Extracellular aggregation of β-amyloid peptides (Aβ) and hyperphosphorylated tau protein (neurofibrillary tangles) may be the most important causes of neural degeneration in Alzheimer’s disease (AD).1 Moreover, accumulating data have implied that deregulated calcium signaling may have an important contribution to the neural cell death in AD.2 Interestingly, altered intracellular calcium homeostasis emerges earlier than neuropathological abnormalities observed in AD.3 This evidence concerns the gene MAPT and Alzheimer disease.