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Tau protein pathology in neurodegenerative diseases
Spillantini MG, Goedert M.. Trends in neurosciences, 1998-10-01
Topic: Brain proteins, microglia and lab models
Abundant tau-positive neurofibrillary lesions constitute a defining neuropathological characteristic of Alzheimer's disease. Filamentous tau pathology is also central to a number of other dementing disorders, such as Pick's disease, progressive supranuclear palsy, corticobasal degeneration and familial frontotemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17). The discovery of mutations in the tau gene in FTDP-17 has firmly established the relevance of tau pathology for the neurodegenerative process. Experimental studies have provided a system for the assembly of full-length tau into Alzheimer-like filaments, providing an assay for the testing of compounds that inhabit the formation of tau filaments.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Spillantini, M. G., & Goedert, M. (1998). Tau protein pathology in neurodegenerative diseases. Trends in neurosciences. https://doi.org/10.1016/s0166-2236(98)01337-x
Vancouver
Spillantini MG, Goedert M. Tau protein pathology in neurodegenerative diseases. Trends in neurosciences. 1998. doi:10.1016/s0166-2236(98)01337-x. PMID: 9786340.
BibTeX
@article{spillantini1998-9786340,
author = {Spillantini, M. G. and Goedert, M.},
title = {{Tau protein pathology in neurodegenerative diseases}},
journal = {Trends in neurosciences},
year = {1998},
doi = {10.1016/s0166-2236(98)01337-x},
pmid = {9786340},
url = {https://doi.org/10.1016/s0166-2236(98)01337-x}
}
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
- Abundant tau-positive neurofibrillary lesions constitute a defining neuropathological characteristic of Alzheimer's disease.
- Filamentous tau pathology is also central to a number of other dementing disorders, such as Pick's disease, progressive supranuclear palsy, corticobasal degeneration and familial frontotemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17).
- The discovery of mutations in the tau gene in FTDP-17 has firmly established the relevance of tau pathology for the neurodegenerative process.
- Experimental studies have provided a system for the assembly of full-length tau into Alzheimer-like filaments, providing an assay for the testing of compounds that inhabit the formation of tau filaments.
Why it matters
This review states that tau-positive neurofibrillary lesions define Alzheimer's disease and are central to several other dementias, and that tau mutations in FTDP-17 established tau's relevance to neurodegeneration. It mentions laboratory assays for testing compounds that block tau filament formation, but reports no treatment or cure.
Study details
- Evidence strengthLow
How this study scored 49/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Trends in neurosciences) |
| Journal's citation record | 3 / 4 | Trends in Neurosciences: journal h-index 439 (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 | 1998 — 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 | 6 / 7 | Cited 686 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 22.9 citations a year over 30 year(s) since 1998 |
| Impact for its field and year | 3 / 6 | Cited 5.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 24 other studies in this library |
| Still being cited | 2 / 4 | Cited 36 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Michel Goedert: h-index 147 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Cambridge: institution h-index 1,973 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 9786340) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 49 / 100 | — |
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