schizophrenia was reported by case-control as well as family studies (110,111). Other studies have reported no significant association between the IL-1β C-511T or IL-1β C3954T SNP and schizophrenia (112), which disagrees with a meta-analysis in a specific population that reported a moderate association of IL-1β C-511T and C3954T polymorphisms with schizophrenia in Caucasian samples, suggesting that the genetic effect of IL-1β on schizophrenia may be ethnicity dependent (113).…”

Section: Cytokine Polymorphisms In Schizophreniamentioning

confidence: 99%

Cytokine Imbalance in Schizophrenia. From Research to Clinic: Potential Implications for Treatment

2021

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Cytokines are one of the most important components of the immune system. They orchestrate the brain's response to infectious and other exogenous insults and are crucial mediators of the cross-talk between the nervous and immune systems. Epidemiological studies have demonstrated that severe infections and autoimmune disorders, in addition to genetic predisposition, are risk factors for schizophrenia. Furthermore, maternal infection during pregnancy appears to increase the risk of schizophrenia, and proinflammatory cytokines may be negatively involved in the neurodevelopmental process. A cytokine imbalance has been described in the blood and cerebrospinal fluid of schizophrenia patients, particularly in the T helper type 1 [Th1] and type 2 [Th2] cytokines, albeit the results of such studies appear to be contradictory. Chronic stress, likewise, appears to contribute to a lasting proinflammatory state and likely also promotes the disorder. The aim of this mini-review is to investigate the roles of different cytokines in the pathophysiology of schizophrenia and define how cytokines may represent key molecular targets to regulate for the prevention and treatment of schizophrenia. How current antipsychotic drugs impact cytokine networks is also evaluated. In this context, we propose to change the focus of schizophrenia from a traditionally defined brain disorder, to one that is substantially impacted by the periphery and immune system.

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Section: Cytokine Polymorphisms In Schizophreniamentioning

confidence: 99%

Cytokine Imbalance in Schizophrenia. From Research to Clinic: Potential Implications for Treatment

2021

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“…Genome-wide association studies have revealed genetic polymorphism of immune-related genes in SCZ etiopathophysiology. For example, genetic polymorphisms of C4 complement factor, major histocompatibility complex (MHC) locus on chromosome 6 ( Shi et al, 2009 ; Sekar et al, 2016 ), interleukin-1β, IL-6, the soluble IL-6 receptor (sIL6R), and IL-10 are associated with increased risk of SCZ ( Xu and He, 2010 ; Gao et al, 2014 ; Shibuya et al, 2014 ; Hudson and Miller, 2018 ). In contrast, polymorphism of IL-2, IL-4, tumor necrosis factor-α (TNF-α), or transforming growth factor- β1 (TGF-β1), are not associated with increased risk of SCZ ( Qin et al, 2013 ; Hudson and Miller, 2018 ).…”

Section: Altered Gut Microbiota Inflammation and Neurodevelopmental D...mentioning

confidence: 99%

Understanding the Role of the Gut Microbiome in Brain Development and Its Association With Neurodevelopmental Psychiatric Disorders

Dash

Syed

Khan

2022

Front. Cell Dev. Biol.

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The gut microbiome has a tremendous influence on human physiology, including the nervous system. During fetal development, the initial colonization of the microbiome coincides with the development of the nervous system in a timely, coordinated manner. Emerging studies suggest an active involvement of the microbiome and its metabolic by-products in regulating early brain development. However, any disruption during this early developmental process can negatively impact brain functionality, leading to a range of neurodevelopment and neuropsychiatric disorders (NPD). In this review, we summarize recent evidence as to how the gut microbiome can influence the process of early human brain development and its association with major neurodevelopmental psychiatric disorders such as autism spectrum disorders, attention-deficit hyperactivity disorder, and schizophrenia. Further, we discuss how gut microbiome alterations can also play a role in inducing drug resistance in the affected individuals. We propose a model that establishes a direct link of microbiome dysbiosis with the exacerbated inflammatory state, leading to functional brain deficits associated with NPD. Based on the existing research, we discuss a framework whereby early diet intervention can boost mental wellness in the affected subjects and call for further research for a better understanding of mechanisms that govern the gut-brain axis may lead to novel approaches to the study of the pathophysiology and treatment of neuropsychiatric disorders.

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“…Yet, another study found increased secretion of IL-1β from monocytes derived from individuals with schizophrenia, which normalizes with antipsychotic medication treatment [52][53][54]. A meta-analysis from 8724 case-control and 201 samples from 16 studies failed to identify an association between IL1β C511T single nucleotide polymorphism (SNP) of the IL-1β gene and schizophrenia [55]. However, a study in a different population found that the IL1β C-511T and C395T polymorphisms were moderately associated with schizophrenia in a group of Caucasian individuals [56], suggesting that the relationship might be specific only to certain racial or ethnic groups.…”

Section: Interleukin 1 Beta (Il-1β)mentioning

confidence: 99%

The impact of inflammation on neurocognition and risk for psychosis: a critical review

Kogan

Ospina

Mittal

et al. 2019

Eur Arch Psychiatry Clin Neurosci

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Neurocognitive difficulties are highly prevalent among people with schizophrenia and have been linked to increased inflammation, as well as dysfunction and disability. Poor neurocognitive functioning has also been documented in individuals at clinical high risk for psychosis (CHR) and a burgeoning literature point to alterations in inflammation markers in this population. However, there is limited information regarding the putative link between inflammation and neurocognition in CHR individuals, and the potential role of inflammation in the development of cognitive difficulties and psychosis. As previous reports indicate that early treatment in schizophrenia is associated with better outcomes, there is an urgent need to identify neurobiological mechanisms underlying cognitive deterioration and psychosis in CHR individuals to provide them with care prior to significant cognitive and functional declines. To address this gap in the literature, we review and summarize the relevant literatures on inflammation and neurocognitive dysfunction in schizophrenia and CHR individuals, point to remaining gaps, and suggest directions for future research.

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Interleukin 1 beta gene and risk of schizophrenia: detailed case–control and family‐based studies and an updated meta‐analysis

Abstract: The present study does not support a role for IL1B in schizophrenia susceptibility.

Cited by 19 publications

References 28 publications

Cytokine Imbalance in Schizophrenia. From Research to Clinic: Potential Implications for Treatment

Cytokine Imbalance in Schizophrenia. From Research to Clinic: Potential Implications for Treatment

Understanding the Role of the Gut Microbiome in Brain Development and Its Association With Neurodevelopmental Psychiatric Disorders

The impact of inflammation on neurocognition and risk for psychosis: a critical review

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