RYR2 and Alzheimer disease: In accord with the idea that GSH elevation could be a therapeutic strategy in AD treatment (Pocernich and Butterfield, 2012), we propose that the restoration of cellular oxidative tone induced by NAC is essential to counteract the oxidative stress induced by AβOs-injections, which is likely to promote non-physiological oxidation of redox-sensitive proteins, such as the RyR2 channels, which contribute to the memory deficits induced by AβOs.