By constructing an AD mouse model with OLs deficient in BACE1, it was found that BACE1-deficient mice had significantly fewer Aβ plaques in the visual cortex, post-splenial cortex, and motor cortex compared to controls, particularly in cortical layers V and VI, a region highly susceptible to early plaque deposition and cognitive decline in AD [84]. This evidence concerns the gene BACE1 and Alzheimer disease.