BMP4-SMAD1/5/9-RUNX2 pathway activation inhibits neurogenesis and oligodendrogenesis in Alzheimer’s patients’ iPSCs in senescence-related conditions

(Stem Cell Reports 18, 688–705; March 14, 2023) The originally published version of Table S1 contained a few minor errors as follows: (1) one of the iPSC lines was mistakenly written as “HPS3636” when it should have appeared as “HPS3676” instead, (2) one of the exogenes in the HPS1745 and HPS1747 iPSC lines was incorrectly listed as “mp53DD” when “p53 shRNA” should have been listed instead, and (3) the sex of the AG25367 iPSC line was erroneously stated as “Male” when “Female” should have been stated instead. All of these errors in Table S1 have now been corrected, and the authors sincerely apologize for these mistakes. BMP4-SMAD1/5/9-RUNX2 pathway activation inhibits neurogenesis and oligodendrogenesis in Alzheimer’s patients’ iPSCs in senescence-related conditionsNakatsu et al.Stem Cell ReportsFebruary 9, 2023In BriefRecent studies demonstrated the defects in neurogenesis in AD brains. Nakatsu et al. created a neuronal differentiation system in which sporadic and familial AD-derived iPSCs showed neurogenesis inhibition. They demonstrated that SMAD1/5/9 activation in AD iPSCs, which was induced by enhanced BMP4 secretion, inhibited neurogenesis and oligodendrogenesis via RUNX2 expression regulation while enhancing astrocyte differentiation. Full-Text PDF Open Access