Analysis of tauopathies with transgenic mice
Abstract
Intraneuronal filamentous inclusions composed of the microtubule-associated protein tau are a feature of several neurodegenerative diseases (including Alzheimer's disease) known as tauopathies. A pivotal finding was the identification in 1998 of mutations in tau associated with frontotemporal dementia with parkinsonism linked to chromosome 17. This demonstrated that tau dysfunction is sufficient to cause neurodegeneration, and indicated that tau is likely to play a crucial role in the pathogenesis of other tauopathies. However, the mechanism by which tau filamentous lesions form and their role in neurodegeneration remains uncertain. Recent progress in the development of transgenic mouse models of human tauopathy is allowing these questions to be addressed.
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Mouse models over-expressing WT or mutant tau develop robust tau pathologies.
“These models develop robust tau pathologies, including pathologically phosphorylated, misfolded, oligomeric and/or fibrillar forms of tau pathology.”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Hutton et al., 2001
Cites
Association of missense and 5′-splice-site mutations in tau with the inherited dementia FTDP-17
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Self-citationThe microtubule binding domain of tau protein
Lee, G., Neve, R. L., & Kosik, K. S. (1989) · Neuron · doi:10.1016/0896-6273(89)90050-0 · Cited by 500 · see citing works
Tau filament formation in transgenic mice expressing P301L tau
Götz, J., Chen, F., Barmettler, R., & Nitsch, R. M. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m006531200 · Cited by 495 · see citing works
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Animal models of neurodegenerative diseases
Dawson, T. M., Golde, T. E., & Lagier-Tourenne, C. (2018) · Nature Neuroscience · doi:10.1038/s41593-018-0236-8 · Cited by 576 · see citing works
Neuroprotective effects of curcumin
Cole, G. M., Teter, B., & Frautschy, S. A. (2007) · ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY · doi:10.1007/978-0-387-46401-5_8 · Cited by 516 · see citing works
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- Authors
- Hutton, M., Lewis, J., Dickson, D., Yen, S.-H., & McGowan, E.
- Affiliations
- Mayo Clinic in Florida (US)
- Corresponding author
- Hutton, Mike
- Venue
- Trends in Molecular Medicine
- Publisher
- Elsevier BV
- Published
- 2001-10
- Volume
- 7
- Issue
- 10
- Pages
- 467-470
- ISSN
- 1471-4914 (ISSN-L)
- OpenAlex
- W2091798758
- Cited by
- 91
- References
- 3
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 5 · 2021: 3 · 2020: 3 · 2019: 1 · 2018: 2 · 2017: 1 · 2016: 1 · 2013: 4 · 2012: 1
- FWCI
- 0.92
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Trends in Molecular Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- tauopathy, tau protein, transgenic mouse model, neurodegeneration, frontotemporal dementia with parkinsonism, Alzheimer's disease, tau mutations
- MeSH terms
- Animals, Disease Models, Animal, Mice, Transgenic, Microtubule-Associated Proteins, Neurofibrils, Up-Regulation, tau Proteins, Protein Serine-Threonine Kinases, Transgenes, Tauopathies, Glycogen Synthase Kinase 3, Mice
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