Evidence map›Paper›PMID 24252164›Full record

ReviewActa neuropathologica communications2013

The prion hypothesis in Parkinson's disease: Braak to the future.

Naomi P Visanji, Patricia L Brooks, Lili-Naz Hazrati, Anthony E Lang

Abstract readReview
In one paragraph

Review in Acta neuropathologica communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.

0numbers the graph read from it
0cells of the map it votes in
127citing 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

127 citing papers in PubMed.

  1. Review
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  10. Nutrients · 2025
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  16. Exploring Intrinsic Disorder in Human Synucleins and Associated Proteins.International journal of molecular sciences · 2024
    Article
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  19. Article
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67 more citing papers are in PubMed but not listed here.

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.

Naomi P VisanjiDivision of Patient Based Clinical Research, Toronto Western Research Institute, and the Edmond J, Safra Program in Parkinson's Disease, Toronto Western Hospital, McLaughlin Pavilion, 7th Floor Rm 7-403, 399 Bathurst Street, Toronto, Ontario M5T 2S8, Canada. lang@uhnres.utoronto.ca.
Patricia L Brooks
Lili-Naz Hazrati
Anthony E Lang

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disorder typified by the presence of intraneuronal inclusions containing aggregated alpha synuclein (αsyn). The progression of parkinsonian pathology and clinical phenotype has been broadly demonstrated to follow a specific pattern, most notably described by Braak and colleagues. In more recent times it has been hypothesized that αsyn itself may be a critical factor in mediating transmission of disease pathology from one brain area to another. Here we investigate the growing body of evidence demonstrating the ability of αsyn to spread transcellularly and induce pathological aggregation affecting neurons by permissive templating and provide a critical analysis of some irregularities in the hypothesis that the progression of PD pathology may be mediated by such a prion-like process. Finally we discuss some key questions that remain unanswered which are vital to determining the potential contribution of a prion-like process to the pathogenesis of PD.

Indexed as

AnimalsHumansModels, NeurologicalParkinson DiseasePrionsSeverity of Illness IndexPrions

Identifiers

PMID24252164
PMCPMC3776210

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.