Following the hypothesis that PrPC-Aβ interaction could be crucial for AD-related neuronal impairment (Laurén et al., 2009; Um and Strittmatter, 2013), we investigated whether soluble Aβ(1–42) oligomers (Supplementary Figure 5) perturb the control of PrPC over SOCE by monitoring PM Ca2+ transients. Here, PRNP is linked to Alzheimer disease.