To investigate if NHE6/Slc9a6 deficiency contributes to APP processing by BACE1 in neurons, we used primary neurons derived from AppSwe (Tg2576) mice, an Alzheimer’s disease (AD) mouse model that overexpresses human APP with the ‘Swedish’ mutation (Hsiao et al., 1996). The gene discussed is SLC9A6; the disease is early-onset autosomal dominant Alzheimer disease.