What role does inflammation play in schizophrenia?

Müller, Norbert

doi:10.1080/14737175.2016.1256206

Cited by 10 publications

(8 citation statements)

References 49 publications

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“…Just as schizophrenia is not a classic autoimmune disorder, it is also not a classic inflammatory disorder. In schizophrenia, the detectable inflammation has been ascribed to be of a low-grade nature with peripheral and central inflammatory states measured using a variety of biomarkers in different research labs (Bechter, 2013; Catts et al, 2014; Dickerson et al, 2016; Fillman et al, 2013; Fillman et al, 2014; Fillman et al, 2016; Kirkpatrick and Miller, 2013; Miller et al, 2011; Muller, 2016; Severance et al, 2012a; Severance et al, 2013). In most cases, the source of this inflammation in these studies is not known, but it is evident in the form of pro- and anti-inflammatory cytokine dysregulation, disrupted tryptophan and kynurenine metabolism, exposure to microbial pathogens and antigens, food hypersensitivities, complement activation, post-mortem pathologies and brain imaging.…”

Section: Autoimmunity In Schizophreniamentioning

confidence: 99%

Autoimmune phenotypes in schizophrenia reveal novel treatment targets

Severance

Dickerson

Yolken

2018

Pharmacology & Therapeutics

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Typical and atypical antipsychotics are the first-line treatments for schizophrenia, but these classes of drugs are not universally effective, and they can have serious side effects that impact compliance. Antipsychotic drugs generally target the dopamine pathways with some variation. As research of schizophrenia pathophysiology has shifted away from a strictly dopamine-centric focus, the development of new pharmacotherapies has waned. A field of inquiry with centuries-old roots is gaining traction in psychiatric research circles and may represent a new frontier for drug discovery in schizophrenia. At the forefront of this investigative effort is the immune system and its many components, pathways and phenotypes, which are now known to actively engage the brain. Studies in schizophrenia reveal an intricate association of environmentally-driven immune activation in concert with a disrupted genetic template. A consistent conduit through this gene-environmental milieu is the gut-brain axis, which when dysregulated can generate pathological autoimmunity. In this review, we present epidemiological and biochemical evidence in support of an autoimmune component in schizophrenia and depict gut processes and a dysbiotic microbiome as a source and perpetuator of autoimmune dysfunction in the brain. Within this framework, we review the role of infectious agents, inflammation, gut dysbioses and autoantibody propagation on CNS pathologies such as neurotransmitter receptor hypofunction and complement pathway-mediated synaptic pruning. We then review the new pharmacotherapeutic horizon and novel agents directed to impact these pathological conditions. At the core of this discourse is the understanding that schizophrenia is etiologically and pathophysiologically heterogeneous and thus its treatment requires individualized attention with disease state variants diagnosed with objective biomarkers.

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Section: Autoimmunity In Schizophreniamentioning

confidence: 99%

Autoimmune phenotypes in schizophrenia reveal novel treatment targets

Severance

Dickerson

Yolken

2018

Pharmacology & Therapeutics

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“…SCZ patients have been reported to show increased levels of oxidative stress (2), and the SCZoxidative stress association has been noted in functional studies (19). Moreover, there is compelling evidence linking reactive oxygen species with immune-inflammatory pathways (20,21), which have also been implicated in SCZ (22,23).…”

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confidence: 97%

A Comprehensive Analysis of Nuclear-Encoded Mitochondrial Genes in Schizophrenia

Gonçalves

Cappi

Hagen

et al. 2018

Biological Psychiatry

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“…Specifically, IP’s values on most of the biomarkers of aging were generally in the less metabolically dysregulated, less pro-inflammatory and more anti-inflammatory direction compared to the NC and SC participants, while SC B group in this study generally showed more unhealthy marker levels compared to the NC B group. Given the potential relationship of immune and brain function, it is possible there could be a biological link underlying cognitive/brain and biomarker function (Misiak et al, 2017; Muller, 2016). On the other hand, relatively strong cognitive and brain reserve may indirectly lead to better biomarker values through environmental factors.…”

Section: Discussionmentioning

confidence: 99%

Avoidance of accelerated aging in schizophrenia?: Clinical and biological characterization of an exceptionally high functioning individual

Palmer¹,

Moore²,

Eyler³

et al. 2018

Schizophrenia Research

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Although speculative, results suggest a possible model in which superior working memory permits a person to be aware of the potentially psychotic nature of a thought or perception, and adjust response accordingly. Compensatory overactivity of brain regions during affective processing may also reflect heightened meta-awareness in emotional situations. Biomarker levels raise the possibility that IP partially avoided the accelerated biological aging associated with schizophrenia.

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What role does inflammation play in schizophrenia?

Cited by 10 publications

References 49 publications

Autoimmune phenotypes in schizophrenia reveal novel treatment targets

Autoimmune phenotypes in schizophrenia reveal novel treatment targets

A Comprehensive Analysis of Nuclear-Encoded Mitochondrial Genes in Schizophrenia

Avoidance of accelerated aging in schizophrenia?: Clinical and biological characterization of an exceptionally high functioning individual

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