Relation of Schizophrenia to Psychosis with Respect to Immune Dysregulation and Its Impact on Memory and Learning

Relation Abstract Since decades, immune dysfunction and the involvement of infectious agents in the pathophysiology of schizophrenia are under greater importance. Schizophrenia is a long lasting state of mental uncertainty that leads to unreliable perception, not suitable actions and feelings, and a sense of mental fragmentation. Patients with schizophrenia show different characteristics of immunological diseases, such as previous infections, anti-inflammatory cytokines or other inflammatory proteins in blood-co-existence of other autoimmune diseases. Its diagnosis is done over a large period of time showing continuous signs of the disturbance that persists for at least six months. Once detected, the psychiatrist diagnosis is made through a series of psychic tests, to avoid the diagnosis of other mental states or diseases. Currently, hundreds of genes across many chromosomes have been identified for schizophrenia, including some genes from the Major Histocompatibility Complex (MHC). Genetic studies offer the hope of gaining new insight into the mechanisms that increase a person‟s susceptibility to develop schizophrenia, in correlation between schizophrenia and (autoimmune and atopic diseases) and lastly its treatment with respect to the immune system. accelerated serum C-reactive protein concentrations at baseline. Moreover longitudinal studies are needed to confirm whether the increase in serum concentrations of pro anti-inflammatory cytokines in schizophrenia and linked psychosis is the cause or effect of contamination, even though these findings suggest causal mechanisms. [22] Antipsychotic-naive first-episode psychosis and acute psychotic relapse are also related with increased serum concentrations of interleukin 6 and other pro anti-inflammatory cytokines, together with tumor necrosis component α (TNFα), interleukin 1β, interferon γ, and decreased serum concentrations of anti-inflammatory cytokine interleukin 10, which can be normalized after remission of symptoms with antipsychotic treatment. Decreased interleukin 2 which is manufacturing in vitro by way of T cells accumulated from sufferers with schizophrenia become thought to be pointing towards the direction of autoimmune reasons of psychosis. However, acute psychosis is not associated with changes in serum interleukin 2 concentrations. The concentration of soluble interleukin 2 receptor will increase in schizophrenia that is probably to be a compensatory mechanism that inhibits interleukin 2 manufacturing. For that reason, the statistics are constant with an increase in pro anti-inflammatory cytokines in acute psychosis. But few studies have adjusted for critical immune-modulatory factors consisting of body mass or smoking, or examined cytokines in cerebrospinal fluid, in which an increase in interleukin 6 concentration has been said in schizophrenia.