Evidence map›Paper›PMID 26785838›Full record

ReviewNeuropathology and applied neurobiology2016

Review: Multiple system atrophy: emerging targets for interventional therapies.

N Stefanova, G K Wenning

Open access · hybridAbstract readReview
In one paragraph

Review in Neuropathology and applied neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
6.5field-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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  10. Signs of early cellular dysfunction in multiple system atrophy.Neuropathology and applied neurobiology · 2021
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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

2 authors at 1 institution in 1 country.

N StefanovaDivision of Neurobiology, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
G K WenningDivision of Neurobiology, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
Innsbruck Medical University · AT

Funding

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

Abstract

Multiple system atrophy (MSA) is a fatal orphan neurodegenerative disorder that manifests with rapidly progressive autonomic and motor dysfunction. The disease is characterized by the accumulation of α-synuclein fibrils in oligodendrocytes that form glial cytoplasmic inclusions, a neuropathological hallmark and central player in the pathogenesis of MSA. Here, we summarize the current knowledge on the etiopathogenesis and neuropathology of MSA. We discuss the role of α-synuclein pathology, microglial activation, oligodendroglial dysfunction and putative cell death mechanisms as candidate therapeutic targets in MSA.

Indexed as

alpha-SynucleinAnimalsHumansMultiple System Atrophyalpha-Synucleinaetiologyclinical trialmultiple system atrophyneuropathologypathogenesisα-synuclein

Identifiers

PMID26785838
PMCPMC4788141
OpenAlexW2301227099

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.