Home › Research › Lewy body dementia
Tau protein isoforms, phosphorylation and role in neurodegenerative disorders
Buée L, Bussière T, Buée-Scherrer V, Delacourte A, Hof PR.. Brain research. Brain research reviews, 2000-08-01
Topic: Brain proteins, microglia and lab models
Tau proteins belong to the family of microtubule-associated proteins. They are mainly expressed in neurons where they play an important role in the assembly of tubulin monomers into microtubules to constitute the neuronal microtubules network. Microtubules are involved in maintaining the cell shape and serve as tracks for axonal transport. Tau proteins also establish some links between microtubules and other cytoskeletal elements or proteins. Tau proteins are translated from a single gene located on chromosome 17. Their expression is developmentally regulated by an alternative splicing mechanism and six different isoforms exist in the human adult brain. Tau proteins are the major constituents of intraneuronal and glial fibrillar lesions described in Alzheimer's disease and numerous neurodegenerative disorders referred to as 'tauopathies'. Molecular analysis has revealed that an abnormal phosphorylation might be one of the important events in the process leading to their aggregation. Moreover, a specific set of pathological tau proteins exhibiting a typical biochemical pattern, and a different regional and laminar distribution could characterize each of these disorders. Finally, a direct correlation has been established between the progressive involvement of the neocortical areas and the increasing severity of dementia, suggesting that pathological tau proteins are reliable marker of the neurodegenerative process. The recent discovery of tau gene mutations in frontotemporal dementia with parkinsonism linked to chromosome 17 has reinforced the predominant role attributed to tau proteins in the pathogenesis of neurodegenerative disorders, and underlined the fact that distinct sets of tau isoforms expressed in different neuronal populations could lead to different pathologies.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Buée, L., Bussière, T., Buée-Scherrer, V., Delacourte, A., & Hof, P. R. (2000). Tau protein isoforms, phosphorylation and role in neurodegenerative disorders. Brain research. Brain research reviews. https://doi.org/10.1016/s0165-0173(00)00019-9
Vancouver
Buée L, Bussière T, Buée-Scherrer V, Delacourte A, Hof PR. Tau protein isoforms, phosphorylation and role in neurodegenerative disorders. Brain research. Brain research reviews. 2000. doi:10.1016/s0165-0173(00)00019-9. PMID: 10967355.
BibTeX
@article{buee2000-10967355,
author = {Buée, L. and Bussière, T. and Buée-Scherrer, V. and Delacourte, A. and Hof, P. R.},
title = {{Tau protein isoforms, phosphorylation and role in neurodegenerative disorders}},
journal = {Brain research. Brain research reviews},
year = {2000},
doi = {10.1016/s0165-0173(00)00019-9},
pmid = {10967355},
url = {https://doi.org/10.1016/s0165-0173(00)00019-9}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- Molecular analysis has revealed that an abnormal phosphorylation might be one of the important events in the process leading to their aggregation.
- Finally, a direct correlation has been established between the progressive involvement of the neocortical areas and the increasing severity of dementia, suggesting that pathological tau proteins are reliable marker of the neurodegenerative process.
Why it matters
This 2000 review explains that tau, a protein that helps build the microtubule "tracks" inside nerve cells, comes from one gene on chromosome 17 in six adult-brain forms, and that it is the main component of the tangles found in Alzheimer's disease and other "tauopathies". The authors suggest that abnormal phosphorylation "might be" a key step in tau clumping, that each tauopathy may have its own pattern of tau forms and brain distribution, and they report that the spread of tau lesions through the neocortex tracks the severity of dementia. These are descriptions of brain pathology and associations, not evidence about any test, treatment or way to prevent the disease.
Study details
- Evidence strengthLow
How this study scored 54/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on senior author's track record, so that was left out: it earned 52 of the 96 points we could judge it on, which is 54 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Brain research. Brain research reviews) |
| Journal's citation record | 3 / 4 | Brain Research Reviews: journal h-index 267 (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 | 2000 — older than 20 years, still counted |
| 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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 7 / 7 | Cited 2,021 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 72.2 citations a year over 28 year(s) since 2000 |
| Impact for its field and year | 5 / 6 | Cited 26.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 36 other studies in this library |
| Still being cited | 4 / 4 | Cited 204 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | — / 4 | OpenAlex's profile for last-listed author Patrick R. Hof holds only 4 work(s), too few to judge a track record — left out of this score |
| Institution's track record | 2 / 3 | Inserm: institution h-index 1,988 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 10967355) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 52 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 52 of the 96 points we could judge it on is 54 out of 100. |
| Total | 54 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
May need a subscription OpenAlex found no free copy of the full text (checked 6 Feb 1020), so the publisher may charge for it. The PubMed abstract is free.
Studies this one cites
Referenced by this study and also in the alzhub library, so you can read them here. Showing 12 of 26.
Later studies that cite this one
36 studies in the alzhub library list this one in their references. Showing the 8 highest-scoring.
Related studies in Lewy body dementia
Also tagged “phosphorylated”
732 studies in the library carry the topic tag “phosphorylated”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 732 tagged studies.