Evidence map›Paper›PMID 22412900›Full record

ArticlePloS one2012

Genetic biomarkers for ALS disease in transgenic SOD1(G93A) mice.

Ana C Calvo, Raquel Manzano, Gabriela Atencia-Cibreiro, Sara Oliván, María J Muñoz, Pilar Zaragoza, Pilar Cordero-Vázquez, Jesús Esteban-Pérez, Alberto García-Redondo, Rosario Osta

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  10. Identification of a novel mutation in MEF2C gene in an atypical patient with frontotemporal lobar degeneration.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Article
  11. Review
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  13. Inflammasome in ALS Skeletal Muscle:International journal of molecular sciences · 2021
    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

10 authors at 3 institutions in 1 country.

Ana C CalvoLaboratorio de Genética Bioquímica (LAGENBIO-I3A), Aragon's Institute of Health Sciences (IACS), Facultad de Veterinaria, Universidad de Zaragoza, Zaragoza, Spain.
Raquel Manzano
Gabriela Atencia-Cibreiro
Sara Oliván
María J Muñoz
Pilar Zaragoza
Pilar Cordero-Vázquez
Jesús Esteban-Pérez
Alberto García-Redondo
Rosario Osta
Universidad de Zaragoza · ESCentre for Biomedical Network Research on Rare Diseases · ESResearch Institute Hospital 12 de Octubre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathophysiological mechanisms of both familial and sporadic Amyotrophic Lateral Sclerosis (ALS) are unknown, although growing evidence suggests that skeletal muscle tissue is a primary target of ALS toxicity. Skeletal muscle biopsies were performed on transgenic SOD1(G93A) mice, a mouse model of ALS, to determine genetic biomarkers of disease longevity. Mice were anesthetized with isoflurane, and three biopsy samples were obtained per animal at the three main stages of the disease. Transcriptional expression levels of seventeen genes, Ankrd1, Calm1, Col19a1, Fbxo32, Gsr, Impa1, Mef2c, Mt2, Myf5, Myod1, Myog, Nnt, Nogo A, Pax7, Rrad, Sln and Snx10, were tested in each muscle biopsy sample. Total RNA was extracted using TRIzol Reagent according to the manufacturer's protocol, and variations in gene expression were assayed by real-time PCR for all of the samples. The Pearson correlation coefficient was used to determine the linear correlation between transcriptional expression levels throughout disease progression and longevity. Consistent with the results obtained from total skeletal muscle of transgenic SOD1(G93A) mice and 74-day-old denervated mice, five genes (Mef2c, Gsr, Col19a1, Calm1 and Snx10) could be considered potential genetic biomarkers of longevity in transgenic SOD1(G93A) mice. These results are important because they may lead to the exploration of previously unexamined tissues in the search for new disease biomarkers and even to the application of these findings in human studies.

Indexed as

Amyotrophic Lateral SclerosisAnimalsBiopsyDenervationDisease Models, AnimalDisease ProgressionFemaleGene Expression ProfilingGene Expression RegulationGenetic MarkersHumansLongevityMaleMiceMice, TransgenicMuscle, SkeletalGenetic MarkersMutant ProteinsSOD1 protein, humanSod1 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1

Identifiers

PMID22412900
PMCPMC3296719
OpenAlexW2010983646

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.