Evidence map›Paper›PMID 19853650›Full record

ReviewExperimental gerontology2010

Total and phosphorylated tau protein as biological markers of Alzheimer's disease.

Harald Hampel, Kaj Blennow, Leslie M Shaw, Yvonne C Hoessler, Henrik Zetterberg, John Q Trojanowski

Open access · greenAbstract readReview
In one paragraph

Review in Experimental gerontology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed, 1 pooled it
10.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

180 citing papers in PubMed, 1 synthesis or guideline pooled it, 389 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. bioRxiv : the preprint server for biology · 2026
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  4. Article
  5. Review
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  8. Circulating neurodegenerative brain injury markers and hip fracture and fall hospitalizations: the Cardiovascular Health Study.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025
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  11. Review
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120 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 4 countries.

Harald HampelDiscipline of Psychiatry, School of Medicine & Trinity College Institute of Neuroscience, Laboratory of Neuroimaging & Biomarker Research, Trinity College, University of Dublin, The Adelaide and Meath Hospital Incorporating The National Children's Hospital, Tallaght, Dublin, Ireland. harald.hampel@med.uni-muenchen.de
Kaj Blennow
Leslie M Shaw
Yvonne C Hoessler
Henrik Zetterberg
John Q Trojanowski
Ludwig-Maximilians-Universität München · DEUniversity of Gothenburg · SEUniversity of Pennsylvania · US

Funding

Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
UPenn ADCC Biomarker CoreP30AG010124 · NIA · UNIVERSITY OF PENNSYLVANIA · PI DETRE, JOHN A · 1991 to 2020
$35.1M
NIA NIH HHS AG-10124NIA NIH HHS AG-24904NIA NIH HHS P30 AG010124NIA NIH HHS U01 AG024904
6 · The paper itself

Abstract

Advances in our understanding of tau-mediated neurodegeneration in Alzheimer's disease (AD) are moving this disease pathway to center stage for the development of biomarkers and disease modifying drug discovery efforts. Immunoassays were developed detecting total (t-tau) and tau phosphorylated at specific epitopes (p-tauX) in cerebrospinal fluid (CSF), methods to analyse tau in blood are at the experimental beginning. Clinical research consistently demonstrated CSF t- and p-tau increased in AD compared to controls. Measuring these tau species proved informative for classifying AD from relevant differential diagnoses. Tau phosphorylated at threonine 231 (p-tau231) differentiated between AD and frontotemporal dementia, tau phosphorylated at serine 181 (p-tau181) enhanced classification between AD and dementia with Lewy bodies. T- and p-tau are considered "core" AD biomarkers that have been successfully validated by controlled large-scale multi-center studies. Tau biomarkers are implemented in clinical trials to reflect biological activity, mechanisms of action of compounds, support enrichment of target populations, provide endpoints for proof-of-concept and confirmatory trials on disease modification. World-wide quality control initiatives are underway to set required methodological and protocol standards. Discussions with regulatory authorities gain momentum defining the role of tau biomarkers for trial designs and how they may be further qualified for surrogate marker status.

Indexed as

AgedAlzheimer DiseaseBiomarkersHumansNerve DegenerationPhosphorylationPredictive Value of Teststau ProteinsBiomarkerstau Proteins

Identifiers

PMID19853650
PMCPMC2815003
OpenAlexW2147576743

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.