Inhibition of CXCR4: A perspective on miracle fruit seed for Alzheimer's disease treatment

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
出处
期刊:Experimental Neurology [Elsevier BV]
卷期号:379: 114841-114841 被引量:3
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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