Evidence map›Paper›PMID 33071772›Full record

ReviewFrontiers in synaptic neuroscience2020

From Synaptic Protein to Prion: The Long and Controversial Journey of α-Synuclein.

Antonio Heras-Garvin, Nadia Stefanova

Abstract readReview
In one paragraph

Review in Frontiers in synaptic neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. BDNF/TrkB activators in Parkinson's disease: A new therapeutic strategy.Journal of cellular and molecular medicine · 2024
    Review
  6. Review
  7. Review
  8. Review
  9. Neuropathology of multiple system atrophy: Kurt Jellinger`s legacy.Journal of neural transmission (Vienna, Austria : 1996) · 2021
    Review
  10. Is Multiple System Atrophy a Prion-like Disorder?International journal of molecular sciences · 2021
    Review
  11. Review
  12. Review
  13. Review
  14. Article
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

2 authors.

Antonio Heras-GarvinDivision of Neurobiology, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
Nadia StefanovaDivision of Neurobiology, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since its discovery 30 years ago, α-synuclein (α-syn) has been one of the most studied proteins in the field of neuroscience. Dozens of groups worldwide have tried to reveal not only its role in the CNS but also in other organs. α-syn has been linked to several processes essential in brain homeostasis such as neurotransmitter release, synaptic function, and plasticity. However, despite the efforts made in this direction, the main function of α-syn is still unknown. Moreover, α-syn became a protein of interest for neurologists and neuroscientists when mutations in its gene were found associated with Parkinson's disease (PD) and even more when α-syn protein deposits were observed in the brain of PD, dementia with Lewy bodies (DLB), and multiple system atrophy (MSA) patients. At present, the abnormal accumulation of α-syn constitutes one of the pathological hallmarks of these disorders, also referred to as α-synucleinopathies, and it is used for post-mortem diagnostic criteria. Whether α-syn aggregation is cause or consequence of the pathogenic events underlying α-synucleinopathies remains unclear and under discussion. Recently, different

Indexed as

neurodegenerationParkinson’s diseaseprionα-synucleinα-synucleinopathies

Identifiers

PMID33071772
PMCPMC7536368

What OpenQuestion holds

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Registered trials

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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.