Park et al. (2019) used a CRISPR-Cas9 nanoparticle complex that effectively crossed the blood–brain barrier (BBB), entered neurons in adult mice, and produced high-frequency indels at target sites in the BACE1 gene, thereby reducing BACE1 expression and activity. This alleviated Aβ-related pathology and cognitive deficits in two AD mouse models (5XFAD and APP knock-in). Singer et al. (2005) used a lentiviral vector expressing siRNA targeting BACE1 to reduce BACE1 levels, thereby decreasing amyloid production as well as neurodegenerative and behavioral deficits in APP transgenic mice. Here, BACE1 is linked to Alzheimer disease.