数据日期 2026-10-29 · 生成时间 2026-10-29 06:03
研究问题
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia worldwide [1,2,3].
方法
This analysis was performed to assess the external support of computational target prediction rather than to confirm all predicted interactions.；This network included the two bile acids, their respective AD-intersecting targets, significantly enriched KEGG pathways, and the disease node (AD).；Known inhibitors or activators were not included as reference ligands because the objective of this study was to compare the predicted interaction patterns of UDCA and TUDCA under a consistent docking framework rather than to evaluate competitive binding against established pharmacological modulators.；Trajectory analyses included root-mean-square deviation (RMSD), root-mean-square fluctuation (RMSF), radius of gyration (Rg), solvent accessible surface area (SASA), ligand RMSD, hydrogen-bond analysis, and MM/GBSA binding free energy calculations.
核心结论
结论：This study was designed to compare the predicted AD-related mechanisms of UDCA and TUDCA from the perspectives of target overlap, pathway preference, and representative ligand–target binding.
局限
These predicted structural interactions were consistent with the enrichment patterns observed in nuclear receptor-associated functions; however, docking results alone cannot establish target preference or functional regulation [21,22].；Therefore, whether their distinct molecular profiles translate into any beneficial interaction when used in combination remains to be determined experimentally [11,22,23,27].；Although both UDCA and TUDCA have been discussed in the literature for their neuroprotective potential, the present computational analysis does not establish the extent to which either compound reaches the central nervous system in vivo.
对本项目的价值
★★☆☆☆ 脑老化是最大未满足需求，也是终点最难量化的领域；biomarker 与认知读数选择最敏感。设计 多组学。
全文来源
PMC JATS 全文（正文 60,648 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：Comparative Network Pharmacology and Molecular Docking Analysis of Ursodeoxycholic Acid and Tauroursodeoxycholic Acid in Alzheimer's Disease-Associated Molecular Networks.
- 期刊与标识：Pharmaceuticals (Basel) · PMID 42943209 · DOI 10.3390/ph19101512**
B 级证据分级：B 级（同行评议临床前研究，主要为动物模型）
本文核心结论来自动物模型或体外细胞学，属临床前证据，不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义，与人类临床结局之间仍有距离。
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