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P301S Mutant Human Tau Transgenic Mice Manifest Early Symptoms of Human Tauopathies with Dementia and Altered Sensorimotor Gating
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Tauopathies are neurodegenerative disorders characterized by the accumulation of abnormal tau protein leading to cognitive and/or motor dysfunction. To understand the relationship between tau pathology and behavioral impairments, we comprehensively assessed behavioral abnormalities in a mouse tauopathy model expressing the human P301S mutant tau protein in the early stage of disease to detect its initial neurological manifestations. Behavioral abnormalities, shown by open field test, elevated plus-maze test, hot plate test, Y-maze test, Barnes maze test, Morris water maze test, and/or contextual fear conditioning test, recapitulated the neurological deficits of human tauopathies with dementia. Furthermore, we discovered that prepulse inhibition (PPI), a marker of sensorimotor gating, was enhanced in these animals concomitantly with initial neuropathological changes in associated brain regions. This finding provides evidence that our tauopathy mouse model displays neurofunctional abnormalities in prodromal stages of disease, since enhancement of PPI is characteristic of amnestic mild cognitive impairment, a transitional stage between normal aging and dementia such as Alzheimer's disease (AD), in contrast with attenuated PPI in AD patients. Therefore, assessment of sensorimotor gating could be used to detect the earliest manifestations of tauopathies exemplified by prodromal AD, in which abnormal tau protein may play critical roles in the onset of neuronal dysfunctions.
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“The presence of spatial memory deficits in the PS19 line is controversial, with some studies pointing towards the development of deficits in the MWM test from a relatively young age of 5 [28] or 6.5 months [41], while others report initial deficits in spatial memory at 10 [42] or even 12 months of age [29], respectively.”
From Characterization of a Mouse Model of Alzheimer’s Disease Expressing Aβ4-42 and Human Mutant Tau (2021) · cites this paper as [28]
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“This is consistent with a hyperactivity phenotype in 6-month-old PS19 mice, presenting with better, albeit not statistically significant, performance on the rotarod compared to WT control animals [28].”
From Characterization of a Mouse Model of Alzheimer’s Disease Expressing Aβ4-42 and Human Mutant Tau (2021) · cites this paper as [28]
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“Both models rely on transgene overexpression and familial mutations (such as ADAD mutations in 5xFAD mice and frontotemporal dementia mutations in PS19 mice) and are not well suited for studying the causative events that lead to the development of pathology in sporadic AD [44–47].”
From APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology (2025) · cites this paper as [46]
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“Although behavioral and electrophysiological deficits have been reported in the PS19 line at the ages assessed in our study (Yoshiyama et al., 2007, Takeuchi et al., 2011, Briggs et al., 2017, Chalermpalanupap et al., 2018), we did not observe robust differences in spine density when PS19 mice were compared to NTG littermates.”
From Dendritic Spine Remodeling and Synaptic Tau Levels in PS19 Tauopathy Mice (2021) · cites this paper as Takeuchi et al., 2011
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Cognitive Disorders: Impairment, Aging, and Dementia
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Metadata
- Authors
- Takeuchi, H., Iba, M., Inoue, H., Higuchi, M., Takao, K., Tsukita, K., Karatsu, Y., Iwamoto, Y., Miyakawa, T., Suhara, T., Trojanowski, J. Q., Lee, V. M. Y., & Takahashi, R.
- Affiliations
- Kyoto University (JP)
- Hospital of the University of Pennsylvania (US)
- National Institute of Radiological Sciences (JP)
- National Institute for Physiological Sciences (JP)
- Fujita Health University (JP)
- Corresponding author
- Inoue, Haruhisa
- ORCID
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2011-06-15
- Volume
- 6
- Issue
- 6
- Pages
- e21050
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3115982
- OpenAlex
- W2158765009
- Cited by
- 247
- References
- 65
- Citations by year
- 2026: 27 · 2025: 36 · 2024: 24 · 2023: 18 · 2022: 24 · 2021: 24 · 2020: 21 · 2019: 13 · 2018: 7 · 2017: 11 · 2016: 9 · 2015: 11 · 2014: 13 · 2013: 5 · 2012: 3
- FWCI
- 4.80
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by-nc-nd)
- QST-Repository (National Institutes for Quantum and Radiological Science and Technology) (submittedVersion)
- Kyoto University Research Information Repository (Kyoto University) (submittedVersion, cc-by)
- Funders
- National Institutes of Health (AG 10 124)
- Japan Society for the Promotion of Science (22700338, 23390235, 21300121)
- Japan Science and Technology Agency
- RIKEN
- National Institute on Aging (P30AG010124, P01AG017586, AG17586, AG-10124)
- RIKEN Brain Science Institute
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- tauopathy, transgenic mouse model, dementia, sensorimotor gating, prepulse inhibition, prodromal Alzheimer's disease, amnestic mild cognitive impairment, behavioral abnormalities, early disease detection, cognitive impairment
- MeSH terms
- Animals, Dementia, Disease Models, Animal, Humans, Mice, Transgenic, tau Proteins, Maze Learning, Mice, Sensory Gating
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