Evidence map›Paper›PMID 40487537›Full record

ArticleAlzheimer's & dementia (Amsterdam, Netherlands)

Brain-derived tau to measure treatment effect in Alzheimer's disease and frontotemporal dementia.

Cassandra Marotta, Fernando Gonzalez-Ortiz, Michael Turton, Henrik Zetterberg, Peter Harrison, Christopher M Hovens, Benjamin Sinclair, Terence J O'Brien, Kaj Blennow, Lucy Vivash

Abstract read
In one paragraph

Article in Alzheimer's & dementia (Amsterdam, Netherlands). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
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

10 authors.

Cassandra MarottaDepartment of Neuroscience School of Translational Medicine Monash University Melbourne Victoria Australia.ORCID https://orcid.org/0009-0008-8430-4824
Fernando Gonzalez-OrtizDepartment of Psychiatry and Neurochemistry Institute of Neuroscience and Physiology The Sahlgrenska Academy, University of Gothenburg Gothenburg Sweden.
Michael TurtonDepartment of Neurodegenerative Disease UCL Institute of Neurology Queen Square London UK.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry Institute of Neuroscience and Physiology The Sahlgrenska Academy, University of Gothenburg Gothenburg Sweden.
Peter HarrisonBioventix Plc, 7 Romans Business Park Farnham Surrey UK.
Christopher M HovensDepartment of Surgery Royal Melbourne Hospital University of Melbourne Parkville Victoria Australia.
Benjamin SinclairDepartment of Neuroscience School of Translational Medicine Monash University Melbourne Victoria Australia.
Terence J O'BrienDepartment of Neuroscience School of Translational Medicine Monash University Melbourne Victoria Australia.
Kaj BlennowDepartment of Psychiatry and Neurochemistry Institute of Neuroscience and Physiology The Sahlgrenska Academy, University of Gothenburg Gothenburg Sweden.
Lucy VivashDepartment of Neuroscience School of Translational Medicine Monash University Melbourne Victoria Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionBrain-derived tau (BD-tau) measures tau specifically from brain-derived sources and can differentiate Alzheimer's disease (AD) from other diseases. This study investigated BD-tau as a potential biomarker of treatment effect.

methodsBD-tau and phosphorylated tau-217 (p-tau217) levels were measured after treatment with an anti-tau drug in AD and behavioral variant frontotemporal dementia (bvFTD) clinical trials, and the association with total tau (t-tau), p-tau181

resultsCerebrospinal fluid (CSF) BD-tau decreased after treatment in the AD cohort; however, no change was seen in bvFTD or p-tau217 in either cohort. CSF t-tau and p-tau181 correlated with BD-tau in AD ( DISCUSSION: CSF BD-tau shows potential as a biomarker of treatment effect in AD but not bvFTD. Further research is needed to investigate this effect in blood-based samples and in other neurodegenerative diseases. Highlights: Cerebrospinal fluid (CSF) brain-derived tau (BD-tau) levels decreased with sodium selenate treatment in patients with Alzheimer's disease (AD).CSF BD-tau levels did not change with sodium selenate treatment in bvFTD.Baseline CSF BD-tau correlated with CSF total tau (t-tau) and phosphorylated tau-181 (p-tau181) in AD and behavioral variant frontotemporal dementia (bvFTD).Baseline serum and plasma BD-tau levels did not correlate with CSF BD-tau in bvFTD.CSF p-tau217 did not change with sodium selenate treatment in AD or bvFTD.

Indexed as

Alzheimer's diseaseanti‐tau treatmentbehavioral variant frontotemporal dementiabrain‐derived taufluid biomarkerstreatment effect

Identifiers

PMID40487537
PMCPMC12140970

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.