Age- and amyloid-β-dependent initiation of neurofibrillary tau tangles: an improved mouse model of Alzheimer’s disease without mutations inMAPT

Abstract

Introducing heterozygous humanized tau toAppNL-F/NL-Fknock-in mice results in the first mouse model of Alzheimers disease in which age and amyloidβ pathology interact to initiate neurofibrillary tau tangle pathology, not dependent on mutations inMAPT. Gradual progression from amyloidβ to tau pathology in NLFTaum/hmice opens possibilities for understanding processes precipitating clinical stages of Alzheimers disease and development of translatable therapies to prevent the onset of tau pathology.