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Inhibition of CXCR4: A perspective on miracle fruit seed for Alzheimer's disease treatment.
Huang, Xue-Yan; Xue, Lu-Lu; Ma, Rui-Fang; Shi, Jing-Shan; Wang, Ting-Hua; Xiong, Liu-Lin; Yu, Chang-Yin.
Affiliation
  • Huang XY; Department of Neurology, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, China.
  • Xue LL; State Key Laboratory of Biotherapy, Sichuan University, Chengdu, Sichuan, China.
  • Ma RF; School of Basic Medical Sciences, Kunming Medical University, Kunming, Yunnan, China.
  • Shi JS; Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Lab of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, China.
  • Wang TH; Department of Neurology, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, China. Electronic address: wangtinghua@vip.163.com.
  • Xiong LL; Department of Anesthesiology, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, China. Electronic address: liulin.xiong@mymail.unisa.edu.au.
  • Yu CY; Department of Neurology, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, China. Electronic address: yuchangyin6812@126.com.
Exp Neurol ; 379: 114841, 2024 Sep.
Article in En | MEDLINE | ID: mdl-38821198
ABSTRACT
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 the 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 in hippocampal tissues in the AD model group, which was then reversed after MFS treatment. Moreover, CXCR4 knockout led to improving 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 of MFS 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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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Receptors, CXCR4 / Alzheimer Disease Limits: Animals Language: En Journal: Exp Neurol Year: 2024 Type: Article Affiliation country: China

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Receptors, CXCR4 / Alzheimer Disease Limits: Animals Language: En Journal: Exp Neurol Year: 2024 Type: Article Affiliation country: China