The recent findings from Alzheimer’s disease mouse models revealed that lentiviral vector-mediated overexpression of NEUROG2 and ASCL1 can ameliorate learning and memory impairment, and the ASCL1gene treatment could be linked to inhibition of the neuroinflammatory response and enhancement of neuroprotection and neurogenesis [31]. This evidence concerns the gene NEUROG2 and early-onset autosomal dominant Alzheimer disease.