数据日期 2026-10-29 · 生成时间 2026-10-29 06:03
研究问题
A variety of evidence now supports two interrelated hypotheses concerning Alzheimer's disease (AD) neurofibrillary pathology (NFT), its prevention and treatment.
方法
In this review, we focus our discussion on its ability to dephosphorylate the glycogen synthase kinase 3s (α and β) in ways that downregulate their activities (below).；The p value for this association survived conservative, Bonferroni correction for the large number of repeated comparisons in this study.；Early in the process of developing this structure–activity relationship, we conducted in silico molecular docking studies with quercetin and the best available molecular model for PTPRD’s phosphatase [13].
核心结论
Much of this effect of PTPRD is likely to result from its role in modulating the neuronal activities of the key tau hyperphosphorylating kinases, glycogen synthase kinase 3s (GSK3 α and β) [13].；In this review, we focus our discussion on its ability to dephosphorylate the glycogen synthase kinase 3s (α and β) in ways that downregulate their activities (below).；Common PTPRD allelic variation thus provides the second strongest genetic influence on the densities of neurofibrillary tangles in a strong GWAS study and confers about 50% individual differences in levels of brain PTPRD expression. ‖ 结论：We review the convergence of evidence from human, mouse, in vitro and in silico studies that enhances the likely translational relevance of these hypotheses.
局限
全文未设独立 limitations 节；结构上为综述/二次研究，因果推断强度受限。
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。队列：FHS；最大样本量约 119；设计 Meta 分析、观察性。
全文来源
PMC JATS 全文（正文 45,209 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：Alzheimer's Disease Neurofibrillary Pathophysiology: PTPRD- and Flavonol-Modified Mechanisms, Prevention and Therapeutics.
- 期刊与标识：Biomedicines · PMID 42940016 · DOI 10.3390/biomedicines14102210**
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