Interleukin 18 and cognitive impairment in first episode and drug naïve schizophrenia versus healthy controls

Sex differences in TGFB-β signaling with respect to age of onset and cognitive functioning in schizophrenia

“…Additionally, the leukemia inhibitory factor gene polymorphism has been associated with deterioration in working memory function in patients with schizophrenia 53. With respect to cytokine serum levels in schizophrenia, cognitive impairment has been associated with higher IL-650 and IL-1854 as well as lower IL-255 levels.…”

“…Firstly, it should be noted that our sample size was limited; however, it is one of the largest studies analyzing serum cytokine levels with respect to cognitive functioning in schizophrenia 50,54,55,76. Secondly, all our patients were medicated, while the association of TGF-β level with cognitive functioning in unmedicated first-episode schizophrenia patients would be much more reliable.…”

First-Episode Psychosis: An Inflammatory State?

“…In particular, IL-2 levels were found to be decreased in two studies in drug-naïve patients [22,26], but appeared not significantly different in one of our studies where the subjects were minimally treated with antipsychotics (19 out of 24 patients were treated with antipsychotic medication with a mean ± SEM duration of treatment of 33.5 ± 7.2 days) [18], suggesting a possible effect of antipsychotic treatment in normalizing IL-2 levels. Other mixed findings come from studies reporting increased or unaffected levels of IL-8 [18,20,27], IL-10 [18,20,25], IL-4 [18,24], IL-18 [27,28] and MCP1 [18,27,29]. …”

“…Interestingly, the first study reported a significant negative correlation between MCP1 levels and the cognitive domains of learning and memory, as measured by the Wechsler Memory Scale [31]. The second study found a positive correlation between levels of IL-18 and the visuospatial/constructional domain of cognitive deficit measured with Repeatable Battery for the Assessment of Neuropsychological Status, which suggested a protective rather than detrimental effect of IL-18 on cognitive function [28]. Because of the paucity of studies investigating the association between inflammation and clinical symptoms in first-episode psychosis, it is still too early to draw any definite conclusions about the contribution of inflammation to the severity of clinical presentation.…”

Refining and integrating schizophrenia pathophysiology – Relevance of the allostatic load concept

“…It has been suggested that immune system deregulation is one of the key pathophysiological mechanisms underlying cognitive deficits in schizophrenia. So far associations have been shown between cognitive decline and the following parameters: serum antibodies to herpes simplex virus 1 (Dickerson et al, 2003Shirts et al, 2008), lymphotoxin gene polymorphism (Dickerson et al, 2007a), leukemia inhibitory factor gene polymorphism (Okahisa et al, 2010), interleukin 18 levels (Zhang et al, 2013e) and C-reactive protein levels (Dickerson et al, 2007b). Moreover, additive effects of multiple immune parameters deregulation on cognitive functioning have been observed, suggesting the cumulative effect of various immune insults on cognition in schizophrenia (Dickerson et al, 2012).…”