TRPM2 and endothelial dysfunction: Iadecola’s group first showed that amyloid β1-40 (Aβ1-40), whose extracellular accumulation on brain microvessels is now regarded as the primary trigger of the pathogenic pathways leading to neuronal damage and dementia [294], may induce endothelial dysfunction by promoting TRPM2-mediated cytosolic Ca2+ overload [38].