Evidence map›Paper›PMID 28241427›Full record

ReviewInternational journal of molecular sciences2017

Potential Modes of Intercellular α-Synuclein Transmission.

Dario Valdinocci, Rowan A W Radford, Sue Maye Siow, Roger S Chung, Dean L Pountney

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
–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

63 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. A Randomized First-in-Human Study With UB-312, a UBITh® α-Synuclein Peptide Vaccine.Movement disorders : official journal of the Movement Disorder Society · 2022
    Trial
  4. Review
  5. Article
  6. Review
  7. Autophagy · 2025
    Article
  8. PTEN: a new dawn in Parkinson's disease treatment.Frontiers in cellular neuroscience · 2025
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Circadian clock protein BMAL1 broadly influences autophagy and endolysosomal function in astrocytes.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  20. The Interplay between α-Synuclein and Microglia in α-Synucleinopathies.International journal of molecular sciences · 2023
    Review

3 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

5 authors.

Dario ValdinocciMenzies Health Institute Queensland, Griffith University, Gold Coast 4222, Australia. dario.valdinocci@griffithuni.edu.au.
Rowan A W RadfordDepartment of Biomedical Sciences, Faculty of Medical and Health Sciences, Macquarie University, Sydney 2109, Australia. rowan.radford@students.mq.edu.au.
Sue Maye SiowMenzies Health Institute Queensland, Griffith University, Gold Coast 4222, Australia. suemaye.siow@griffithuni.edu.au.
Roger S ChungDepartment of Biomedical Sciences, Faculty of Medical and Health Sciences, Macquarie University, Sydney 2109, Australia. roger.chung@mq.edu.au.
Dean L PountneyMenzies Health Institute Queensland, Griffith University, Gold Coast 4222, Australia. d.pountney@griffith.edu.au.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intracellular aggregates of the α-synuclein protein result in cell loss and dysfunction in Parkinson's disease and atypical Parkinsonism, such as multiple system atrophy and dementia with Lewy bodies. Each of these neurodegenerative conditions, known collectively as α-synucleinopathies, may be characterized by a different suite of molecular triggers that initiate pathogenesis. The mechanisms whereby α-synuclein aggregates mediate cytotoxicity also remain to be fully elucidated. However, recent studies have implicated the cell-to-cell spread of α-synuclein as the major mode of disease propagation between brain regions during disease progression. Here, we review the current evidence for different modes of α-synuclein cellular release, movement and uptake, including exocytosis, exosomes, tunneling nanotubes, glymphatic flow and endocytosis. A more detailed understanding of the major modes by which α-synuclein pathology spreads throughout the brain may provide new targets for therapies that halt the progression of disease.

Indexed as

Models, Biologicalalpha-SynucleinAnimalsAstrocytesCell CommunicationExosomesExtracellular SpaceHumansIntracellular SpaceLewy BodiesLewy Body DiseaseMicrogliaMultiple System AtrophyParkinson DiseaseProtein Aggregation, PathologicalProtein Bindingalpha-Synucleindementia with Lewy bodiesexosomegliosisglymphaticmultiple system atrophyParkinson’s diseasetunneling nanotubeα-synuclein

Identifiers

PMID28241427
PMCPMC5344001

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.