Scholarlink

Background <p>Alzheimer’s disease (AD) is a leading cause of dementia, imposing a substantial burden on individuals and society. While existing therapies can reduce the symptoms of AD, they do not offer genuine therapeutic effectiveness. Adiponectin Receptor Agonist (ADN-R Ag) has been proposed as a novel therapeutic agent for AD. This study aims to evaluate its efficacy in treating AD model mice.</p> Methods <p>A systematic search of PubMed, Scopus, Cochrane Library, and Web of Science was conducted up to May 3, 2025. Research investigating the impact of ADN-R Ag on cognitive performance and associated molecular pathways in Alzheimer’s disease models, specifically APP/PS1, P301S, and 5XFAD mice, was incorporated. The Alzheimer’s disease models in the study were male and ranged in age from 5.5 to 8 months. Studies evaluating the effect of ADN-R Ag on AD model mice through cognitive function tests and related molecular mechanisms were included. Methodological quality assessment was performed using the CAMARADES tool for animal studies. The meta-analysis was performed following Cochrane guidelines.</p> Results <p>Six articles were included for the review. ADN-R Ag significantly improved cognitive function in the meta-analysis. The weighted mean difference of ADN-R Ag was 21.75 (95% CI: 16.61–26.88; <i>p</i> &lt; 0.001) for alternation rate percentage in the Y-maze, 20.46 (95% CI: 11.41–29.51, <i>p</i> &lt; 0.001) for novel object exploration time percentage in the novel object recognition (NOR) test, -15.83 (95% CI: -23.33 to -8.32, <i>p</i> &lt; 0.001) for escape latency in the Morris water maze (MWM), and 13.89 (95% CI: 8.84–18.94; <i>p</i> &lt; 0.001) for target quadrant time in the probe test. Additionally, ADN-R Ag was reported to mitigate AD pathology by reducing Aβ depositions through inhibition of GSK3β/BACE1/NF-κB pathway, suppressing neuronal inflammation by suppressing microglial and astrocytes activity and reducing and IL1β and TNFα levels, enhancing autophagy, and improving mitochondrial function with significant involvement of the AMPK pathway.</p> Conclusion <p>Based on the current study, ADN-R Ag has therapeutic effects on AD. However, considering the complex underlying molecular mechanisms and limited prior studies, further research is needed.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Neuroprotection through adiponectin receptor agonist: an updated meta-analysis of preclinical Alzheimer’s disease studies

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年8月4日

查看全文
  • Tannaz Novinbahador,
  • Amin Abbasi,
  • Roghayeh Molani-Gol,
  • Leili Aghebati-Maleki,
  • Amirhesam Pouraghaei,
  • Hassan Soleimanpour

摘要

Background

Alzheimer’s disease (AD) is a leading cause of dementia, imposing a substantial burden on individuals and society. While existing therapies can reduce the symptoms of AD, they do not offer genuine therapeutic effectiveness. Adiponectin Receptor Agonist (ADN-R Ag) has been proposed as a novel therapeutic agent for AD. This study aims to evaluate its efficacy in treating AD model mice.

Methods

A systematic search of PubMed, Scopus, Cochrane Library, and Web of Science was conducted up to May 3, 2025. Research investigating the impact of ADN-R Ag on cognitive performance and associated molecular pathways in Alzheimer’s disease models, specifically APP/PS1, P301S, and 5XFAD mice, was incorporated. The Alzheimer’s disease models in the study were male and ranged in age from 5.5 to 8 months. Studies evaluating the effect of ADN-R Ag on AD model mice through cognitive function tests and related molecular mechanisms were included. Methodological quality assessment was performed using the CAMARADES tool for animal studies. The meta-analysis was performed following Cochrane guidelines.

Results

Six articles were included for the review. ADN-R Ag significantly improved cognitive function in the meta-analysis. The weighted mean difference of ADN-R Ag was 21.75 (95% CI: 16.61–26.88; p < 0.001) for alternation rate percentage in the Y-maze, 20.46 (95% CI: 11.41–29.51, p < 0.001) for novel object exploration time percentage in the novel object recognition (NOR) test, -15.83 (95% CI: -23.33 to -8.32, p < 0.001) for escape latency in the Morris water maze (MWM), and 13.89 (95% CI: 8.84–18.94; p < 0.001) for target quadrant time in the probe test. Additionally, ADN-R Ag was reported to mitigate AD pathology by reducing Aβ depositions through inhibition of GSK3β/BACE1/NF-κB pathway, suppressing neuronal inflammation by suppressing microglial and astrocytes activity and reducing and IL1β and TNFα levels, enhancing autophagy, and improving mitochondrial function with significant involvement of the AMPK pathway.

Conclusion

Based on the current study, ADN-R Ag has therapeutic effects on AD. However, considering the complex underlying molecular mechanisms and limited prior studies, further research is needed.