Inflammation Theories in Psychotic Disorders: A Critical Review

Abstract

Recent research suggests that inflammation and immunity may have a role in the etiology of psychotic disorders. There is evidence of proinflammatory activation of the innate immune system and an activation of the T-cells of the adaptive immune system in both schizophrenia and bipolar disorder. Studies of antipsychotic-naïve patients with first-episode psychosis have found that inflammation is present already at this stage. Some of these abnormalities resolve after the initiation of treatment, suggesting that they are state markers of acute psychosis, but other abnormalities persist. There is also evidence for prenatal infections being involved in the etiology of schizophrenia. Several hypotheses link inflammation and immunity with psychotic disorders. In this review, we focus on hypotheses related to prenatal development, disturbed regulation of neurogenesis, microglial activation, autoimmunity and microbial environment, and consider the potential confounding effects related to stress, childhood adversities, lifestyle and medical comorbidity as well as some methodological limitations. We also review the current evidence for the effectiveness of anti-inflammatory medication in the treatment of psychotic disorders.

Seroreactive marker for inflammatory bowel disease and associations with antibodies to dietary proteins in bipolar disorder

“…One objective of our study design was to enable comparisons between recently diagnosed individuals and those individuals who have had their disease for greater amounts of time. For measures of inflammatory indices that are known to fluctuate over time, the ability to compare individuals in different stages of disease is especially pertinent (6, 8, 9, 32, 45). Toward this end, we recruited 226 individuals diagnosed with bipolar disorder without a recent onset of psychosis, 38 individuals with bipolar disorder and a recent onset of psychosis, and 207 individuals who did not have a history of psychiatric disorders from inpatient and outpatient treatment sites and published announcements.…”

Intermittent or sustained systemic inflammation and the preterm brain

“…Schizophrenia and some other chronic psychotic disorders have inflammatory characteristics (16). Treatment with anti-inflammatory compounds appears to reduce the severity of some symptoms.…”

Comorbidities in Neurology: Is adenosine the common link?

“…This remarkable overlap suggests the existence of common pathogenic mechanisms, which include synaptic dysfunction and synaptotocicity (Jensen, 2011; Noebels, 2011; Swann and Rho, 2014; Zhou and Roper, 2012), inflammatory processes (Kobow et al, 2012; Miller and Spencer, 2014; Perry, 2012), and glial activation (Ravizza et al, 2013; Stanimirovic and Friedman, 2012; Suvisaari and Mantere, 2013). Although several mechanisms might contribute to the development of comorbid symptomatology, we will here address and focus on the ‘adenosine hypothesis of comorbidities’, which suggests that adenosine deficiency per se can be a sufficient cause for the generation of a wide spectrum of symptoms shared among seemingly distinct neurological conditions.…”