ArticleMolecular medicine (Cambridge, Mass.)2025
FCGR2B knockdown alleviates diabetes-induced cognitive dysfunction by altering neuronal excitability.
Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- PRDM16 protects retinal ganglion cells from ischemia-reperfusion Injury by regulating the RPL5/p53 axis.Cellular and molecular life sciences : CMLS · 2026Article
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4 authors.
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Abstract
backgroundDiabetes mellitus (DM) patients with cognitive impairment seriously affect their quality of life. The onset and development of diabetes-induced cognitive dysfunction are associated with neuronal excitability. In this work, we aimed to reveal the pathogenesis of DM-induced cognitive impairment.
methodsDM mouse model was constructed by high-fat diet combined with streptozocin. Morris water maze test and novel object recognition was used to examine spatial learning and memory ability of mice. The protein expression levels of Fc gamma receptor 2b (FCGR2B), SHC1, p-PI3K and p-AKT were measured by Western blot. Neuronal markers c-Fos and GABAA were detected by Immunohistochemistry.
resultsFCGR2B was highly expressed in hippocampus of DM mice, which was directly associated with Shc1. In vivo, DM mice exhibited decrease of spatial learning and memory ability and up-regulation of FCGR2B. FCGR2B knockdown improved spatial learning and memory ability of DM mice. Not only that, FCGR2B silencing increased the expression of SHC1, p-PI3K and p-AKT in hippocampus of DM mice. Excitatory neuron marker c-Fos was markedly increased and inhibitory neuron marker γ-aminobutyric acid type A (GABAA) receptor was markedly decreased in the hippocampus of DM mice with FCGR2B silencing.
conclusionKnock-down FCGR2B within hippocampus of DM mice activated PI3K/AKT signaling pathway via SHC1 in DM mice and alleviated DM-induced cognition impairment. Knock-down FCGR2B alleviated DM-induced cognition impairment by regulating hippocampal neuronal excitability. Thus, this work suggested that FCGR2B may be a potential target for treatment of DM-induced cognitive dysfunction.
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