Age- and amyloid-β-dependent initiation of neurofibrillary tau tangles: an improved mouse model of Alzheimer’s disease without mutations in MAPT
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Introducing heterozygous humanized tau to App NL-F/NL-F knock-in mice results in the first mouse model of Alzheimer’s disease in which age and amyloid-β pathology interact to initiate neurofibrillary tau tangle pathology, not dependent on mutations in MAPT. Gradual progression from amyloid-β to tau pathology in NLFTau m/h mice opens possibilities for understanding processes precipitating clinical stages of Alzheimer’s disease and development of translatable therapies to prevent the onset of tau pathology.
