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Transmission and spreading of tauopathy in transgenic mouse brain
Clavaguera F, Bolmont T, Crowther RA, Abramowski D, Frank S, Probst A, Fraser G, Stalder AK et al.. Nature cell biology, 2009-06-07
Topic: Brain proteins, microglia and lab models
Plain-language summary
Hyperphosphorylated tau makes up the filamentous intracellular inclusions of several neurodegenerative diseases, including Alzheimer's disease. In the disease process, neuronal tau inclusions first appear in the transentorhinal cortex from where they seem to spread to the hippocampal formation and neocortex. Cognitive impairment becomes manifest when inclusions reach the hippocampus, with abundant neocortical tau inclusions and extracellular beta-amyloid deposits being the defining pathological hallmarks of Alzheimer's disease. An abundance of tau inclusions, in the absence of beta-amyloid deposits, defines Pick's disease, progressive supranuclear palsy, corticobasal degeneration and other diseases. Tau mutations cause familial forms of frontotemporal dementia, establishing that tau protein dysfunction is sufficient to cause neurodegeneration and dementia. Thus, transgenic mice expressing mutant (for example, P301S) human tau in nerve cells show the essential features of tauopathies, including neurodegeneration and abundant filaments made of hyperphosphorylated tau protein. By contrast, mouse lines expressing single isoforms of wild-type human tau do not produce tau filaments or show neurodegeneration. Here we have used tau-expressing lines to investigate whether experimental tauopathy can be transmitted. We show that injection of brain extract from mutant P301S tau-expressing mice into the brain of transgenic wild-type tau-expressing animals induces assembly of wild-type human tau into filaments and spreading of pathology from the site of injection to neighbouring brain regions.
What this study adds
Evidence grade: Low
In this mouse study, brain extract from mice carrying a mutant (P301S) form of human tau was injected into the brains of mice carrying normal human tau, a strain that on its own does not form tau filaments. The study reports that the injection made the normal human tau assemble into filaments, and that the pathology spread from the injection site to neighbouring brain regions.
Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Clavaguera, F., Bolmont, T., Crowther, R. A., Abramowski, D., Frank, S., Probst, A., et al. (2009). Transmission and spreading of tauopathy in transgenic mouse brain. Nature cell biology. https://doi.org/10.1038/ncb1901
Vancouver
Clavaguera F, Bolmont T, Crowther RA, Abramowski D, Frank S, Probst A, et al. Transmission and spreading of tauopathy in transgenic mouse brain. Nature cell biology. 2009. doi:10.1038/ncb1901. PMID: 19503072.
BibTeX
@article{clavaguera2009-19503072,
author = {Clavaguera, F. and Bolmont, T. and Crowther, R. A. and Abramowski, D. and Frank, S. and Probst, A. and Fraser, G. and Stalder, A. K. and others},
title = {{Transmission and spreading of tauopathy in transgenic mouse brain}},
journal = {Nature cell biology},
year = {2009},
doi = {10.1038/ncb1901},
pmid = {19503072},
url = {https://doi.org/10.1038/ncb1901}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
Key findings
- Tau mutations cause familial forms of frontotemporal dementia, establishing that tau protein dysfunction is sufficient to cause neurodegeneration and dementia.
- Thus, transgenic mice expressing mutant (for example, P301S) human tau in nerve cells show the essential features of tauopathies, including neurodegeneration and abundant filaments made of hyperphosphorylated tau protein.
- By contrast, mouse lines expressing single isoforms of wild-type human tau do not produce tau filaments or show neurodegeneration.
- Here we have used tau-expressing lines to investigate whether experimental tauopathy can be transmitted.
- We show that injection of brain extract from mutant P301S tau-expressing mice into the brain of transgenic wild-type tau-expressing animals induces assembly of wild-type human tau into filaments and spreading of pathology from the site of injection to neighbouring brain regions.
Why it matters
In this mouse study, brain extract from mice carrying a mutant (P301S) form of human tau was injected into the brains of mice carrying normal human tau, a strain that on its own does not form tau filaments. The study reports that the injection made the normal human tau assemble into filaments, and that the pathology spread from the injection site to neighbouring brain regions. It is animal research on how tau pathology can be transmitted and spread; it does not test a treatment and does not show that Alzheimer's spreads between people.
Study details
- Evidence strengthLow
How this study scored 58/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Nature cell biology) |
| Journal's citation record | 3 / 4 | Nature Cell Biology: journal h-index 486 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2009 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Laboratory or animal study (title names “transgenic”) — scores zero |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 7 / 7 | Cited 1,814 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 95.5 citations a year over 19 year(s) since 2009 |
| Impact for its field and year | 6 / 6 | Cited 51.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 63 other studies in this library |
| Still being cited | 4 / 4 | Cited 257 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Markus Tolnay: h-index 59 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Tübingen: institution h-index 940 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 8 institution(s) in 3 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 19503072) |
| Free to read | 2 / 2 | Free to read |
| Total | 58 / 100 | — |
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