Evidence map›Paper›PMID 35813946›Full record

ReviewFrontiers in aging neuroscience2022

The Future of Seed Amplification Assays and Clinical Trials.

Thomas Coysh, Simon Mead

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Review
  3. Digital seed amplification assay for TDP-43 aggregate quantification in CSF.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  4. Review
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  6. Review
  7. Article
  8. Article
  9. Protein misfolding: understanding biology to classify and treat synucleinopathies.Journal of neural transmission (Vienna, Austria : 1996) · 2025
    Review
  10. Digital seed amplification assay for TDP-43 aggregate quantification in CSF.medRxiv : the preprint server for health sciences · 2025
    Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
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  17. Review
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  20. ⍺-Synuclein Structural Diversity and the Cellular Environment in ⍺-Synuclein Transmission Models and Humans.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
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

2 authors at 2 institutions in 1 country.

Thomas CoyshMRC Prion Unit at UCL, UCL Institute of Prion Diseases, London, United Kingdom.
Simon MeadMRC Prion Unit at UCL, UCL Institute of Prion Diseases, London, United Kingdom.
MRC Prion Unit · GBNational Hospital for Neurology and Neurosurgery · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prion-like seeded misfolding of host proteins is the leading hypothesised cause of neurodegenerative diseases. The exploitation of the mechanism in the protein misfolding cyclic amplification (PMCA) and real-time quaking-induced conversion (RT-QuIC) assays have transformed prion disease research and diagnosis and have steadily become more widely used for research into other neurodegenerative disorders. Clinical trials in adult neurodegenerative diseases have been expensive, slow, and disappointing in terms of clinical benefits. There are various possible factors contributing to the failure to identify disease-modifying treatments for adult neurodegenerative diseases, some of which include: limited accuracy of antemortem clinical diagnosis resulting in the inclusion of patients with the "incorrect" pathology for the therapeutic; the role of co-pathologies in neurodegeneration rendering treatments targeting one pathology alone ineffective; treatment of the primary neurodegenerative process too late, after irreversible secondary processes of neurodegeneration have become established or neuronal loss is already extensive; and preclinical models used to develop treatments not accurately representing human disease. The use of seed amplification assays in clinical trials offers an opportunity to tackle these problems by sensitively detecting

Indexed as

biomarkerneurodegenerative diseasespre-symptomatic carrierspre-symptomatic diagnosisprionprotein aggregationRT-QuICseed amplification assays

Identifiers

PMID35813946
PMCPMC9257179
OpenAlexW4283394158

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.