奶油
莫里斯水上航行任务
海马体
突触可塑性
氧化应激
内分泌学
免疫印迹
化学
原肌球蛋白受体激酶B
标记法
磷酸化
内科学
细胞生物学
细胞凋亡
神经科学
生物
医学
神经营养因子
生物化学
受体
转录因子
基因
作者
Ying Zhang,Qian Zhou,Lu Lu,Yu Sui,Wujie Shi,Hu Zhang,Ran Liu,Yuepu Pu,Lihong Yin
出处
期刊:Nutrients
[MDPI AG]
日期:2023-02-15
卷期号:15 (4): 972-972
被引量:16
摘要
It has been reported that disordered Cu metabolism is associated with several neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD). However, the underlying mechanism is still unclear. In this study, 4-week-old male mice were exposed to Cu by free-drinking water for three months. Then, the effects of Cu on cognitive functions in mice were tested by Morris water maze tests, and the potential mechanisms were investigated by the ELISA, immunochemistry, TUNEL, and Western blot tests. It was found that Cu exacerbates learning and memory impairment, and leads to Cu-overload in the brain and urine of mice. The results showed that Cu induces neuronal degeneration and oxidative damage, promotes the expression of apoptosis-related protein Bax, cuproptosis-related proteins FDX1 and DLAT and the proteotoxic stress marker HSP70, and decreases Fe-S cluster proteins. In addition, Cu affects the pre-synaptic and post-synaptic regulatory mechanisms through inhibiting the expression of PSD-95 and SYP. Cu also suppresses phosphorylation levels in CREB and decreases the expression of BDNF and TrkB in the mouse hippocampus. In conclusion, Cu might mediate cuproptosis, damage synaptic plasticity and inhibit the CREB/BDNF pathway to cause cognitive dysfunction in mice.
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