Therefore, in order to determine how mis-expression of human mutant APP (Aβ42), MAPT (0N4R Tau), and Ank2 may lead to changes in neuronal function and AD relevant phenotypes, we expressed the genetically encoded Ca2+ reporter, GCaMP6f using the same OK107-Gal4 MB promoter as for the memory experiments and then measuring peak intracellular Ca2+ in response to high [K+] solution that non-specifically depolarizes neurons (Malik et al., 2013). This evidence concerns the gene LGALS4 and Alzheimer disease.