P301S Mutant Human Tau Transgenic Mice Manifest Early Symptoms of Human Tauopathies with Dementia and Altered Sensorimotor Gating
Open accessAbstract
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 deficits in the MWM test from 5 or 6.5 months, while others report initial deficits in spatial memory at 10 or 12 months of age.
“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]
The Results (Spatial learning abilities; page unavailable) report impaired Morris water maze performance in the transgenic mice. Materials and Methods (Experimental design; page unavailable) specifies that the water-maze mice were six months old, not exactly five or 6.5 months old. The study supports an early spatial-memory deficit, but a single age of testing does not establish when deficits first appeared. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe slightly better rotarod performance of PS19 mice is consistent with a hyperactivity phenotype in 6-month-old PS19 mice, presenting better albeit not statistically significant performance on the rotarod compared to WT control animals.
“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]
The Results section ('Locomotor activity and motor coordination'; page unavailable) reports no statistically significant rotarod difference from wild-type mice, and the Results section on hyperactivity reports that the mutant mice were more hyperactive. However, Materials and Methods ('Rotarod test'; page unavailable) specifies 15-week-old mice, not 6-month-old mice, and the text does not report better rotarod performance in the mutants. (LLM, conf=0.88)
Experimental — accuracy not yet measuredBoth models rely on transgene overexpression and familial mutations and are not well suited for studying causative events that lead to development of pathology in sporadic AD.
“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]
The Introduction (page unavailable) identifies the studied mice as transgenic animals expressing human P301S tau, a mutation associated with hereditary frontotemporal dementia. The Materials and Methods, Animals section (page unavailable) confirms the transgenic model. Our copy does not establish that this model overexpresses the transgene or assess whether either model is unsuitable for studying the causes of sporadic Alzheimer’s disease; it also does not describe 5xFAD mice. (LLM, conf=0.85)
Experimental — accuracy not yet measuredIn PS19 mice, there were no robust differences in spine density when PS19 mice were compared to NTG littermates, despite reported behavioral and electrophysiological deficits at the ages assessed.
“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
The Results sections on open-field behavior and sensorimotor gating report behavioral differences and altered prepulse inhibition in young P301S tau mice; the Methods place the prepulse-inhibition test at 16 weeks. Our copy does not report electrophysiological deficits. The spine-density comparison is the citing authors’ own finding, not a finding attributed to Takeuchi et al. (LLM, conf=0.83)
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- 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
- Health Sciences › Medicine › Physiology › 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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