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CSF phosphorylated tau protein correlates with neocortical neurofibrillary pathology in Alzheimer's disease
Katharina Büerger, Michael Ewers, Tuula Pirttilä, Raymond P. Zinkowski, Irina I. Alafuzoff, Stefan Johannes Teipel, John F. DeBernardis, Daniel J. Kerkman, Cheryl McCulloch, Hilkka S. Soininen, Harald Juergen Hampel. Brain, 2006-09-29
Topic: Brain proteins, microglia and lab models
Hyperphosphorylated tau protein (P-tau) in CSF is a core biomarker candidate of Alzheimer's disease. Hyperphosphorylation of tau is thought to lead to neurofibrillary changes, a neuropathological hallmark of this type of dementia. Currently, the question is unresolved whether CSF levels of P-tau reflect neurofibrillary changes within the brain of a patient with the illness. Twenty-six patients were included with intra-vitam CSF as well as post-mortem neuropathological data. In the CSF, P-tau phosphorylated at threonine 231 (P-tau231P) was analysed. Post-mortem, scores of neurofibrillary tangles (NFT) and neuritic plaques (NP) were assessed in frontal, temporal, parietal and hippocampal cortical areas. In the same cortical regions, load of hyperphosphorylated tau protein (HP-tau load) was determined. Concentrations of P-tau231P were measured in frontal cortex homogenates. We found significant correlations between CSF P-tau231P concentrations and scores of NFTs and HP-tau load in all neocortical regions studied. The score of NPs was correlated with CSF P-tau231P only within the frontal cortex. There was a correlation between P-tau231P in CSF and brain homogenates. These findings indicate that CSF P-tau231P may serve as an in vivo surrogate biomarker of neurofibrillary pathology in Alzheimer's disease.
Why it matters
In patients with spinal fluid taken in life and brain examination after death, levels of a phosphorylated tau protein (P-tau231P) in the spinal fluid correlated with the amount of tangle pathology in all neocortical regions studied. The authors say this marker may serve as an in vivo stand-in measure of tangle pathology in Alzheimer's disease.
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How this study scored 51/100
Published in a leading specialty 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 strength of evidence, so that was left out: it earned 48 of the 95 points we could judge it on, which is 51 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Brain) |
| Journal's citation record | 4 / 4 | Brain: journal h-index 503 (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 | — / 5 | No evidence rating recorded — left out of this score |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2006 — 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 586 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 26.6 citations a year over 22 year(s) since 2006 |
| Impact for its field and year | 4 / 6 | Cited 12.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 2 / 4 | Cited 47 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Harald Juergen Hampel: h-index 136 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Ludwig-Maximilians-Universität München: institution h-index 1,224 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 17012293) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 48 / 95 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 48 of the 95 points we could judge it on is 51 out of 100. |
| Total | 51 / 100 | — |
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Read the original
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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 names 11 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
APA 7th
Büerger, K., Ewers, M., Pirttilä, T., Zinkowski, R. P., Alafuzoff, I. I., Teipel, S. J., et al. (2006). CSF phosphorylated tau protein correlates with neocortical neurofibrillary pathology in Alzheimer's disease. Brain. https://doi.org/10.1093/brain/awl269
Vancouver
Büerger K, Ewers M, Pirttilä T, Zinkowski RP, Alafuzoff II, Teipel SJ, et al. CSF phosphorylated tau protein correlates with neocortical neurofibrillary pathology in Alzheimer's disease. Brain. 2006. doi:10.1093/brain/awl269. PMID: 17012293.
BibTeX
@article{buerger2006-17012293,
author = {Büerger, Katharina and Ewers, Michael and Pirttilä, Tuula and Zinkowski, Raymond P. and Alafuzoff, Irina I. and Teipel, Stefan Johannes and DeBernardis, John F. and Kerkman, Daniel J. and McCulloch, Cheryl and Soininen, Hilkka S. and Hampel, Harald Juergen},
title = {{CSF phosphorylated tau protein correlates with neocortical neurofibrillary pathology in Alzheimer's disease}},
journal = {Brain},
year = {2006},
doi = {10.1093/brain/awl269},
pmid = {17012293},
url = {https://doi.org/10.1093/brain/awl269}
}
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