Tau prion strains dictate patterns of cell pathology, progression rate, and regional vulnerability in vivo
Open accessAbstract
Tauopathies are neurodegenerative disorders that affect distinct brain regions, progress at different rates, and exhibit specific patterns of tau accumulation. The source of this diversity is unknown. We previously characterized two tau strains that stably maintain unique conformations in vitro and in vivo, but did not determine the relationship of each strain to parameters that discriminate between tauopathies such as regional vulnerability or rate of spread. We have now isolated and characterized 18 tau strains in cells based on detailed biochemical and biological criteria. Inoculation of PS19 transgenic tau (P301S) mice with these strains causes strain-specific intracellular pathology in distinct cell types and brain regions, and induces different rates of network propagation. In this system, strains alone are sufficient to account for diverse neuropathological presentations, similar to those that define human tauopathies. Further study of these strains can thus establish a structural logic that governs these biological effects.
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Tau forms strains, defined assembly conformations that propagate faithfully in vivo, creating unique transmissible pathologies.
“Tau also forms strains, which are defined assembly conformations that propagate faithfully in vivo, creating unique transmissible pathologies (Sanders et al., 2014; Kaufman et al., 2016).”
From Spontaneous pathology in PS19 tauopathy mice progresses via brain networks (2025) · cites this paper as Kaufman et al., 2016
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- Authors
- Kaufman, S. K., Sanders, D. W., Thomas, T. L., Ruchinskas, A. J., Vaquer-Alicea, J., Sharma, A. M., Miller, T. M., & Diamond, M. I.
- Affiliations
- Washington University in St. Louis (US)
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Diamond, Marc I.
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2016-11
- Volume
- 92
- Issue
- 4
- Pages
- 796-812
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC5392364
- OpenAlex
- W2545421204
- Cited by
- 450
- References
- 11
- Citations by year
- 2026: 28 · 2025: 45 · 2024: 34 · 2023: 46 · 2022: 42 · 2021: 52 · 2020: 55 · 2019: 58 · 2018: 52 · 2017: 35 · 2016: 3
- FWCI
- 39.73
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH/NIA (F30AG048653, R01AG048678)
- NIH (F31NS086251)
- NIH/NINDS (R01NS071835)
- Tau Consortium
- Cure Alzheimer’s Fund
- Hope Center Alafi Neuroimaging Laboratory at Washington University in St. Louis
- Neuro-Models Facility
- Whole Brain Microscopy Facility
- Moody Foundation Flow Cytometry Facility
- High Throughput Screening Core at University of Texas Southwestern
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- tauopathy, tau conformation, regional vulnerability, disease progression rate, network propagation, P301S tau, cell type specificity, neurodegeneration
- MeSH terms
- Prion Proteins, Animals, Brain, Humans, Mice, Transgenic, tau Proteins, Disease Progression, Tauopathies, Mice, HEK293 Cells
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