Notably, the downregulation of BACE1-AS in an AD mouse model lowers the amyloid-β levels and ameliorates adult neurogenesis while reduced levels of SMN1-AS increases the transcription of SMN2 gene in patient-derived cells, in SMA neurons, and in a mouse model of severe SMA (Modarresi et al., 2011; d’Ydewalle et al., 2017). Here, SMN1 is linked to Alzheimer disease.