In attempts to convert adult human fibroblasts to neurons, another group turned to using the 5 factors that we initially found in mouse to be the most critical of the 19 tested candidate factors. The resulting cells possessed a series of neuronal properties including certain functional properties such as the ability to generate action potentials when depolarized (Qiang et al., 2011). The acquisition of more mature functional properties such as synaptic transmission was less clear. This observation is similar to ours when adult fibroblasts were infected with BAM and Neurod1 (Pang et al., 2011). Nevertheless, iN cells were generated from Familial Alzheimer’s Disease (FAD) patients with mutations in PRESENELIN genes and were found to exhibit disease-specific traits, providing important proof-of-concept that iN cells can be used to model human disease. Specifically, the FAD-iN cells showed the presence of amyloid precursor protein (APP) puncta in endosomes, which was not readily detected in the originating FAD fibroblasts. This phenotype could be rescued by overexpression of wild-type PRESENELIN1. Of note, one of the reprogramming factors used in this study is Olig2, another member
