Evidence map›Paper›PMID 29627580›Full record

ArticleNeurobiology of disease2018

Poloxamer 188 decreases membrane toxicity of mutant SOD1 and ameliorates pathology observed in SOD1 mouse model for ALS.

Jacob J Riehm, Lijun Wang, Ghanashyam Ghadge, Michael Teng, Ana M Correa, Jeremy D Marks, Raymond P Roos, Michael J Allen

Open access · hybridAbstract read
In one paragraph

Article in Neurobiology of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Preparation, characterization, andAsian journal of pharmaceutical sciences · 2018
    Article
  9. 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

8 authors at 1 institution in 1 country.

Jacob J RiehmDepartment of Medicine, Section of Pulmonary Critical Care, The University of Chicago, Chicago, IL, USA.
Lijun WangDepartment of Neurology, The University of Chicago, Chicago, IL, USA.
Ghanashyam GhadgeDepartment of Neurology, The University of Chicago, Chicago, IL, USA.
Michael TengDepartment of Medicine, Section of Pulmonary Critical Care, The University of Chicago, Chicago, IL, USA.
Ana M CorreaDepartment of Biochemistry and Molecular Biology, The University of Chicago, Chicago, IL, USA.
Jeremy D MarksDepartment of Pediatrics, The University of Chicago, Chicago, IL, USA.
Raymond P RoosDepartment of Neurology, The University of Chicago, Chicago, IL, USA. Electronic address: rroos@neurology.bsd.uchicago.edu.
Michael J AllenDepartment of Medicine, Section of Pulmonary Critical Care, The University of Chicago, Chicago, IL, USA.
University of Chicago · US

Funding

Synthetic Antigen Binder CoreU54GM087519 · NIGMS · UNIVERSITY OF CHICAGO · PI PEROZO, EDUARDO A · 2010 to 2017
$31.9M
Mechanisms of Co-Polymer-Mediated NeuroprotectionR01NS056313 · NINDS · UNIVERSITY OF CHICAGO · PI MARKS, JEREMY D · 2007 to 2011
$1.8M
The Role of Toxic Ion Channels in ALS PathogenesisR01NS067247 · NINDS · UNIVERSITY OF CHICAGO · PI ALLEN, MICHAEL J · 2009 to 2013
$1.7M
NIGMS NIH HHS U54 GM087519NINDS NIH HHS R01 NS056313NINDS NIH HHS R01 NS067247
6 · The paper itself

Abstract

Here we report a gain in function for mutant (mt) superoxide dismutase I (SOD1), a cause of familial amyotrophic lateral sclerosis (FALS), wherein small soluble oligomers of mtSOD1 acquire a membrane toxicity. Phosphatidylglycerol (PG) lipid domains are selectively targeted, which could result in membrane damage or "toxic channels" becoming active in the bilayer. This PG-selective SOD1-mediated membrane toxicity is largely reversible in vitro by a widely-available FDA-approved surfactant and membrane-stabilizer P188. Treatment of G93ASOD1 transgenic mice with P188 significantly delayed symptoms onset, extended survival and decreased motoneuron death. The use of P188 or an analogue, which targets mtSOD1 misfolding-induced membrane toxicity, may provide a new direction for ALS treatment.

Indexed as

Amyotrophic Lateral SclerosisAnimalsCell MembraneHumansMaleMiceMice, TransgenicMutationPoloxamerSuperoxide Dismutase-1Surface-Active AgentsPoloxamerSod1 protein, mouseSuperoxide Dismutase-1Surface-Active AgentsAFMALSAtomic force microscopyElectrophysiologyF68G93ALipid peroxidationMembrane toxicityP188PoloxamerProtein misfoldingSOD1Superoxide dismutase

Identifiers

PMID29627580
PMCPMC5943144
OpenAlexW2795810606

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.