Evidence map›Paper›PMID 18219386›Full record

ArticleThe Journal of clinical investigation2008

Revisiting oxidative damage in ALS: microglia, Nox, and mutant SOD1.

Séverine Boillée, Don W Cleveland

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
7.3field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Neuroimmunometabolism: A New Pathological Nexus Underlying Neurodegenerative Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Neurotheranostics as personalized medicines.Advanced drug delivery reviews · 2019
    Review
  11. Neuron-targeted caveolin-1 improves neuromuscular function and extends survival in SOD1FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Expression of the ALS-causing variant hSOD1(G93A) leads to an impaired integrity and altered regulation of claudin-5 expression in an in vitro blood-spinal cord barrier model.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015
    Article
  20. CCR2 antagonism alters brain macrophage polarization and ameliorates cognitive dysfunction induced by traumatic brain injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 2 countries.

Séverine BoilléeLudwig Institute for Cancer Research, Department of Medicine, and Department of Neuroscience, UCSD, La Jolla, California 92030, USA.
Don W Cleveland
Ludwig Cancer Research · BE

Funding

Neurofilaments, SOD1 and Motor Neuron DiseasesR37NS027036 · NINDS · LUDWIG INSTITUTE FOR CANCER RES LTD · PI CLEVELAND, DON W · 2005 to 2011
$4.1M
NINDS NIH HHS R37 NS027036
6 · The paper itself

Abstract

Mutation in superoxide dismutase-1 (SOD1) causes the inherited degenerative neurological disease familial amyotrophic lateral sclerosis (ALS), a non-cell-autonomous disease: mutant SOD1 synthesis in motor neurons and microglia drives disease onset and progression, respectively. In this issue of the JCI, Harraz and colleagues demonstrate that SOD1 mutants expressed in human cell lines directly stimulate NADPH oxidase (Nox) by binding to Rac1, resulting in overproduction of damaging ROS (see the related article beginning on page 659). Diminishing ROS by treatment with the microglial Nox inhibitor apocynin or by elimination of Nox extends survival in ALS mice, reviving the proposal that ROS mediate ALS pathogenesis, but with a new twist: it's ROS produced by microglia.

Indexed as

Oxidative StressAcetophenonesAmyotrophic Lateral SclerosisAnimalsEnzyme InhibitorsHumansMiceMicrogliaMotor NeuronsNADPH Oxidasesrac1 GTP-Binding ProteinReactive Oxygen SpeciesSuperoxide DismutaseSuperoxide Dismutase-1SuperoxidesAcetophenonesacetovanilloneEnzyme InhibitorsNADPH Oxidasesrac1 GTP-Binding ProteinRAC1 protein, humanReactive Oxygen SpeciesSOD1 protein, humanSod1 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1Superoxides

Identifiers

PMID18219386
PMCPMC2213376
OpenAlexW2064923216

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.