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Phosphorylated tau in Alzheimer's disease
Julia Telser, Kirsten Grossmann, Niklas Wohlwend, Lorenz Risch, Christoph H Saely, Philipp Werner. Advances in clinical chemistry, 2023-06-09
Topic: Plasma and spinal-fluid biomarkers
There is a need for blood biomarkers to detect individuals at different Alzheimer's disease (AD) stages because obtaining cerebrospinal fluid-based biomarkers is invasive and costly. Plasma phosphorylated tau proteins (p-tau) have shown potential as such biomarkers. This systematic review was conducted according to the PRISMA guidelines and aimed to determine whether quantification of plasma tau phosphorylated at threonine 181 (p-tau181), threonine 217 (p-tau217) and threonine 231 (p-tau231) is informative in the diagnosis of AD. All p-tau isoforms increase as a function of Aβ-accumulation and discriminate healthy individuals from those at preclinical AD stages with high accuracy. P-tau231 increases earliest, followed by p-tau181 and p-tau217. In advanced stages, all p-tau isoforms are associated with the clinical classification of AD and increase with disease severity, with the greatest increase seen for p-tau217. This is also reflected by a better correlation of p-tau217 with Aβ scans, whereas both, p-tau217 and p-tau181 correlated equally with tau scans. However, at the very advanced stages, p-tau181 begins to plateau, which may mirror the trajectory of the Aβ pathology and indicate an association with a more intermediate risk of AD. Across the AD continuum, the incremental increase in all biomarkers is associated with structural changes in widespread brain regions and underlying cognitive decline. Furthermore, all isoforms differentiate AD from non-AD neurodegenerative disorders, making them specific for AD. Incorporating p-tau181, p-tau217 and p-tau231 in clinical use requires further studies to examine ideal cut-points and harmonize assays.
Key findings
- In advanced stages, all p-tau isoforms are associated with the clinical classification of AD and increase with disease severity, with the greatest increase seen for p-tau217.
- Across the AD continuum, the incremental increase in all biomarkers is associated with structural changes in widespread brain regions and underlying cognitive decline.
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Study details
- Study designsystematic review
- Evidence strengthHigh
How this study scored 70/100
Published in a peer-reviewed journal, and it is a systematic review of all the studies on the question. Scored zero for sample size, effect reported and studied in people because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multi-centre collaboration and free to read, so those were left out: it earned 39 of the 56 points we could judge it on, which is 70 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Advances in clinical chemistry) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 12 / 12 | A systematic review of all the studies on the question |
| Strength of evidence | 5 / 5 | Rated “high” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 3 / 5 | 2023 — within 6 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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | A review of other studies — randomisation is not credited here |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 37852722) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 39 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 39 of the 56 points we could judge it on is 70 out of 100. |
| Total | 70 / 100 | — |
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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APA 7th
Telser, J., Grossmann, K., Wohlwend, N., Risch, L., Saely, C. H., & Werner, P. (2023). Phosphorylated tau in Alzheimer's disease. Advances in clinical chemistry. https://doi.org/10.1016/bs.acc.2023.05.001
Vancouver
Telser J, Grossmann K, Wohlwend N, Risch L, Saely CH, Werner P. Phosphorylated tau in Alzheimer's disease. Advances in clinical chemistry. 2023. doi:10.1016/bs.acc.2023.05.001. PMID: 37852722.
BibTeX
@article{telser2023-37852722,
author = {Telser, Julia and Grossmann, Kirsten and Wohlwend, Niklas and Risch, Lorenz and Saely, Christoph H and Werner, Philipp},
title = {{Phosphorylated tau in Alzheimer's disease}},
journal = {Advances in clinical chemistry},
year = {2023},
doi = {10.1016/bs.acc.2023.05.001},
pmid = {37852722},
url = {https://doi.org/10.1016/bs.acc.2023.05.001}
}
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