Transcriptomics and metabolomics reveal the mechanism of cognitive impairment induced by long-term selenium deficiency in miceMendeley Data
As the aging population increases, cognitive impairment is emerging as a growing health issue worldwide. Low selenium status has been reported to correlate with cognitive decline in older adults. Nonetheless, the impact of prolonged selenium deficiency on cognitive function in adult mice and the und...
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Elsevier
2025-07-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651325007031 |
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| author | Wanpeng Cheng Yani Wang Peiyue Sa Luyun Liang Lantian Zhang Guangyan Shen Jincheng Luo Mengdi Li |
| author_facet | Wanpeng Cheng Yani Wang Peiyue Sa Luyun Liang Lantian Zhang Guangyan Shen Jincheng Luo Mengdi Li |
| author_sort | Wanpeng Cheng |
| collection | DOAJ |
| description | As the aging population increases, cognitive impairment is emerging as a growing health issue worldwide. Low selenium status has been reported to correlate with cognitive decline in older adults. Nonetheless, the impact of prolonged selenium deficiency on cognitive function in adult mice and the underlying mechanisms remain poorly understood. In this research, male C57BL/6 J mice were given either a normal diet (0.2 mg/kg Se) or a selenium-deficient diet (0.02 mg/kg Se) for 24 weeks to evaluate the impact of long-term selenium insufficiency on their cognitive abilities. We performed hippocampus transcriptome sequencing, real-time PCR, Golgi-Cox staining, transmission electron microscopy, western blotting, and untargeted brain metabolomics to uncover the underlying regulatory mechanism. We found that chronic selenium deficiency impaired the capabilities of object recognition, spatial memory, and self-caring in mice, and disrupted the expression of key genes related to cognitive behavior, dendrite morphogenesis, and synaptic plasticity. Additionally, prolonged selenium deficiency compromised neurite integrity, decreased dendritic spine density, impaired synaptic ultrastructure, and reduced synaptic protein expression. Brain metabolomics revealed that differential metabolites (methylmalonic acid, N-acetyl-1-aspartylglutamic acid, and S-adenosylmethionine) may be involved in the process of cognitive impairment. These findings suggest that perturbation in cognition-related transcriptome profiles, lesions in neurites and synapses, and remodeling of the brain metabolic pattern are involved in the cognitive impairment induced by long-term selenium deficiency. Our study offers a new perspective on the pathogenesis of cognitive impairment, highlighting the critical role of selenium supplementation in maintaining healthy cognitive function. |
| format | Article |
| id | doaj-art-0568033ae40c4b9ea9d8f321edbcd221 |
| institution | DOAJ |
| issn | 0147-6513 |
| language | English |
| publishDate | 2025-07-01 |
| publisher | Elsevier |
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| series | Ecotoxicology and Environmental Safety |
| spelling | doaj-art-0568033ae40c4b9ea9d8f321edbcd2212025-08-20T03:07:50ZengElsevierEcotoxicology and Environmental Safety0147-65132025-07-0129911836710.1016/j.ecoenv.2025.118367Transcriptomics and metabolomics reveal the mechanism of cognitive impairment induced by long-term selenium deficiency in miceMendeley DataWanpeng Cheng0Yani Wang1Peiyue Sa2Luyun Liang3Lantian Zhang4Guangyan Shen5Jincheng Luo6Mengdi Li7Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, Xuzhou 221004, China; Department of Pathogen Biology and Immunology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou 221004, ChinaJiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, Xuzhou 221004, China; Department of Anatomy, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou 221004, ChinaJiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, Xuzhou 221004, China; Department of Anatomy, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou 221004, ChinaJiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, Xuzhou 221004, China; The First Clinical College of Xuzhou Medical University, Xuzhou 221004, ChinaJiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, Xuzhou 221004, China; Department of Anatomy, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou 221004, ChinaThe First Clinical College of Hainan Medical University, Haikou 571199, ChinaKey Laboratory for Gout Research, School of Public Health, Jiamusi University, Jiamusi 154007, ChinaJiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, Xuzhou 221004, China; Department of Anatomy, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou 221004, China; Corresponding author at: Department of Anatomy, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou 221004, China.As the aging population increases, cognitive impairment is emerging as a growing health issue worldwide. Low selenium status has been reported to correlate with cognitive decline in older adults. Nonetheless, the impact of prolonged selenium deficiency on cognitive function in adult mice and the underlying mechanisms remain poorly understood. In this research, male C57BL/6 J mice were given either a normal diet (0.2 mg/kg Se) or a selenium-deficient diet (0.02 mg/kg Se) for 24 weeks to evaluate the impact of long-term selenium insufficiency on their cognitive abilities. We performed hippocampus transcriptome sequencing, real-time PCR, Golgi-Cox staining, transmission electron microscopy, western blotting, and untargeted brain metabolomics to uncover the underlying regulatory mechanism. We found that chronic selenium deficiency impaired the capabilities of object recognition, spatial memory, and self-caring in mice, and disrupted the expression of key genes related to cognitive behavior, dendrite morphogenesis, and synaptic plasticity. Additionally, prolonged selenium deficiency compromised neurite integrity, decreased dendritic spine density, impaired synaptic ultrastructure, and reduced synaptic protein expression. Brain metabolomics revealed that differential metabolites (methylmalonic acid, N-acetyl-1-aspartylglutamic acid, and S-adenosylmethionine) may be involved in the process of cognitive impairment. These findings suggest that perturbation in cognition-related transcriptome profiles, lesions in neurites and synapses, and remodeling of the brain metabolic pattern are involved in the cognitive impairment induced by long-term selenium deficiency. Our study offers a new perspective on the pathogenesis of cognitive impairment, highlighting the critical role of selenium supplementation in maintaining healthy cognitive function.http://www.sciencedirect.com/science/article/pii/S0147651325007031Selenium deficiencyCognitive impairmentTranscriptomicsNeurite morphologySynapseMetabolomics |
| spellingShingle | Wanpeng Cheng Yani Wang Peiyue Sa Luyun Liang Lantian Zhang Guangyan Shen Jincheng Luo Mengdi Li Transcriptomics and metabolomics reveal the mechanism of cognitive impairment induced by long-term selenium deficiency in miceMendeley Data Ecotoxicology and Environmental Safety Selenium deficiency Cognitive impairment Transcriptomics Neurite morphology Synapse Metabolomics |
| title | Transcriptomics and metabolomics reveal the mechanism of cognitive impairment induced by long-term selenium deficiency in miceMendeley Data |
| title_full | Transcriptomics and metabolomics reveal the mechanism of cognitive impairment induced by long-term selenium deficiency in miceMendeley Data |
| title_fullStr | Transcriptomics and metabolomics reveal the mechanism of cognitive impairment induced by long-term selenium deficiency in miceMendeley Data |
| title_full_unstemmed | Transcriptomics and metabolomics reveal the mechanism of cognitive impairment induced by long-term selenium deficiency in miceMendeley Data |
| title_short | Transcriptomics and metabolomics reveal the mechanism of cognitive impairment induced by long-term selenium deficiency in miceMendeley Data |
| title_sort | transcriptomics and metabolomics reveal the mechanism of cognitive impairment induced by long term selenium deficiency in micemendeley data |
| topic | Selenium deficiency Cognitive impairment Transcriptomics Neurite morphology Synapse Metabolomics |
| url | http://www.sciencedirect.com/science/article/pii/S0147651325007031 |
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