Evidence map›Paper›PMID 30572656›Full record

ReviewInternational journal of molecular sciences2018

Extracellular Interactions of Alpha-Synuclein in Multiple System Atrophy.

Dario Valdinocci, Rowan A W Radford, Michael Goulding, Junna Hayashi, Roger S Chung, Dean L Pountney

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
25.2field-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

20 citing papers in PubMed, 159 citations in OpenAlex.

  1. Trial
  2. Article
  3. Reduced coupling of global brain function and cerebrospinal fluid dynamics in Parkinson's disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Article
  4. Article
  5. Review
  6. Serotonin Transporter Imaging in Multiple System Atrophy and Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2022
    Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Decoupling of Global Brain Activity and Cerebrospinal Fluid Flow in Parkinson's Disease Cognitive Decline.Movement disorders : official journal of the Movement Disorder Society · 2021
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

6 authors at 3 institutions in 1 country.

Dario ValdinocciSchool of Medical Science, Griffith University, Gold Coast 4222, Australia. dario.valdinocci@griffithuni.edu.au.
Rowan A W RadfordCentre for Motor Neuron Disease Research, Department of Biomedical Sciences, Faculty of Medical and Health Sciences, Macquarie University, Sydney 2109, Australia. rowan.radford@students.mq.edu.au.
Michael GouldingSchool of Medical Science, Griffith University, Gold Coast 4222, Australia. michael.goulding@griffithuni.edu.au.
Junna HayashiResearch School of Chemistry, Australian National University, Canberra 2601, Australia. junna.hayashi@anu.edu.au.
Roger S ChungCentre for Motor Neuron Disease Research, Department of Biomedical Sciences, Faculty of Medical and Health Sciences, Macquarie University, Sydney 2109, Australia. roger.chung@mq.edu.au.
Dean L PountneySchool of Medical Science, Griffith University, Gold Coast 4222, Australia. d.pountney@griffith.edu.au.
Griffith University · AUMacquarie University · AUAustralian National University · AU

Funding

Griffith University NoneMacquarie University None
6 · The paper itself

Abstract

Multiple system atrophy, characterized by atypical Parkinsonism, results from central nervous system (CNS) cell loss and dysfunction linked to aggregates of the normally pre-synaptic α-synuclein protein. Mostly cytoplasmic pathological α-synuclein inclusion bodies occur predominantly in oligodendrocytes in affected brain regions and there is evidence that α-synuclein released by neurons is taken up preferentially by oligodendrocytes. However, extracellular α-synuclein has also been shown to interact with other neural cell types, including astrocytes and microglia, as well as extracellular factors, mediating neuroinflammation, cell-to-cell spread and other aspects of pathogenesis. Here, we review the current evidence for how α-synuclein present in the extracellular milieu may act at the cell surface to drive components of disease progression. A more detailed understanding of the important extracellular interactions of α-synuclein with neuronal and non-neuronal cell types both in the brain and periphery may provide new therapeutic targets to modulate the disease process.

Indexed as

alpha-SynucleinAnimalsAstrocytesExtracellular SpaceHumansMicrogliaMultiple System AtrophyNeuronsOligodendrogliaalpha-Synucleinchaperonegliosisglymphaticmultiple system atrophyneuroinflammationα-synuclein

Identifiers

PMID30572656
PMCPMC6320782
OpenAlexW2903644235

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.