Case Control Study
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Psychiatry. Dec 19, 2024; 14(12): 1804-1814
Published online Dec 19, 2024. doi: 10.5498/wjp.v14.i12.1804
Interaction between serum inflammatory cytokines and brain-derived neurotrophic factor in cognitive function among first-episode schizophrenia patients
Li-Jun Cui, Li-Li Cai, Wan-Qiu Na, Rui-Long Jia, Jie-Lin Zhu, Xin Pan
Li-Jun Cui, Key Laboratory of Psychiatry, Huzhou Third Municipal Hospital, the Affiliated Hospital of Huzhou University, Huzhou 313000, Zhejiang Province, China
Li-Li Cai, Wan-Qiu Na, Xin Pan, Department of Psychiatry, Huzhou Third Municipal Hospital, The Affiliated Hospital of Huzhou University, Huzhou 313000, Zhejiang Province, China
Rui-Long Jia, School of Information Engineering, Huzhou University, Huzhou 313000, Zhejiang Province, China
Jie-Lin Zhu, Department of Clinical Laboratory, Huzhou Third Municipal Hospital, The Affiliated Hospital of Huzhou University, Huzhou 313000, Zhejiang Province, China
Author contributions: Cui LJ, Cai LL and Na WQ contributed to the writing of the manuscript; Jia RL contributed to data analysis and statistical processing; Zhu JL contributed to conduct experimental operations; Cai LL and Pan X devised the study design; all authors have read and agreed to the published version of the manuscript.
Supported by Huzhou Public Welfare Research Project Social Development Category, No. 2021GYB09, No. 2021GY38, No. 2019GY26 and No. 2019GZB02.
Institutional review board statement: This study was approved by the Ethics Committee of Huzhou Third Municipal Hospital (Ethical Approval No. 2021-018).
Informed consent statement: Fully inform all participants and their guardians of the content of this study and sign an informed consent form before enrollment.
Conflict-of-interest statement: The authors declare no conflicts of interest for this article.
Data sharing statement: The data for this study can be obtained from the corresponding author upon request.
STROBE statement: The authors have read the STROBE Statement—checklist of items, and the manuscript was prepared and revised according to the STROBE Statement—checklist of items.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Xin Pan, Doctor, Chief Doctor, Department of Psychiatry, Huzhou Third Municipal Hospital, The Affiliated Hospital of Huzhou University, No. 2088 East Tiaoxi Road, Huzhou 313000, Zhejiang Province, China. huzhoupanxin@163.com
Received: May 1, 2024
Revised: August 24, 2024
Accepted: September 14, 2024
Published online: December 19, 2024
Processing time: 209 Days and 21.8 Hours
Abstract
BACKGROUND

The pathogenesis of cognitive impairment in schizophrenia (SCZ) remains unclear. Accumulating studies showed that inflammatory-immune dysregulation and altered brain derived neurotrophic factor (BDNF) levels play a crucial role in the psychopathology of SCZ. However, their association with cognitive dysfunction in first-episode SCZ patients has not been thoroughly investigated.

AIM

To explore the interaction effects between cognitive function and inflammatory cytokines and BDNF in first-episode SCZ.

METHODS

The current study is a cross-sectional case-control investigation that recruited 84 patients with first-episode SCZ (SCZ group) and 80 healthy controls (HCs group) at the Huzhou Third Municipal Hospital between August 2021 and September 2023. ELISA was employed to measure the serum levels of interleukin (IL)-1β, IL-4, IL-6, IL-10, and BDNF. The Chinese brief cognitive test (C-BCT) and the positive and negative syndrome scales were measured the severity of cognitive impairment and psychiatric symptoms.

RESULTS

Compared to the HC group, the SCZ group exhibited elevated IL-1β and IL-6 levels, decreased BDNF levels, and reduced C-BCT scores (all P < 0.001). In SCZ, BDNF was negatively correlated with IL-6 (r = -0.324, P < 0.05). Information processing speed was negatively correlated with IL-6 (r = -0.315, P < 0.05) and positively with BDNF (r = 0.290, P < 0.05); attention, working memory, comprehensive ability, and executive function were negatively correlated with IL-1β and IL-6 (all P < 0.05) and positively with BDNF (all P < 0.05). Multiple regression analysis showed IL-6 influenced C-BCT dimensions (β = -0.218 to -0.327, all P < 0.05); attention and executive ability were influenced by IL-1β (β = -0.199 to -0.261, all P < 0.05); comprehensive executive ability was influenced by BDNF (β = 0.209, P < 0.05).

CONCLUSION

Our findings suggested that interrelationships between immune dysfunction and neurotrophic deficiency might underlie the pathological mechanisms of cognitive impairments in first-episode SCZ patients.

Keywords: Brain-derived neurotrophic factor; Inflammatory cytokines; First-episode schizophrenia; Cognitive function; Pro-inflammatory cytokines; Neuroinflammation; Serum biomarkers

Core Tip: The previous literature has demonstrated that dysregulation of the inflammatory immune and alterations in brain derived neurotrophic factor (BDNF) levels play a pivotal role in the pathophysiology of schizophrenia (SCZ). In this study, 84 patients with first-episode SCZ and 80 healthy volunteers were recruited. We assessed the cognitive function and psychiatric symptoms of the subjects, measured their serum inflammatory cytokines and BDNF levels, and explored the interaction between cognitive impairment and serum inflammatory cytokines and BDNF in first-episode SCZ. The findings of this study suggest that cognitive impairment in first-episode SCZ was related to immune inflammation imbalance and neurotrophic deficiency.