Evidence map›Paper›PMID 29480459›Full record

ReviewCell and tissue research2018

The concept of alpha-synuclein as a prion-like protein: ten years after.

Jennifer A Steiner, Emmanuel Quansah, Patrik Brundin

Open access · greenAbstract readReview
In one paragraph

Review in Cell and tissue research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed, 1 pooled it
8.7field-weighted citation impact, top 1% 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

111 citing papers in PubMed, 1 synthesis or guideline pooled it, 184 citations in OpenAlex.

  1. Pooled it
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  9. Article
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  11. Review
  12. The history and status of dopamine cell therapies for Parkinson's disease.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024
    Review
  13. Review
  14. Article
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  16. Article
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  19. Article
  20. Single-Domain Antibody-Based Protein Degrader for Synucleinopathies.bioRxiv : the preprint server for biology · 2024
    Article

51 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

3 authors at 1 institution in 1 country.

Jennifer A SteinerCenter for Neurodegenerative Science, Van Andel Research Institute, 333 Bostwick Ave. NE, Grand Rapids, MI, 49503, USA. jennifer.steiner@vai.org.
Emmanuel QuansahCenter for Neurodegenerative Science, Van Andel Research Institute, 333 Bostwick Ave. NE, Grand Rapids, MI, 49503, USA.
Patrik BrundinCenter for Neurodegenerative Science, Van Andel Research Institute, 333 Bostwick Ave. NE, Grand Rapids, MI, 49503, USA.
Van Andel Institute · US

Funding

Linking Synucleinopathy and Dysfunction of Olfactory PathwaysR01DC016519 · NIDCD · VAN ANDEL RESEARCH INSTITUTE · PI MOORE, DARREN JOHN, WESSON, DANIEL W · 2017 to 2021
$2.8M
Does Microglial Activation Influence Propagation of Alpha-synuclein PathologyR21NS093993 · NINDS · VAN ANDEL RESEARCH INSTITUTE · PI BRUNDIN, PATRIK · 2016 to 2017
$523k
Promoting survival of dopamine neurons in models of Parkinsons disease using a novel transcriptional regulatorR21NS105436 · NINDS · VAN ANDEL RESEARCH INSTITUTE · PI BRUNDIN, PATRIK, TAYLOR, MERRITT KEARNY · 2018 to 2019
$508k
NIDCD NIH HHS R01 DC016519NINDS NIH HHS R21 NS093993NINDS NIH HHS R21 NS105436
6 · The paper itself

Abstract

Parkinson's disease is characterized by the loss of nigrostriatal dopaminergic signaling and the presence of alpha-synuclein aggregates (also called Lewy bodies and neurites) throughout the brain. In 2003, Braak and colleagues created a staging system for Parkinson's disease describing the connection between the alpha-synuclein pathology and disease severity. Later, they suggested that the pathology might initially be triggered by exogenous insults targeting the gut and olfactory system. In 2008, we and other groups documented Lewy pathology in grafted neurons in people with Parkinson's disease who had been transplanted over a decade prior to autopsy. We proposed that the Lewy pathology in the grafted neurons was the result of permissive templating or prion-like spread of alpha-synuclein pathology from neurons in the host to those in the grafts. During the following ten years, several studies described the transmission of alpha-synuclein pathology between neurons, both in cell culture and in experimental animals. Recent research has also begun to identify underlying molecular mechanisms. Collectively, these experimental studies tentatively support the idea that the progression from one Braak stage to the next is the consequence of prion-like propagation of Lewy pathology. However, definitive proof that intercellular propagation of alpha-synuclein pathology occurs in Parkinson's disease cases has proven difficult to secure. In this review, we highlight several open questions that currently prevent us from concluding with certainty that prion-like transfer of alpha-synuclein contributes to the progression of Parkinson's disease.

Indexed as

alpha-SynucleinAnimalsConnectomeHumansNeuronsParkinson DiseasePrionsProtein Aggregatesalpha-SynucleinPrionsProtein AggregatesParkinson’s diseaseTransmissionα-synuclein, aggregation

Identifiers

PMID29480459
PMCPMC6541204
OpenAlexW2792619350

What OpenQuestion holds

Textmetadata
LicenceTDM
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.