CXCR4型
神经保护
基因剔除小鼠
痴呆
趋化因子
疾病
趋化因子受体
医学
神经科学
海马体
阿尔茨海默病
下调和上调
免疫学
生物
受体
炎症
内科学
生物化学
基因
作者
Xueyan Huang,Lu‐Lu Xue,Ruifang Ma,Jingshan Shi,Ting‐Hua Wang,Liu‐Lin Xiong,Changyin Yu
标识
DOI:10.1016/j.expneurol.2024.114841
摘要
Alzheimer's disease (AD) is the most prevalent type of dementia, and its causes are currently diverse and not fully understood. In a previous study, we discovered that short-term treatment with miracle fruit seed (MFS) had a therapeutic effect on AD model mice, however, the precise mechanism behind this effect remains unclear. In this research, we aimed to establish the efficacy and safety of long-term use of MFS in AD model mice. A variety of cytokines and chemokines have been implicated in the development of AD. Previous studies have validated a correlation between the expression levels of C-X-C chemokine receptor type 4 (CXCR4) and disease severity in AD. In this research, we observed an upregulation of CXCR4 expression 1n hippocampal tissues in the AD model group, which was then reversed after MFS treatment. Moreover, CXCR4 knockout resulted in improved cognitive function in AD model mice, and MFS showed the ability to regulate CXCR4 expression. Finally, our findings indicate that CXCR4 knockout and long-term MFS treatment produce comparable effects in treating AD model mice. In conclusion, this research demonstrates that therapeutic efficacy and safety of long-term use in AD model mice. MFS treatment and the subsequent reduction of CXCR4 expression exhibit a neuroprotective role in the brain, highlighting their potential as therapeutic targets for AD.
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