Evidence map›Paper›PMID 27259295›Full record

ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2016

Neuroprotection by Epigenetic Modulation in a Transgenic Model of Multiple System Atrophy.

Edith Sturm, Lisa Fellner, Florian Krismer, Werner Poewe, Gregor K Wenning, Nadia Stefanova

Open access · hybridAbstract read
In one paragraph

Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2016. 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
1.6field-weighted citation impact, top 17% 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, 17 citations in OpenAlex.

  1. Recent Advances in Clinical Trials in Multiple System Atrophy.Current neurology and neuroscience reports · 2024
    Review
  2. Review
  3. A Mouse Model of Multiple System Atrophy: Bench to Bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  4. Review
  5. Current experimental disease-modifying therapeutics for multiple system atrophy.Journal of neural transmission (Vienna, Austria : 1996) · 2021
    Review
  6. Signs of early cellular dysfunction in multiple system atrophy.Neuropathology and applied neurobiology · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Multiple System Atrophy - State of the Art.Current neurology and neuroscience reports · 2017
    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 2 institutions in 1 country.

Edith SturmDivision of Neurobiology, Department of Neurology, Medical University of Innsbruck, Anichstr. 35, 6020, Innsbruck, Austria.
Lisa FellnerDivision of Neurobiology, Department of Neurology, Medical University of Innsbruck, Anichstr. 35, 6020, Innsbruck, Austria.
Florian KrismerDivision of Neurobiology, Department of Neurology, Medical University of Innsbruck, Anichstr. 35, 6020, Innsbruck, Austria.
Werner PoeweDivision of Neurobiology, Department of Neurology, Medical University of Innsbruck, Anichstr. 35, 6020, Innsbruck, Austria.
Gregor K WenningDivision of Neurobiology, Department of Neurology, Medical University of Innsbruck, Anichstr. 35, 6020, Innsbruck, Austria.
Nadia StefanovaDivision of Neurobiology, Department of Neurology, Medical University of Innsbruck, Anichstr. 35, 6020, Innsbruck, Austria. nadia.stefanova@i-med.ac.at.
Innsbruck Medical University · ATUniversität Innsbruck · AT

Funding

Austrian Science Fund FWF F 4414Austrian Science Fund FWF P 25161
6 · The paper itself

Abstract

Similar to Parkinson disease, multiple system atrophy (MSA) presents neuropathologically with nigral neuronal loss; however, the hallmark intracellular α-synuclein (αSyn) accumulation in MSA affects typically oligodendrocytes to form glial cytoplasmic inclusions. The underlying pathogenic mechanisms remain unclear. As MSA is predominantly sporadic, epigenetic mechanisms may play a role. We tested the effects of the pan-histone deacetylase inhibitor (HDACi) sodium phenylbutyrate in aged mice overexpressing αSyn under the control of the proteolipid protein promoter (PLP-αSyn) designed to model MSA and characterized by αSyn accumulation in oligodendrocytes and nigral neurodegeneration. HDACi improved motor behavior and survival of nigral neurons in PLP-αSyn mice. Furthermore, HDACi reduced the density of oligodendroglial αSyn aggregates, which correlated with the survival of nigral neurons in PLP-αSyn mice. For the first time, we suggest a role of HDACi in the pathogenesis of MSA-like neurodegeneration and support the future development of selective HDACi for MSA therapy.

Indexed as

Agingalpha-SynucleinAnimalsBrainDisease Models, AnimalEpigenesis, GeneticFemaleGait Disorders, NeurologicMaleMiceMice, Inbred C57BLMice, TransgenicMultiple System AtrophyMyelin Proteolipid ProteinNeurogliaNeurons4-phenylbutyric acidalpha-SynucleinMyelin Proteolipid ProteinNeuroprotective AgentsPhenylbutyratesPlp1 protein, mouseProtein Deglycase DJ-1histone acetylationneuroprotectionnigral degenerationphenylbutyrateα-Synuclein

Identifiers

PMID27259295
PMCPMC5081120
OpenAlexW2416697945

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.