To date, two strategies have been proposed for the pharmacological modulation of TRPC6 activity for the treatment of Alzheimer’s disease and cerebral ischemia: (1) TRPC6 activation to allow Ca2+ influx via neuronal SOCE and sustain the stability of postsynaptic contacts (for AD) and to attenuate NMDAR activity and prevent calcium-dependent excitotoxicity [15,16] (for ischemia); (2) inhibition of TRPC6 in order to prevent calcium overload and the subsequent cell damage [23,64] (for AD and ischemia). This evidence concerns the gene TRPC6 and ischemia.