Evidence map›Paper›PMID 24524809›Full record

ArticleJournal of veterinary internal medicine

Breed distribution of SOD1 alleles previously associated with canine degenerative myelopathy.

R Zeng, J R Coates, G C Johnson, L Hansen, T Awano, A Kolicheski, E Ivansson, M Perloski, K Lindblad-Toh, D P O'Brien and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of veterinary internal medicine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.8field-weighted citation impact, top 4% 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

60 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
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  11. Absence ofVeterinary sciences · 2025
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  15. Whole exome sequencing as a screening tool in dogs: A pilot study.Computational and structural biotechnology journal · 2025
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  18. Common Neurologic Diseases in Geriatric Dogs.Animals : an open access journal from MDPI · 2024
    Review
  19. Ethical Concerns about Fashionable Dog Breeding.Animals : an open access journal from MDPI · 2024
    Review
  20. HomozygousGenes · 2024
    Article
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

13 authors at 5 institutions in 2 countries.

R ZengDepartment of Veterinary Pathology, University of Missouri, Columbia, MO.
J R Coates
G C Johnson
L Hansen
T Awano
A Kolicheski
E Ivansson
M Perloski
K Lindblad-Toh
D P O'Brien
J Guo
M L Katz
G S Johnson
Missouri College · USBroad Institute · USColumbia University Irving Medical Center · USUppsala University · SEVirginia Mason Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrevious reports associated 2 mutant SOD1 alleles (SOD1:c.118A and SOD1:c.52T) with degenerative myelopathy in 6 canine breeds. The distribution of these alleles in other breeds has not been reported.

objectiveTo describe the distribution of SOD1:c.118A and SOD1:c.52T in 222 breeds. ANIMALS: DNA from 33,747 dogs was genotyped at SOD1:c.118, SOD1:c.52, or both. Spinal cord sections from 249 of these dogs were examined.

methodsRetrospective analysis of 35,359 previously determined genotypes at SOD1:c.118G>A or SOD1:c.52A>T and prospective survey to update the clinical status of a subset of dogs from which samples were obtained with a relatively low ascertainment bias.

resultsThe SOD1:c.118A allele was found in cross-bred dogs and in 124 different canine breeds whereas the SOD1:c.52T allele was only found in Bernese Mountain Dogs. Most of the dogs with histopathologically confirmed degenerative myelopathy were SOD1:c.118A homozygotes, but 8 dogs with histopathologically confirmed degenerative myelopathy were SOD1:c.118A/G heterozygotes and had no other sequence variants in their SOD1 amino acid coding regions. The updated clinical conditions of dogs from which samples were obtained with a relatively low ascertainment bias suggest that SOD1:c.118A homozygotes are at a much higher risk of developing degenerative myelopathy than are SOD1:c.118A/G heterozygotes. CONCLUSIONS AND CLINICAL IMPORTANCE: We conclude that the SOD1:c.118A allele is widespread and common among privately owned dogs whereas the SOD1:c.52T allele is rare and appears to be limited to Bernese Mountain Dogs. We also conclude that breeding to avoid the production of SOD1:c.118A homozygotes is a rational strategy.

Indexed as

AllelesAnimalsDog DiseasesDogsGene FrequencyGenetic Predisposition to DiseaseGenotypeHomozygoteMuscular Atrophy, SpinalMutation, MissenseSpecies SpecificitySuperoxide DismutaseSuperoxide DismutaseAmyotrophic lateral sclerosisCytoplasmic aggregatesDNA testSpinal cord

Identifiers

PMID24524809
PMCPMC4238831
OpenAlexW2152934293

What OpenQuestion holds

Textmetadata
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.