# Protein Kinase Expression of the AKT/mTOR Signaling Pathway in Peripheral Mononuclear Cells of Schizophrenia Patients: A Pilot Study

## TL;DR

This pilot study explores the AKT/mTOR signaling pathway in schizophrenia patients, finding altered protein kinase expression that may contribute to the disease's biology.

## Contribution

The study is among the first to investigate AKT/mTOR signaling in peripheral mononuclear cells of schizophrenia patients.

## Key findings

- AKT1 and p70S6K expression was significantly increased in schizophrenia patients.
- GSK3-α and GSK3-β expression was elevated in patients with schizophrenia lasting more than 5 years.
- AKT/mTOR signaling may be a potential target for new diagnostic and therapeutic approaches in schizophrenia.

## Abstract

A comprehensive study of the contribution of dysfunction AKT/mTOR signaling to the pathogenesis of schizophrenia is needed. The aim of the study is to determine the expression of the protein kinase AKT/mTOR signaling pathway in peripheral mononuclear cells (PMCs) of patients with schizophrenia. Determination of AKT1, mTOR, p70S6K, GSK3-α, and GSK3-β in mononuclears was performed on multiplex analyzers. Statistical data processing was carried out using SPSS. The critical significance level for the differences was 0.05. The study included 58 patients with schizophrenia (F20) and 60 healthy individuals. We found an increase in the expression of AKT1 and p706SK in PM׳s of patients (p = 0.006, p = 0.001). Analysis of kinase expression was carried out depending on clinical characteristics (type of course, leading symptoms and duration of the schizophrenia). Increased expression of GSK3-α and GSK3-β was detected in patients with a duration of disease more than 5 years (p = 0.019, p = 0.018). The AKT/mTOR signaling cascade may play a significant role in the pathogenesis of schizophrenia. We can assume that signaling pathways are involved in neurobiological processes and can be targets for new methods of pharmacotherapy, prognosis and diagnosis of mental disorders.