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Characterization of Novel CSF Tau and ptau Biomarkers for Alzheimer’s Disease
Open accessAbstract
Cerebral spinal fluid (CSF) Aβ42, tau and p181tau are widely accepted biomarkers of Alzheimer's disease (AD). Numerous studies show that CSF tau and p181tau levels are elevated in mild-to-moderate AD compared to age-matched controls. In addition, these increases might predict preclinical AD in cognitively normal elderly. Despite their importance as biomarkers, the molecular nature of CSF tau and ptau is not known. In the current study, reverse-phase high performance liquid chromatography was used to enrich and concentrate tau prior to western-blot analysis. Multiple N-terminal and mid-domain fragments of tau were detected in pooled CSF with apparent sizes ranging from <20 kDa to ~40 kDa. The pattern of tau fragments in AD and control samples were similar. In contrast, full-length tau and C-terminal-containing fragments were not detected. To quantify levels, five tau ELISAs and three ptau ELISAs were developed to detect different overlapping regions of the protein. The discriminatory potential of each assay was determined using 20 AD and 20 age-matched control CSF samples. Of the tau ELISAs, the two assays specific for tau containing N-terminal sequences, amino acids 9-198 (numbering based on tau 441) and 9-163, exhibited the most significant differences between AD and control samples. In contrast, CSF tau was not detected with an ELISA specific for a more C-terminal region (amino acids 159-335). Significant discrimination was also observed with ptau assays measuring amino acids 159-p181 and 159-p231. Interestingly, the discriminatory potential of p181 was reduced when measured in the context of tau species containing amino acids 9-p181. Taken together, these results demonstrate that tau in CSF occurs as a series of fragments and that discrimination of AD from control is dependent on the subset of tau species measured. These assays provide novel tools to investigate CSF tau and ptau as biomarkers for other neurodegenerative diseases.
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“In CSF, full-length tau can only be detected by western blot, but not by other methods such as ELISA and IP-MS [216–219].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [217]
In the citing paper
“Both full-length and truncated tau isoforms can be secreted.”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [217]
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“whereas the presence of full-length tau in the CSF is questionable.”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [217]
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“However, only the existence of truncated tau in CSF has been confirmed [216–218]”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [217]
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Self-citationCerebrospinal fluid biomarker signature in Alzheimer's disease neuroimaging initiative subjects
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Self-citationInverse relation between in vivo amyloid imaging load and cerebrospinal fluid Aβ 42 in humans
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CSF Biomarkers and Incipient Alzheimer Disease in Patients With Mild Cognitive Impairment
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Self-citationPET imaging of amyloid deposition in patients with mild cognitive impairment
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Cicognola, C., Hansson, O., Scheltens, P., Kvartsberg, H., Zetterberg, H., Teunissen, C. E., & Blennow, K. (2021) · Figshare · doi:10.6084/m9.figshare.13787431
Self-citationGobom, J., Benedet, A. L., Mattsson, N., Montoliu‐Gaya, L., Schultz, N., Ashton, N. J., Janelidze, S., Servaes, S., Sauer, M., Pascoal, T. A., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26553350
Self-citationFeatherby, S. J., Faulkner, E. C., Gordon, A. D., & Ettelaie, C. (2026) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-025-01658-7
Identification et caractérisation fonctionnelle de nouveaux sites de clivage de la protéine Tau
Derisbourg, M. J. (2015) · theses.fr (ABES) · doi:10.70675/ef5f45b0zf4e8z433fz9beaz8d2cc6de65bc
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Tau368 improves p-tau diagnostic accuracy for FTLD-tau from FTLD-TDP
Kac, P. R., Cousins, K. A. Q., Szadziewska, A., Shaw, L. M. J., Turton, M., Deerlin, V. M. V., Harrison, P., Zetterberg, H., Wolk, D. A., McMillan, C. T., et al. (2026) · Acta Neuropathologica · doi:10.1007/s00401-026-03042-1
Self-citationTau-mediated Mechanisms in Alzheimerʼs Disease Pathogenesis
Narayanappa, T. S., Ananthanarayana, V., & Chinnathambi, S. (2026) · Molecular Neurobiology · doi:10.1007/s12035-026-06057-7
Metadata
- Authors
- Meredith Jr., J. E., Sankaranarayanan, S., Guss, V., Lanzetti, A. J., Berisha, F., Neely, R. J., Slemmon, J. R., Portelius, E., Zetterberg, H., Blennow, K., Soares, H., Ahlijanian, M., & Albright, C. F.
- Affiliations
- Bristol-Myers Squibb (United States) (US)
- University of Gothenburg (SE)
- UCL Queen Square Institute of Neurology (GB)
- ORCID
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-10-07
- Volume
- 8
- Issue
- 10
- Pages
- e76523
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3792042
- OpenAlex
- W2024790026
- Cited by
- 209
- References
- 60
- Citations by year
- 2026: 6 · 2025: 13 · 2024: 14 · 2023: 14 · 2022: 11 · 2021: 19 · 2020: 23 · 2019: 28 · 2018: 29 · 2017: 16 · 2016: 11 · 2015: 13 · 2014: 11
- FWCI
- 8.10
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- UCL Discovery (University College London) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Funders
- Bristol-Myers Squibb
- Vetenskapsrådet
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Clinical Neurology › Cerebrospinal fluid and hydrocephalus
- Keywords
- Alzheimer's disease, cerebrospinal fluid, tau protein, phosphorylated tau, biomarkers, preclinical Alzheimer's disease, tau isoforms, diagnostic discrimination
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Chromatography, High Pressure Liquid, Enzyme-Linked Immunosorbent Assay, Humans, Male, Middle Aged, Molecular Weight, Peptide Fragments, Phosphorylation, Sensitivity and Specificity, Blotting, Western, Reproducibility of Results, Biomarkers, tau Proteins, Chromatography, Reverse-Phase
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