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Updated: Apr 22, 2026
14:08
Study of Protein-protein Interactions in Autophagy Research
Published on: September 9, 2017
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mTOR-driven autophagy-inflammation crosstalk underlies schizophrenia pathophysiology
Ling Yan1,2, Xiaona Wang2, Yongping Zhang2
1Laboratory of Animal Genetics, Breeding and Reproduction in the Plateau Mountainous Region, Ministry of Education, Medical College, Guizhou University, Guiyang, China.
Translational Psychiatry
|April 20, 2026
Summary
In schizophrenia, impaired autophagy and increased inflammation are linked via mTOR pathway. Inhibiting mTOR restores autophagy, reducing neuroinflammation and offering a potential therapeutic strategy.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Schizophrenia (SZ) involves immune dysregulation and reduced autophagy.
- The mechanistic link between autophagy and inflammation in SZ is not well understood.
Purpose of the Study:
- To investigate the relationship between autophagy and inflammation in SZ patients.
- To explore the role of mTOR-regulated autophagy in a maternal immune activation (MIA)-induced SZ mouse model.
Main Methods:
- Assessed autophagic activity and inflammatory markers in PBMCs from SZ patients and controls.
- Utilized flow cytometry, Western blotting, and qPCR.
- Analyzed behavioral, molecular, and neurochemical changes in MIA-induced SZ-like mice treated with rapamycin.
Main Results:
- SZ patients showed reduced autophagic-lysosome function and increased inflammation markers (IL-1β, IL-6, IFN-γ, NLRP3 inflammasome).
- Hyperactivation of the PI3K/AKT/mTOR pathway suppressed autophagy.
- MIA mice exhibited SZ-like behaviors, neuroinflammation, and monoaminergic disruptions, which were reversed by rapamycin treatment.
Conclusions:
- mTOR hyperactivation suppresses autophagy, elevating pro-inflammatory cytokines in SZ.
- Inhibiting mTOR restores autophagy, reduces neuroinflammation, and glial activation.
- Autophagy presents a promising therapeutic target for schizophrenia.
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