Selenium ameliorates cognitive impairment through activating BDNF/TrkB pathway

IF 3.6 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Trace Elements in Medicine and Biology Pub Date : 2025-01-15 DOI:10.1016/j.jtemb.2025.127599
Yu Liu , Ye Liu , Liping Shi , Xue Zhang , Kunmei Liu , Shulan He
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引用次数: 0

Abstract

Background

Alzheimer's disease (AD) is a neurodegenerative disorder that primarily affects older adults. Selenium, an essential micronutrient for humans, plays a crucial role in the body's normal physiological and metabolic processes. A long-term deficiency in selenium intake can lead to various diseases and even contribute to the ageing process. This study aims to explore the ameliorative effect of selenium on cognitive impairment in 3 × Tg-AD mice and to determine if its effects are related to the BDNF/TrkB pathway.

Methods

We employed the APP/PS1/tau 3 × Tg-AD mouse model for dietary selenium intervention. Behavioural experiments were conducted to assess learning and memory. Additionally, we measured selenium and GSH-Px levels in whole blood and brain tissue. Neuronal apoptosis in the hippocampus was observed using transmission electron microscopy. The expressions of Aβ, P-tau, BDNF, TrkB, and CREB were measured via RT-qPCR, while the expressions of Aβ, P-tau, BDNF, TrkB, p-CREB, and CREB were quantified using Western blot analysis.

Results

Our findings indicate that selenium supplementation can improve spatial learning and memory deficiencies in 3 × Tg-AD mice. Selenium supplementation increased selenium and GSH-Px levels in the brain tissue of 3 × Tg-AD mice and significantly enhanced neuronal conditions. Furthermore, the expression levels of proteins related to the BDNF/TrkB pathway significantly increased following selenium supplementation.

Conclusions

Our study demonstrates that selenium can ameliorate memory impairment in 3 × Tg-AD mice by activating the BDNF/TrkB pathway.
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硒通过激活BDNF/TrkB通路改善认知障碍。
背景:阿尔茨海默病(AD)是一种主要影响老年人的神经退行性疾病。硒是人体必需的微量元素,在人体正常的生理和代谢过程中起着至关重要的作用。长期缺乏硒会导致各种疾病,甚至会导致衰老过程。本研究旨在探讨硒对3 × Tg-AD小鼠认知功能障碍的改善作用,并确定其作用是否与BDNF/TrkB通路有关。方法:采用APP/PS1/tau 3 × Tg-AD小鼠模型对膳食硒进行干预。进行了行为实验来评估学习和记忆。此外,我们还测量了全血和脑组织中硒和GSH-Px的水平。透射电镜观察海马神经元凋亡。RT-qPCR检测Aβ、P-tau、BDNF、TrkB和CREB的表达,Western blot检测Aβ、P-tau、BDNF、TrkB、p-CREB和CREB的表达。结果:补充硒可以改善3 × Tg-AD小鼠的空间学习和记忆缺陷。补充硒可提高3 × Tg-AD小鼠脑组织中硒和GSH-Px水平,并显著改善神经元状况。此外,添加硒后,BDNF/TrkB通路相关蛋白的表达水平显著增加。结论:我们的研究表明硒可以通过激活BDNF/TrkB通路改善3 × Tg-AD小鼠的记忆障碍。
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来源期刊
CiteScore
6.60
自引率
2.90%
发文量
202
审稿时长
85 days
期刊介绍: The journal provides the reader with a thorough description of theoretical and applied aspects of trace elements in medicine and biology and is devoted to the advancement of scientific knowledge about trace elements and trace element species. Trace elements play essential roles in the maintenance of physiological processes. During the last decades there has been a great deal of scientific investigation about the function and binding of trace elements. The Journal of Trace Elements in Medicine and Biology focuses on the description and dissemination of scientific results concerning the role of trace elements with respect to their mode of action in health and disease and nutritional importance. Progress in the knowledge of the biological role of trace elements depends, however, on advances in trace elements chemistry. Thus the Journal of Trace Elements in Medicine and Biology will include only those papers that base their results on proven analytical methods. Also, we only publish those articles in which the quality assurance regarding the execution of experiments and achievement of results is guaranteed.
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