Evidence map›Paper›PMID 26010802›Full record

ArticleThe Journal of comparative neurology2015

Identification of B6SJL mSOD1(G93A) mouse subgroups with different disease progression rates.

Melissa M Haulcomb, Nichole A Mesnard-Hoaglin, Richard J Batka, Rena M Meadows, Whitney M Miller, Kathryn P Mcmillan, Todd J Brown, Virginia M Sanders, Kathryn J Jones

Abstract read
In one paragraph

Article in The Journal of comparative neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–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

4 citing papers in PubMed.

  1. Article
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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

9 authors.

Melissa M HaulcombNeuroscience Program, Loyola University Medical Center, Maywood, Illinois, 60153.
Nichole A Mesnard-HoaglinNeuroscience Program, Loyola University Medical Center, Maywood, Illinois, 60153.
Richard J BatkaDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana, 46202.
Rena M MeadowsDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana, 46202.
Whitney M MillerDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana, 46202.
Kathryn P McmillanDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana, 46202.
Todd J BrownDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana, 46202.
Virginia M SandersDepartment of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, Columbus, Ohio, 43210.
Kathryn J JonesDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana, 46202.

Funding

Immune Regulation of Neuronal Injury and RepairR01NS040433 · NINDS · LOYOLA UNIVERSITY CHICAGO · PI JONES, KATHRYN JANE · 2001 to 2017
$5.9M
NINDS NIH HHS NS40433NINDS NIH HHS R01 NS040433
6 · The paper itself

Abstract

Disease progression rates among patients with amyotrophic lateral sclerosis (ALS) vary greatly. Although the majority of affected individuals survive 3-5 years following diagnosis, some subgroups experience a more rapidly progressing form, surviving less than 1 year, and other subgroups experience slowly progressing forms, surviving nearly 50 years. Genetic heterogeneity and environmental factors pose significant barriers in investigating patient progression rates. Similar to the case for humans, variation in survival within the mSOD1 mouse has been well documented, but different progression rates have not been investigated. The present study identifies two subgroups of B6SJL mSOD1(G93A) mice with different disease progression rates, a fast progression group (FPG) and slow progression group, as evidenced by differences in the rate of motor function decline. In addition, increased disease-associated gene expression within the FPG facial motor nucleus confirmed the presence of a more severe phenotype. We hypothesize that a more severe disease phenotype could be the result of 1) an earlier onset of axonal disconnection with a consistent degeneration rate or 2) a more severe or accelerated degenerative process. We performed a facial nerve transection axotomy in both mSOD1 subgroups prior to disease onset as a method to standardize the axonal disconnection. Instead of leading to comparable gene expression in both subgroups, this standardization did not eliminate the severe phenotype in the FPG facial nucleus, suggesting that the FPG phenotype is the result of a more severe or accelerated degenerative process. We theorize that these mSOD1 subgroups are representative of the rapid and slow disease phenotypes often experienced in ALS.

Indexed as

Age FactorsAmyotrophic Lateral SclerosisAnimalsDisease Models, AnimalDisease ProgressionFacial NerveFeeding BehaviorLaser Capture MicrodissectionMiceMice, Inbred C57BLMice, TransgenicMotor DisordersMuscle StrengthMutationRNA, MessengerSensation DisordersRNA, MessengerSOD1 G93A proteinSuperoxide DismutaseALSdisease progressionfacial nerve axotomygene expressionMNmotoneuronmSOD1

Identifiers

PMID26010802
PMCPMC4607568

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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.