ID3 and early-onset autosomal dominant Alzheimer disease: Altogether, our demonstration that the overexpression of NeuroD2 or the silencing of Id3 is able to restore a condition of defective differentiation is critical as it points to the possibility to use these targets to treat neurodegenerative diseases where defects of terminal differentiation of new dentate gyrus neurons occur, such as in Alzheimer’s disease, as we have previously proposed (Tirone et al., 2013).