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This page is an AI-assisted Turkish summary of the study presented at the 26th World Congress of Psychiatry. The study belongs to the presenting authors; please refer to the original source when citing it.

EV0674

Genetic predisposition to inflammation drives neuroanatomical deviations from normative trajectories in schizophrenia

INFLAMMATORY GENETIC LIABILITY DRIVES NEUROANATOMICAL DEVIATIONS FROM NORMATIVE TRAJECTORIES IN SCHIZOPHRENIA

Inflammatory polygenic risk scores are the strongest predictors of deviations from normative brain developmental trajectories in schizophrenia, and this pattern is not explained by medication effects.

The study aimed to investigate the genetic predisposition underlying neuroanatomical deviations from normative developmental trajectories in schizophrenia (SZ), while accounting for medication effects. T1-weighted MRI data from 134 patients with SZ were processed using FreeSurfer, and deviations from normative trajectories were quantified using the CentileBrain model; mean absolute Z scores were calculated across regions of interest for subcortical volume (SV), surface area (SA), and cortical thickness (CT). Polygenic risk scores (PRS) for psychiatric disorders and inflammatory regulators were derived from GWAS summary statistics; partial least squares (PLS) regression was used to test whether PRS and z-scored chlorpromazine and lorazepam equivalents predicted structural deviations. The first PLS component explained 8.2% of the variance in structural deviations (coefficient 0.364) and was driven primarily by SV (loading 0.852), followed by SA (loading 0.398) and CT (loading 0.338). Inflammatory PRS had the highest variable importance in projection (VIP) scores. Adding medication variables to the model did not alter this pattern; IL10, IL2RA, IL9, CXCL10, and CXCL12 remained the variables with the strongest positive contributions. The authors conclude that genetic predisposition to inflammation is associated with multidomain neuroanatomical atypicality in SZ, particularly in subcortical structures, and that although medication use contributes to structural variability, it does not explain this neuroimmunological signature.

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