Evidence map›Paper›PMID 39036077›Full record

ArticleBioengineering & translational medicine2024

Rational design of structure-based vaccines targeting misfolded alpha-synuclein conformers of Parkinson's disease and related disorders.

Jose Miguel Flores-Fernandez, Verena Pesch, Aishwarya Sriraman, Enrique Chimal-Juarez, Sara Amidian, Xiongyao Wang, Caleb Duckering, Andrew Fang, Sara Reithofer, Liang Ma and 4 more

Abstract read
In one paragraph

Article in Bioengineering & translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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  6. 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

14 authors.

Jose Miguel Flores-FernandezCentre for Prions and Protein Folding Diseases University of Alberta Edmonton Alberta Canada.
Verena PeschInstitut für Biologische Informationsprozesse, Strukturbiochemie (IBI-7), Forschungszentrum Jülich GmbH Jülich Germany.
Aishwarya SriramanCentre for Prions and Protein Folding Diseases University of Alberta Edmonton Alberta Canada.
Enrique Chimal-JuarezCentre for Prions and Protein Folding Diseases University of Alberta Edmonton Alberta Canada.
Sara AmidianCentre for Prions and Protein Folding Diseases University of Alberta Edmonton Alberta Canada.
Xiongyao WangCentre for Prions and Protein Folding Diseases University of Alberta Edmonton Alberta Canada.
Caleb DuckeringCentre for Prions and Protein Folding Diseases University of Alberta Edmonton Alberta Canada.
Andrew FangCentre for Prions and Protein Folding Diseases University of Alberta Edmonton Alberta Canada.
Sara ReithoferInstitut für Biologische Informationsprozesse, Strukturbiochemie (IBI-7), Forschungszentrum Jülich GmbH Jülich Germany.
Liang MaInstitut für Biologische Informationsprozesse, Strukturbiochemie (IBI-7), Forschungszentrum Jülich GmbH Jülich Germany.
Leonardo M CortezCentre for Prions and Protein Folding Diseases University of Alberta Edmonton Alberta Canada.
Valerie L SimCentre for Prions and Protein Folding Diseases University of Alberta Edmonton Alberta Canada.
Gültekin TamgüneyInstitut für Biologische Informationsprozesse, Strukturbiochemie (IBI-7), Forschungszentrum Jülich GmbH Jülich Germany.ORCID https://orcid.org/0000-0002-6933-5154
Holger WilleCentre for Prions and Protein Folding Diseases University of Alberta Edmonton Alberta Canada.ORCID https://orcid.org/0000-0001-5102-8706

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synucleinopathies, including Parkinson's disease (PD), multiple system atrophy (MSA), and dementia with Lewy bodies (DLB), are neurodegenerative disorders caused by the accumulation of misfolded alpha-synuclein protein. Developing effective vaccines against synucleinopathies is challenging due to the difficulty of stimulating an immune-specific response against alpha-synuclein without causing harmful autoimmune reactions, selectively targeting only pathological forms of alpha-synuclein. Previous attempts using linear peptides and epitopes without control of the antigen structure failed in clinical trials. The immune system was unable to distinguish between native alpha-synuclein and its amyloid form. The prion domain of the fungal HET-s protein was selected as a scaffold to introduce select epitopes from the surface of alpha-synuclein fibrils. Four vaccine candidates were generated by introducing specific amino acid substitutions onto the surface of the scaffold protein. The approach successfully mimicked the stacking of the parallel in-register beta-sheet structure seen in alpha-synuclein fibrils. All vaccine candidates induced substantial levels of IgG antibodies that recognized pathological alpha-synuclein fibrils derived from a synucleinopathy mouse model. Furthermore, the antisera recognized pathological alpha-synuclein aggregates in brain lysates from patients who died from DLB, MSA, or PD, but did not recognize linear alpha-synuclein peptides. Our approach, based on the rational design of vaccines using the structure of alpha-synuclein amyloid fibrils and strict control over the exposed antigen structure used for immunization, as well as the ability to mimic aggregated alpha-synuclein, provides a promising avenue toward developing effective vaccines against alpha-synuclein fibrils.

Indexed as

beta‐solenoid structureparallel in‐register beta‐sheet structureParkinson's diseaseprotein engineeringrational designvaccine

Identifiers

PMID39036077
PMCPMC11256163

What OpenQuestion holds

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Registered trials

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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.