Accumulation of Filamentous Tau in the Cerebral Cortex of Human Tau R406W Transgenic Mice
Open accessAbstract
Missense mutations of the tau gene cause autosomal dominant frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), an illness characterized by progressive personality changes, dementia, and parkinsonism. There is prominent frontotemporal lobe atrophy of the brain accompanied by abundant tau accumulation with neurofibrillary tangles and neuronal cell loss. Using a hamster prion protein gene expression vector, we generated several independent lines of transgenic (Tg) mice expressing the longest form of the human four-repeat tau with the R406W mutation associated with FTDP-17. The TgTauR406W 21807 line showed tau accumulation beginning in the hippocampus and amygdala at 6 months of age, which subsequently spread to the cortices and subcortical areas. The accumulated tau was phosphorylated, ubiquitinated, conformationally changed, argyrophilic, and sarcosyl-insoluble. Activation of GSK-3beta and astrocytic induction of mouse tau were observed. Astrogliosis and microgliosis correlated with prominent tau accumulation. Electron microscopic examination revealed the presence of straight filaments. Behavioral tests showed motor disturbances and progressive acquired memory loss between 10 to 12 months of age. These findings suggested that TgTauR406W mice would be a useful model in the study of frontotemporal dementia and other tauopathies such as Alzheimer's disease (AD).
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Tau deposition can be observed in the astrocyte nucleus in AD brain.
“Although tau primarily accumulates in neurons, tau deposition can also be observed in the astrocyte nucleus in AD brain [432, 433].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [432]
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- Authors
- Ikeda, M., Kawarai, T., Kawarabayashi, T., Matsubara, E., Murakami, T., Sasaki, A., Tomidokoro, Y., Ikarashi, Y., Kuribara, H., Ishiguro, K., Hasegawa, M., Yen, S.-H., Chishti, M. A., Harigaya, Y., Abe, K., Okamoto, K., St. George-Hyslop, P., Westaway, D., & Shoji†, M.
- Affiliations
- Gunma University (JP)
- University Health Network (CA)
- Okayama University (JP)
- Tsumura (Japan) (JP)
- Mitsubishi Chemical (Japan) (JP)
- Tokyo Institute of Psychiatry (JP)
- Mayo Clinic (US)
- Maebashi Red Cross Hospital (JP)
- Corresponding author
- Ikeda, Masaki
- ORCID
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2005-02
- Volume
- 166
- Issue
- 2
- Pages
- 521-531
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC1602315
- OpenAlex
- W2129830770
- Cited by
- 120
- References
- 51
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 3 · 2023: 6 · 2022: 1 · 2021: 6 · 2020: 8 · 2019: 7 · 2018: 2 · 2017: 6 · 2016: 8 · 2015: 4 · 2014: 6 · 2013: 6 · 2012: 7
- FWCI
- 5.82
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal Of Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer Society
- Ministry of Education, Culture, Sports, Science and Technology
- Howard Hughes Medical Institute
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- FTDP-17, tauopathy, transgenic mouse model, cerebral cortex, neurofibrillary tangles, tau phosphorylation, ubiquitination, GSK3β, astrocyte activation, microglial activation, motor disturbances, memory loss, Alzheimer's disease
- MeSH terms
- Glycogen Synthase Kinase 3 beta, Amygdala, Animals, Astrocytes, Behavior, Animal, Brain, Cerebral Cortex, Genetic Vectors, Cricetinae, Hippocampus, Humans, Mice, Transgenic, Microscopy, Electron, Mutation, Phosphorylation, Prions, Protein Conformation, Time Factors, Blotting, Western, tau Proteins, Microglia, Transgenes, Mutation, Missense, Reverse Transcriptase Polymerase Chain Reaction, Ubiquitin, Glycogen Synthase Kinase 3, Mice
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