ArticleTranslational psychiatry2026
Cytokine changes in clinical high risk for psychosis population following antipsychotic medication.
Article in Translational psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Serum cytokine alterations are associated with the usage of antipsychotic medications (AP). However, few studies have been designed to longitudinally measure cytokine changes during AP exposure in individuals at clinical high risk (CHR) for psychosis. This study aimed to assess changes in levels of cytokines after initiating AP in the prodromal phase. This longitudinal study involved individuals with CHR who completed the 1-year follow-up reassessment. Individuals with CHR were grouped into those treated with AP (AP + group) and those without (AP- group). Levels of vascular endothelial growth factor (VEGF), granulocyte-macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, 2, 6, 8, and 10 were measured at baseline and 1 year after completion of the clinical assessment. This study included 88 CHR individuals (median age, 18 years and 40.9% [n = 36] women; AP- group: n = 28, AP + group: n = 60). The baseline serum levels of IL-6 were higher in the AP- group than in the AP + group (z = -2.577, p = 0.010). Self-controlled comparisons showed that VEGF (z = 3.826, p < 0.001), TNF-α (z = 2.642, p = 0.008), IL-8 (z = 2.300, p = 0.021), and GM-CSF (z = 2.346, p = 0.019) levels were significantly increased in the AP- group. In the AP + group, IL-6 (z = 3.512, p < 0.001) was significantly increased, IL-1β (z = 2.563, p = 0.010), and GM-CSF (z = 2.095, p = 0.036) were significantly decreased. Repeated-measures analysis of variance revealed a significant group × visit effect on VEGF (F = 20.348, p < 0.001), GM-CSF (F = 7.042, p = 0.013), and IL-1β(F = 4.670, p = 0.040). The findings revealed significant differences in trajectories between individuals with CHR who were and were not taking AP. There is an association between AP use in CHR individuals and differences in inflammatory and neurotrophic factor trajectories.
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