ABO and Alzheimer disease: AβO‐induced immediate activation of NMDAR enhances mitochondrial Ca2+ accumulation in a mechanism involving endoplasmic reticulum (ER) Ca2+ release through inositol 1,4,5‐trisphosphate receptor (InsP3R) and mitochondrial depolarization (Ferreira et al., 2015), revealing increased susceptibility of glutamatergic synapses and mitochondrial dysfunction in AD.