Evidence map›Paper›PMID 27098666›Full record

ReviewJournal of neural transmission (Vienna, Austria : 1996)2016

Multiple system atrophy: pathogenic mechanisms and biomarkers.

Kurt A Jellinger, Gregor K Wenning

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of neural transmission (Vienna, Austria : 1996), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
7.0field-weighted citation impact, top 3% 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

37 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. The 'α-synucleinopathy syndicate': multiple system atrophy and Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Mild cognitive impairment in multiple system atrophy: a brain network disorder.Journal of neural transmission (Vienna, Austria : 1996) · 2023
    Review
  11. Article
  12. Review
  13. Article
  14. Current experimental disease-modifying therapeutics for multiple system atrophy.Journal of neural transmission (Vienna, Austria : 1996) · 2021
    Review
  15. Review
  16. Article
  17. Article
  18. Review
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  20. 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 at 1 institution in 1 country.

Kurt A JellingerInstitute of Clinical Neurobiology, Alberichgasse 5/13, 1150, Vienna, Austria. kurt.jellinger@univie.ac.at.
Gregor K WenningDivision of Clinical Neurobiology, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
Innsbruck Medical University · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple system atrophy (MSA) is a unique proteinopathy that differs from other α-synucleinopathies since the pathological process resulting from accumulation of aberrant α-synuclein (αSyn) involves the oligodendroglia rather than neurons, although both pathologies affect multiple parts of the brain, spinal cord, autonomic and peripheral nervous system. Both the etiology and pathogenesis of MSA are unknown, although animal models have provided insight into the basic molecular changes of this disorder. Accumulation of aberrant αSyn in oligodendroglial cells and preceded by relocation of p25α protein from myelin to oligodendroglia results in the formation of insoluble glial cytoplasmic inclusions that cause cell dysfunction and demise. These changes are associated with proteasomal, mitochondrial and lipid transport dysfunction, oxidative stress, reduced trophic transport, neuroinflammation and other noxious factors. Their complex interaction induces dysfunction of the oligodendroglial-myelin-axon-neuron complex, resulting in the system-specific pattern of neurodegeneration characterizing MSA as a synucleinopathy with oligodendroglio-neuronopathy. Propagation of modified toxic αSyn species from neurons to oligodendroglia by "prion-like" transfer and its spreading associated with neuronal pathways result in a multi-system involvement. No reliable biomarkers are currently available for the clinical diagnosis and prognosis of MSA. Multidisciplinary research to elucidate the genetic and molecular background of the deleterious cycle of noxious processes, to develop reliable diagnostic biomarkers and to deliver targets for effective treatment of this hitherto incurable disorder is urgently needed.

Indexed as

BiomarkersAnimalsHumansMultiple System AtrophyBiomarkersEtiopathogenesisFluid biomarkerGlial/neuronal inclusionsGlioneuronal degenerationMultiple system atrophyOligodendrogliopathyα-Synuclein

Identifiers

PMID27098666
OpenAlexW2340875712

What OpenQuestion holds

Textmetadata
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.