Evidence map›Paper›PMID 29058121›Full record

ReviewActa neuropathologica2018

Multiple system atrophy: experimental models and reality.

Cassia Overk, Edward Rockenstein, Elvira Valera, Nadia Stefanova, Gregor Wenning, Eliezer Masliah

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Acta neuropathologica, 2018. 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
2.1field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Multiple system atrophy.Nature reviews. Disease primers · 2022
    Review
  4. Article
  5. Failure of Diphtheria Toxin Model to Induce Parkinson-Like Behavior in Mice.International journal of molecular sciences · 2021
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Models of multiple system atrophy.Experimental & molecular medicine · 2019
    Review
  11. Article
  12. Review
  13. Article
  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

6 authors at 4 institutions in 2 countries.

Cassia OverkDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, 92093-0624, USA.
Edward RockensteinDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, 92093-0624, USA.
Elvira ValeraDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, 92093-0624, USA.
Nadia StefanovaDivision of Clinical Neurobiology, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
Gregor WenningDivision of Clinical Neurobiology, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
Eliezer MasliahDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, 92093-0624, USA. emasliah@ucsd.edu.
University of California, San Diego · USInnsbruck Medical University · ATNational Institutes of Health · USUniversität Innsbruck · AT

Funding

B-Synuclein as a Treatment for Lewy Body DiseaseR01AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RISSMAN, ROBERT · 2001 to 2021
$5.2M
Neuroimmune responses and therapeutics of alpha-synucleinopathies of the aging populationZIAAG000936 · NIA · NATIONAL INSTITUTE ON AGING · PI COOKSON, MARK · 2017 to 2025
$4.1M
a-synuclein clearance strategies for the treatment of Lewy body disease.R37AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MASLIAH, ELIEZER · 2006 to 2014
$2.7M
Regulation of the oligodendroglial accumulation of alpha-synuclein in Multiple System AtrophyR01NS092803 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DESPLATS, PAULA ALEJANDRA · 2016 to 2020
$1.8M
Intramural NIH HHS Z99 AG999999Intramural NIH HHS ZIA AG000936NIA NIH HHS R01 AG018440NINDS NIH HHS NS092803NINDS NIH HHS R01 NS092803
6 · The paper itself

Abstract

Multiple system atrophy (MSA) is a rapidly progressing fatal synucleinopathy of the aging population characterized by parkinsonism, dysautonomia, and in some cases ataxia. Unlike other synucleinopathies, in this disorder the synaptic protein, α-synuclein (α-syn), predominantly accumulates in oligodendroglial cells (and to some extent in neurons), leading to maturation defects of oligodendrocytes, demyelination, and neurodegeneration. The mechanisms through which α-syn deposits occur in oligodendrocytes and neurons in MSA are not completely clear. While some studies suggest that α-syn might transfer from neurons to glial cells, others propose that α-syn might be aberrantly overexpressed by oligodendroglial cells. A number of in vivo models have been developed, including transgenic mice overexpressing α-syn under oligodendroglial promoters (e.g.: MBP, PLP, and CNP). Other models have been recently developed either by injecting synthetic α-syn fibrils or brain homogenates from patients with MSA into wild-type mice or by using viral vectors expressing α-syn under the MBP promoter in rats and non-human primates. Each of these models reproduces some of the neuropathological and functional aspects of MSA; however, none of them fully replicate the spectrum of MSA. Understanding better the mechanisms of how α-syn accumulates in oligodendrocytes and neurons will help in developing better models that recapitulate various pathogenic aspects of MSA in combination with translatable biomarkers of early stages of the disease that are necessary to devise disease-modifying therapeutics for MSA.

Indexed as

AnimalsDisease Models, AnimalHumansMultiple System AtrophyIn vivo modelsMultiple system atrophySynucleinopathies

Identifiers

PMID29058121
PMCPMC6156777
OpenAlexW2766463586

What OpenQuestion holds

Textmetadata
LicenceTDM
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.