Evidence map›Paper›PMID 37553663›Full record

ArticleMolecular neurodegeneration2023

Specific detection of tau seeding activity in Alzheimer's disease using rationally designed biosensor cells.

Aurelien Lathuiliere, Youhwa Jo, Romain Perbet, Cameron Donahue, Caitlin Commins, Noé Quittot, Zhanyun Fan, Rachel E Bennett, Bradley T Hyman

Open access · goldAbstract read
In one paragraph

Article in Molecular neurodegeneration, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. In situ seeding assay: A novel technique for direct tissue localization of bioactive tau.Journal of neuropathology and experimental neurology · 2024
    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

9 authors at 2 institutions in 2 countries.

Aurelien LathuiliereDepartment of Neurology, Massachusetts General Hospital/Harvard Medical School, 114 16Th Street, Charlestown, MA, 02129, USA.
Youhwa JoDepartment of Neurology, Massachusetts General Hospital/Harvard Medical School, 114 16Th Street, Charlestown, MA, 02129, USA.
Romain PerbetDepartment of Neurology, Massachusetts General Hospital/Harvard Medical School, 114 16Th Street, Charlestown, MA, 02129, USA.
Cameron DonahueDepartment of Neurology, Massachusetts General Hospital/Harvard Medical School, 114 16Th Street, Charlestown, MA, 02129, USA.
Caitlin ComminsDepartment of Neurology, Massachusetts General Hospital/Harvard Medical School, 114 16Th Street, Charlestown, MA, 02129, USA.
Noé QuittotDepartment of Neurology, Massachusetts General Hospital/Harvard Medical School, 114 16Th Street, Charlestown, MA, 02129, USA.
Zhanyun FanDepartment of Neurology, Massachusetts General Hospital/Harvard Medical School, 114 16Th Street, Charlestown, MA, 02129, USA.
Rachel E BennettDepartment of Neurology, Massachusetts General Hospital/Harvard Medical School, 114 16Th Street, Charlestown, MA, 02129, USA.
Bradley T HymanDepartment of Neurology, Massachusetts General Hospital/Harvard Medical School, 114 16Th Street, Charlestown, MA, 02129, USA. bhyman@mgh.harvard.edu.ORCID http://orcid.org/0000-0002-7959-9401
Harvard University · USUniversity of Geneva · CH

Funding

Research Education ComponentP30AG062421 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI Christine S Ritchie · 2019 to 2026
$36.5M
Are multiple tau species toxic in Alzheimer's Disease?RF1AG059789 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 2018 to 2018
$2.7M
Synergy between amyloid and tau in Alzheimer's DiseaseRF1AG058674 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 2018 to 2018
$2.6M
Complexity and Heterogeneity of Alzheimer diseaseR56AG061196 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 2019 to 2019
$654k
NIA NIH HHS P30 AG062421NIA NIH HHS R56 AG061196NIA NIH HHS RF1 AG058674NIA NIH HHS RF1 AG059789
6 · The paper itself

Abstract

backgroundThe prion-like propagation of tau in neurodegenerative disorders implies that misfolded pathological tau can recruit the normal protein and template its aggregation. Here, we report the methods for the development of sensitive biosensor cell lines for the detection of tau seeding activity.

resultsWe performed the rational design of novel tau probes based on the current structural knowledge of pathological tau aggregates in Alzheimer's disease. We generated Förster resonance energy transfer (FRET)-based biosensor stable cell lines and characterized their sensitivity, specificity, and overall ability to detect bioactive tau in human samples. As compared to the reference biosensor line, the optimized probe design resulted in an increased efficiency in the detection of tau seeding. The increased sensitivity allowed for the detection of lower amount of tau seeding competency in human brain samples, while preserving specificity for tau seeds found in Alzheimer's disease.

conclusionsThis next generation of FRET-based biosensor cells is a novel tool to study tau seeding activity in Alzheimer's disease human samples, especially in samples with low levels of seeding activity, which may help studying early tau-related pathological events.

Indexed as

Alzheimer DiseaseBiosensing TechniquesTauopathiesBrainHumanstau Proteinstau ProteinsAlzheimer’s diseaseBiosensor cellsPrion-like propagationSeedingTau

Identifiers

PMID37553663
PMCPMC10408046
OpenAlexW4385660177

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.