AppNLGF mice harbour three familial Alzheimer’s disease mutations, Swedish (NL), Arctic (G) and Beyreuther/Iberian (F) and exhibit cognitive deficits and neuroinflammation accompanied by progressive Aβ pathology in the brain parenchyma, whereas AppNL mice carry only the Swedish (NL) mutation and overproduce human Aβ without the formation of Aβ plaques for up to 24 months.33,34 Neither AppNLGF nor AppNL mice develop NFTs or neuropil threads composed of tau aggregates, suggesting that these mouse models recapitulate the preclinical stage of Alzheimer’s disease. The gene discussed is MAPT; the disease is Alzheimer disease.