Evidence map›Paper›PMID 24894118›Full record

ReviewParkinsonism & related disorders2014

Multiple system atrophy as emerging template for accelerated drug discovery in α-synucleinopathies.

Florian Krismer, Kurt A Jellinger, Sonja W Scholz, Klaus Seppi, Nadia Stefanova, Angelo Antonini, Werner Poewe, Gregor K Wenning

Abstract readReview
In one paragraph

Review in Parkinsonism & related disorders, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Simplified quantification of [Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Trial
  3. Review
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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

8 authors.

Florian KrismerDepartment of Neurology, Innsbruck Medical University, Innsbruck, Austria. Electronic address: florian.krismer@i-med.ac.at.
Kurt A JellingerInstitute of Clinical Neurobiology, Vienna, Austria. Electronic address: kurt.jellinger@univie.ac.at.
Sonja W ScholzDepartment of Neurology, The Johns Hopkins Hospital, Baltimore, MD 21287, USA. Electronic address: sonja.w.scholz@googlemail.com.
Klaus SeppiDepartment of Neurology, Innsbruck Medical University, Innsbruck, Austria. Electronic address: klaus.seppi@uki.at.
Nadia StefanovaDepartment of Neurology, Innsbruck Medical University, Innsbruck, Austria. Electronic address: nadia.stefanova@i-med.ac.at.
Angelo AntoniniDepartment of Parkinson's Disease and Movement Disorders, IRCCS San Camillo, Venice, Italy. Electronic address: angelo3000@yahoo.com.
Werner PoeweDepartment of Neurology, Innsbruck Medical University, Innsbruck, Austria. Electronic address: werner.poewe@i-med.ac.at.
Gregor K WenningDepartment of Neurology, Innsbruck Medical University, Innsbruck, Austria. Electronic address: Gregor.Wenning@i-med.ac.at.

Funding

Research Education Program for Residents and Fellows in Neurology - PorrasR25NS065729 · NINDS · JOHNS HOPKINS UNIVERSITY · PI HILLIS, ARGYE E. · 2009 to 2024
$3.3M
NINDS NIH HHS R25 NS065729
6 · The paper itself

Abstract

There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated.

Indexed as

Drug DiscoveryMultiple System AtrophyParkinson Diseasealpha-SynucleinHumansalpha-SynucleinDrug developmentMultiple system atrophyParkinson's diseaseSynucleinopathies

Identifiers

PMID24894118
PMCPMC4141743

What OpenQuestion holds

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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.