Evidence map›Paper›PMID 24598411›Full record

ReviewProgress in neurobiology2014

Towards translational therapies for multiple system atrophy.

Daniela Kuzdas-Wood, Nadia Stefanova, Kurt A Jellinger, Klaus Seppi, Michael G Schlossmacher, Werner Poewe, Gregor K Wenning

Open access · hybridAbstract readReview
In one paragraph

Review in Progress in neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Cerebrospinal fluid levels of neurofilament light chain in multiple system atrophy relative to Parkinson's disease: a meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017
    Pooled it
  2. Review
  3. Exidavnemab binds to aggregated α-synuclein in human brains affected by α-synucleinopathies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Synucleinopathies: common features and hippocampal manifestations.Cellular and molecular life sciences : CMLS · 2017
    Review
  12. Article
  13. Article
  14. Multiple system atrophy: pathogenic mechanisms and biomarkers.Journal of neural transmission (Vienna, Austria : 1996) · 2016
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
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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

7 authors at 2 institutions in 2 countries.

Daniela Kuzdas-WoodDepartment of Neurology, Innsbruck Medical University, Anichstraße 35, Innsbruck 6020, Austria.
Nadia StefanovaDepartment of Neurology, Innsbruck Medical University, Anichstraße 35, Innsbruck 6020, Austria.
Kurt A JellingerInstitute of Clinical Neurobiology, Vienna, Austria.
Klaus SeppiDepartment of Neurology, Innsbruck Medical University, Anichstraße 35, Innsbruck 6020, Austria.
Michael G SchlossmacherDivisions of Neuroscience and Neurology, The Ottawa Hospital Research Institute, University of Ottawa, 451 Smyth Road, RGH #1412, Ottawa, ON, K1H 8M5, Canada.
Werner PoeweDepartment of Neurology, Innsbruck Medical University, Anichstraße 35, Innsbruck 6020, Austria.
Gregor K WenningDepartment of Neurology, Innsbruck Medical University, Anichstraße 35, Innsbruck 6020, Austria. Electronic address: gregor.wenning@i-med.ac.at.
Innsbruck Medical University · ATUniversity of Ottawa · CA

Funding

Austrian Science Fund FWF P 25161Austrian Science Fund FWF W 1206
6 · The paper itself

Abstract

Multiple system atrophy (MSA) is a fatal adult-onset neurodegenerative disorder of uncertain etiopathogenesis manifesting with autonomic failure, parkinsonism, and ataxia in any combination. The underlying neuropathology affects central autonomic, striatonigral and olivopontocerebellar pathways and it is associated with distinctive glial cytoplasmic inclusions (GCIs, Papp-Lantos bodies) that contain aggregates of α-synuclein. Current treatment options are very limited and mainly focused on symptomatic relief, whereas disease modifying options are lacking. Despite extensive testing, no neuroprotective drug treatment has been identified up to now; however, a neurorestorative approach utilizing autologous mesenchymal stem cells has shown remarkable beneficial effects in the cerebellar variant of MSA. Here, we review the progress made over the last decade in defining pathogenic targets in MSA and summarize insights gained from candidate disease-modifying interventions that have utilized a variety of well-established preclinical MSA models. We also discuss the current limitations that our field faces and suggest solutions for possible approaches in cause-directed therapies of MSA.

Indexed as

alpha-SynucleinAnimalsBiomarkersClinical Trials as TopicDisease Models, AnimalHumansMitochondriaMultiple System AtrophyOxidative Stressalpha-SynucleinBiomarkersAlpha-synucleinMultiple system atrophyNeurodegenerationOlivopontocerebellar atrophyStriatonigral degeneration

Identifiers

PMID24598411
PMCPMC4068324
OpenAlexW2042224862

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.