Evidence map›Paper›PMID 39932548›Full record

ReviewJournal of neural transmission (Vienna, Austria : 1996)2025

Protein misfolding: understanding biology to classify and treat synucleinopathies.

Tiago Fleming Outeiro, Günter Höglinger, Anthony E Lang, Tuane C R G Vieira

Abstract readReview
In one paragraph

Review in Journal of neural transmission (Vienna, Austria : 1996), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Insights into the Diagnosis, Treatment, and Management of Prion Diseases.CNS & neurological disorders drug targets · 2026
    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

4 authors.

Tiago Fleming OuteiroDepartment of Experimental Neurodegeneration, Center for Biostructural Imaging of Neurodegeneration, University Medical Center Göttingen, Göttingen, Germany. touteir@gwdg.de.ORCID 0000-0003-1679-1727
Günter HöglingerDepartment of Neurology, LMU University Hospital, Ludwig-Maximilians-Universität (LMU) München, Munich, Germany.
Anthony E LangEdmond J. Safra Program in Parkinson's Disease, the Rossy PSP Centre, Division of Neurology, Department of Medicine, University Health Network, University of Toronto, Toronto, Canada.
Tuane C R G VieiraInstitute of Medical Biochemistry Leopoldo de Meis, National Institute of Science and Technology for Structural Biology and Bioimaging, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, 21941-901, Brazil.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein misfolding and aggregation is a major pathological hallmark in a variety of human conditions, including cancer, diabetes, and neurodegeneration. However, we still do not fully understand the role of protein accumulation in disease. Interestingly, recent breakthroughs in artificial intelligence (AI) are having a tremendous impact on our ability to predict three-dimensional protein structures and understand the molecular rules governing protein folding/misfolding. This progress will enable us to understand how intrinsic and extrinsic factors trigger protein misfolding, thereby changing protein function. These changes, in some cases, are related to normal biological responses and, in other cases, associated with pathological alterations, such as those found in many neurodegenerative disorders. Here, we provide a brief historical perspective of how findings in the field of prion diseases and prion biology have enabled tremendous advances that are now forming the basis for our understanding of disease processes and discuss how this knowledge is now emerging as central for our ability to classify, diagnose, and treat devastating neurodegenerative disorders such as Parkinson's and Alzheimer's diseases.

Indexed as

Protein FoldingProteostasis DeficienciesSynucleinopathiesAnimalsHumansAlpha-synucleinBiomarkersDisease classificationNeurodegenerationParkinson’s diseaseProtein aggregation

Identifiers

PMID39932548
PMCPMC12630200

What OpenQuestion holds

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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.