SMAD1 and Alzheimer disease: Additionally, studies on a series of 18 hiPSC lines obtained from sAD and fAD patients and from healthy controls evidenced alterations in the differentiation of the AD-derived lines when senescence was induced; in this case, AD-hiPSCs showed an impaired potential to differentiate into neurons and oligodendrocytes and increased differentiation to astrocytes; this was associated with BMP4 hypersecretion and activation of the SMAD1/5/9-RUNX2 signaling pathway [83].