Experimental evidence (decreased TRPC6 mRNA expression in AD patient samples, improved cognitive function, and increased excitatory synapse formation in mice that overexpress TRPC6 as well as synaptoprotective properties of positive TRPC6 modulators) suggest that TRPC6 is the preferred molecular target in comparison to STIM2 and ORAI2. This evidence concerns the gene STIM2 and Alzheimer disease.