For example, Keskin et al. applied histochemistry, in vivo Ca2+ imaging and behavioral analyses in APP23xPS45 transgenic mice, and demonstrated that BACE inhibition is beneficial to all levels of impairment in the AD mouse model, i.e., inhibition rescued hyperactivity of neurons, impairment of long-range circuitry, and memory defects [34]. This evidence concerns the gene BACE1 and Alzheimer disease.