SynthesisFrontiers in pharmacology2026
Efficacy and possible mechanism of
Synthesis in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Context: Alzheimer's disease (AD) is the most common neurodegenerative disorder, which is associated with impaired cognition. Objectives: This study aimed to investigate the therapeutic potential and underlying mechanisms of KXS for AD. Methods: A systematic search of 7 databases was conducted from inception to October 2025, with language restrictions in both Chinese and English. Behavior and biomarkers were assessed as measures of efficacy and mechanism. The risk of bias was assessed by the SYRCLE's risk of bias tool. The meta-analysis was performed by STATA version 15.0 software packages and RevMan 5.4 software. Subgroup, meta-regression, and sensitivity analyses were used to ascertain the robustness of primary analyses, Egger's test and funnel plots were used to assess potential publication bias, and the evidence of evidence was assessed by the modified GRADE approach. Results: This study included 44 studies, involving a total of 2,681 animals, 3 behavioral tests, such as Morris water maze (MWM), novel object recognition (NOR), Y maze, and 9 biomarkers, such as β-amyloid peptide (Aβ), tau protein, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), malondialdehyde (MDA), superoxide dismutase (SOD), acetylcholinesterase (AchE), and acetylcholine (ACh). KXS could significantly shorten escape latency from the target quadrant, and elevate entry frequency into the target quadrant and time spent in the target quadrant in MWM; meanwhile, KXS could also significantly enhance the relative recognition index in NOR, and improve spontaneous alternation performance in Y-maze. Moreover, KXS could decrease Aβ, tau and AchE in the hippocampus, and TNF-α, IL-1β, IL-6, and MDA in both serum and hippocampus, while increase ACh in the hippocampus and SOD in both serum and hippocampus. Conclusion: These findings suggest that KXS may alleviates cognitive deficits in AD animal models, which may be attributed to its modulation of multiple mechanisms, including Aβ and tau pathology, inflammation, oxidative stress, and cholinergic function. However, due to the high risk of bias, indicating that the true effects of KXS may be smaller than those reported. Therefore, high-quality preclinical studies are essential before clinical efficacy can be considered.
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Registered trials
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.