NLRP3 and Alzheimer disease: Because the mentioned above NLRP3 inflammasome is overtly activated in AD patients as well as in mouse models of the disease and its inhibition was identified as a new therapeutic target for treating both neuronal and microglial dysfunction in AD (33, 51), we hypothesize that caloric restriction has a potential to alleviate the consequences of amyloid ß deposition in mice and humans.