PSEN1 and familial Alzheimer disease: In particular, whereas the role of FAD-linked PS1 and PS2 mutations at the store level was debated [18], the large majority of data converge towards SOCE downregulation, when studied either in cell lines expressing the PS1/2 mutants or in fibroblasts from FAD patients [6,9,10,11,12,13,16,19,20,21,46] as well as in SAD [10,70].