SynthesisBMC neurology2025
Neuroprotection through adiponectin receptor agonist: an updated meta-analysis of preclinical Alzheimer's disease studies.
Synthesis in BMC neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Vitamin D and L-Cysteine as Potential Regulators of Adiponectin in Alzheimer's Disease: A Narrative Review.Nutrients · 2026Review
- Plasma and CSF adiponectin levels in biomarker-confirmed Alzheimer's disease: A cross-sectional study in a tertiary memory clinic.Metabolic brain disease · 2026Article
- Adipokines at the Metabolic-Brain Interface: Therapeutic Modulation by Antidiabetic Agents and Natural Compounds in Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlzheimer’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.
methodsA 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.
resultsSix 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.
conclusionBased 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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.