Fessel Jeffrey
Department of Medicine University of California San Francisco California USA.
Alzheimers Dement (N Y). 2020 May 6;6(1):e12019. doi: 10.1002/trc2.12019. eCollection 2020.
If it is correct that ineffective levels of transforming growth factors beta and their receptor account for old age being a risk factor for Alzheimer's disease (AD), then increasing TGFBR2 might be therapeutic. Pacltaxel is a direct way to increase TGFBR2 levels. Indirect ways that will increase TGFBR2, include decreasing the levels of c-myc because that will lower the miRNA cluster 17-92, particularly its miR-17 and miR-20a components; and raising EGFR because that also will increase TGFBR2. Metformin and desferrioxamine are drugs that decrease c-myc; and statins increase levels of EGF. Clinical trials using those drugs, would demonstrate whether they decrease the progression from amnestic mild cognitive impairment to AD.
如果转化生长因子β及其受体水平不足导致老年成为阿尔茨海默病(AD)的危险因素这一观点正确,那么增加转化生长因子β受体2(TGFBR2)可能具有治疗作用。紫杉醇是增加TGFBR2水平的直接方法。增加TGFBR2的间接方法包括降低c-myc水平,因为这会降低miRNA簇17-92的水平,尤其是其miR-17和miR-20a成分;以及提高表皮生长因子受体(EGFR)水平,因为这也会增加TGFBR2。二甲双胍和去铁胺是降低c-myc的药物;他汀类药物可提高表皮生长因子(EGF)水平。使用这些药物的临床试验将证明它们是否能减缓从遗忘型轻度认知障碍发展为AD的进程。