Gestational Hypoxia Disrupts Medial Ganglionic Eminence Progenitor Dynamics and Interneuron Development in Schizophrenia.

Authors

Peiyan Ni, Qiancheng Zhang, Youhui Jiang, Huiying Yao, Chuqing Zhou, Xiaoyi Tian, Shiyingnan Gao, Jun Zhao, Xinyi Ren, Naxin Xu, Mengshan Fu, Liansheng Zhao, Xueyu Qi, Xueli Yu, Wanjun Guo, Sangmi Chung, Fan Guo, Tao Li

Published in

Advanced science (Weinheim, Baden-Wurttemberg, Germany). Pages e76936. Aug 12, 2026. Epub Aug 12, 2026.

Abstract

Schizophrenia (SCZ) is a neurodevelopmental disorder characterized by heterogeneous symptoms and multifactorial etiologies. Medial ganglionic eminence (MGE) spheroids generated from first-episode schizophrenia (FES) patients revealed accelerated neurodevelopmental trajectories and enhanced hypoxia responses via single-cell transcriptomics. Notably, FES patient-derived MGE spheroids exhibited defective interneuron migration, disrupted synaptic ultrastructure, and diminished network synchronization. To establish causal links, the gestational hypoxia mouse model recapitulated key pathologies, including reduced progenitor proliferation, abbreviated cell cycles, mismatched interneuron subtypes, and schizophrenia-like behavioral deficits in offspring. Critically, maternal administration of N-acetylcysteine (NAC) restored redox homeostasis and rescued both cellular and behavioral phenotypes. Collectively, these results demonstrate that developmental redox disruption directly impairs GABAergic circuit assembly, while supporting targeted antioxidant pharmacotherapy during gestation as a translatable strategy to mitigate neurodevelopmental risk.

PMID:
42584395
Bibliographic data and abstract were imported from PubMed on 12 Aug 2026.

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