Authors
Xinbo Ma, Liu Yang, Xinhua Shao, Jia Cui, Ziqiao Guan, Man Lyu, Shuaifei Yang, Na Fang, Yang Liu, Yanhui Gao, Xiaona Liu, Yanmei Yang
Published in
Journal of Zhejiang University. Science. B. Volume 27. Issue 9. Pages 1013-1030. Aug 06, 2026. Epub Aug 06, 2026.
Abstract
Arsenic exposure is known to cause cognitive deficits, although the underlying mechanisms are yet to be explored. In this study, we investigated the role of nerve growth factor (NGF), a neuroprotective factor, in arsenic-induced cognitive impairment. In mouse models exposed to 25 and 50 mg/L sodium arsenite (NaAsO2), we observed neuronal damage accompanied by the downregulation of NGF, decreased phosphorylation of phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT), reduced phosphorylation of the mitochondrial fission protein dynamin-related protein 1 (Drp1), and downregulation of the mitochondrial fusion protein optic atrophy 1 (OPA1). Similarly, the downregulation of NGF, inactivation of the PI3K/AKT signaling pathway, mitochondrial dynamics imbalance (dysregulation of mitochondrial fission and fusion processes), and increased apoptosis were observed in HT-22 cells exposed to 4 μmol/L NaAsO2. NGF overexpression mitigated these arsenic-induced alterations, while the protective effect of NGF against arsenic toxicity was reduced by LY294002, a PI3K/AKT pathway inhibitor. These findings suggest that a decrease in NGF mediates the arsenic-disrupted mitochondrial dynamics via inhibiting the PI3K/AKT pathway, ultimately impairing cognitive function.
PMID:
42806852
Bibliographic data and abstract were imported from PubMed on 29 Sep 2026.
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