Evidence map›Paper›PMID 31370680›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2019

Seeded propagation of α-synuclein aggregation in mouse brain using protein misfolding cyclic amplification.

Simon Nicot, Jérémy Verchère, Maxime Bélondrade, Charly Mayran, Dominique Bétemps, Daisy Bougard, Thierry Baron

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–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

15 citing papers in PubMed.

  1. Article
  2. Enteric glia, neuropeptides, and Parkinson's: impacts of calcitonin gene-related peptide on gut alpha synuclein.American journal of physiology. Gastrointestinal and liver physiology · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. 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

7 authors.

Simon NicotPathogenesis and Control of Chronic Infections, Etablissement Français du Sang, INSERM, Université de Montpellier, Montpellier, France.
Jérémy VerchèreFrench Agency for Food, Environmental, and Occupational Health and Safety (ANSES), University of Lyon, Lyon, France.
Maxime BélondradePathogenesis and Control of Chronic Infections, Etablissement Français du Sang, INSERM, Université de Montpellier, Montpellier, France.
Charly MayranPathogenesis and Control of Chronic Infections, Etablissement Français du Sang, INSERM, Université de Montpellier, Montpellier, France.
Dominique BétempsFrench Agency for Food, Environmental, and Occupational Health and Safety (ANSES), University of Lyon, Lyon, France.
Daisy BougardPathogenesis and Control of Chronic Infections, Etablissement Français du Sang, INSERM, Université de Montpellier, Montpellier, France.
Thierry BaronFrench Agency for Food, Environmental, and Occupational Health and Safety (ANSES), University of Lyon, Lyon, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

α-Synuclein (α-syn) protein aggregation is associated with several neurodegenerative disorders collectively referred to as synucleinopathies, including Parkinson's disease. We used protein misfolding cyclic amplification (PMCA) to study α-syn aggregation in brain homogenates of wild-type or transgenic mice expressing normal (D line) or A53T mutant (M83 line) human α-syn. We found that sonication-incubation cycles of M83 mouse brain gradually produce large quantities of SDS-resistant α-syn aggregates, involving both human and mouse proteins. These PMCA products, containing partially proteinase K-resistant α-syn species, are competent to accelerate the onset of neurologic symptoms after intracerebral inoculation to young M83 mice and to seed aggregate formation of α-syn following PMCA, including in D and wild-type mouse brain substrates. PMCA seeding activity in the M83 diseased brain correlates positively with regions mostly targeted by the α-syn pathology in this model. Our data indicate that similar to prions, PMCA can reproduce some characteristics of α-syn aggregation and seeded propagation

Indexed as

Gene AmplificationProtein Aggregatesalpha-SynucleinAnimalsBrainHumansMice, Inbred C57BLMice, KnockoutMice, TransgenicMutationProtein Aggregation, PathologicalProteostasis Deficienciesalpha-SynucleinProtein AggregatesPMCAprionseedingα-syn

Identifiers

PMID31370680
PMCPMC6902716

What OpenQuestion holds

Textmetadata
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.