Age- and amyloid-β-dependent initiation of neurofibrillary tau tangles: an improved mouse model of Alzheimer's disease without mutations in MAPT .

Autor: Desai S; Department of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London, WC1E 6BT, United Kingdom.; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, 431 80, Sweden., Camporesi E; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, 431 80, Sweden., Brinkmalm G; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, 431 80, Sweden., Alatza A; Department of Neurodegenerative Disease, University College London Queen Square Institute of Neurology, London, WC1N 3BG, United Kingdom., Wood JI; Department of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London, WC1E 6BT, United Kingdom.; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, 431 80, Sweden., Tripathi T; Department of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London, WC1E 6BT, United Kingdom., Bez S; UK Dementia Research Institute, University College London, Gower Street, London, WC1E 6BT, United Kingdom., Stasyuk N; Department of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London, WC1E 6BT, United Kingdom., Hajar HB; Department of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London, WC1E 6BT, United Kingdom., Saito T; Department of Neurocognitive Science, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467-8601, Japan., Saido TC; Laboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan., Hardy J; Department of Neurodegenerative Disease, University College London Queen Square Institute of Neurology, London, WC1N 3BG, United Kingdom.; UK Dementia Research Institute, University College London, Gower Street, London, WC1E 6BT, United Kingdom., Cummings DM; Department of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London, WC1E 6BT, United Kingdom., Hanrieder J; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, 431 80, Sweden.; Department of Neurodegenerative Disease, University College London Queen Square Institute of Neurology, London, WC1N 3BG, United Kingdom., Edwards FA; Department of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London, WC1E 6BT, United Kingdom.
Jazyk: angličtina
Zdroj: BioRxiv : the preprint server for biology [bioRxiv] 2024 Nov 04. Date of Electronic Publication: 2024 Nov 04.
DOI: 10.1101/2024.11.04.621900
Abstrakt: 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.
Databáze: MEDLINE