Since the most prominent molecular pathology of AD is the neurotoxicity of aggregate Aβ and hyperphosphorylated tau protein, which jointly damage neurons and ultimately lead to cognitive decline, we performed immunofluorescence staining to assess whether hDPSCs had modified their progression.1 The results revealed that the pathological Aβ aggregation and the expression of phosphorylated Tau protein (AT8) in the hippocampus of hDPSCs-treated AD mice were much lesser than those in AD-PBS mice (Fig. 6c, d). Here, MAPT is linked to Alzheimer disease.