Age and amyloidβ-dependent initiation of neurofibrillary tau tangles: an improved mouse model of Alzheimers disease without mutations in MAPT.
Desai, S.; Camporesi, E.; Brinkmalm, G.; Alatza, A.; Wood, J. I.; Tripathi, T.; Bez, S.; Stasyuk, N.; Hajar, H. B.; Saito, T.; Saido, T. C.; Hardy, J.; Cummings, D. M.; Hanrieder, J.; Edwards, F. A.
Show abstract
Introducing heterozygous humanized tau to AppNL-F/NL-F knock-in mice results in the first mouse model of Alzheimers disease in which age and amyloid-{beta} pathology interact to initiate neurofibrillary tau tangle pathology, not dependent on mutations in MAPT. Gradual progression from amyloid-{beta} to tau pathology in NLFTaum/h mice opens possibilities for understanding processes precipitating clinical stages of Alzheimers disease and development of translatable therapies to prevent the onset of tau pathology.
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