Evidence map›Paper›PMID 22488161›Full record

ReviewNeurotoxicity research2012

Nitric oxide-mediated oxidative damage and the progressive demise of motor neurons in ALS.

Derek A Drechsel, Alvaro G Estévez, Luis Barbeito, Joseph S Beckman

Open access · greenAbstract readReview
In one paragraph

Review in Neurotoxicity research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
7.2field-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

69 citing papers in PubMed, 111 citations in OpenAlex.

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  17. NADBiomedicines · 2021
    Review
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9 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 2 countries.

Derek A DrechselDepartment of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331, USA.
Alvaro G Estévez
Luis Barbeito
Joseph S Beckman
Oregon State University · USInstitut Pasteur de Montevideo · UYUniversity of Central Florida · US

Funding

Reducing Susceptibility to Environmental Stress Throughout the Life SpanP30ES000210 · NIEHS · OREGON STATE UNIVERSITY · PI BECKMAN, JOSEPH S · 1985 to 2015
$21.4M
Overall Program/FreiP01AT002034 · NCCIH · OREGON STATE UNIVERSITY · PI FREI, BALZ B · 2003 to 2012
$11.7M
MODE OF ACTION OF ENVIRONMENTAL TOXICANTST32ES007060 · NIEHS · OREGON STATE UNIVERSITY · PI Jamie DeWitt, Siva Kumar Kolluri · 1985 to 2026
$11.6M
Superoxide Dismutase, Peroxynitrite and ALSR01NS058628 · NINDS · OREGON STATE UNIVERSITY · PI BECKMAN, JOSEPH S · 2008 to 2012
$1.6M
NCCIH NIH HHS P01 AT002034NCCIH NIH HHS P01AT002034NIEHS NIH HHS P30 ES000210NIEHS NIH HHS P30ES000210NIEHS NIH HHS T32 ES007060NIEHS NIH HHS T32ES07060NINDS NIH HHS R01 NS058628NINDS NIH HHS R01NS058628A
6 · The paper itself

Abstract

Oxidative damage is a common and early feature of Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and other neurodegenerative disorders. Dr. Mark Smith and his colleagues have built the case for oxidative stress being a primary progenitor rather than a secondary end-stage epiphenomenon of neurodegeneration. They proposed that reactive oxygen species contribute to the "age-related cascade of neurodegeneration," whereby accumulative oxidative damage with age promotes other characteristic pathological changes in afflicted brain regions, including protein aggregation, metabolic deficiencies, and inflammation. Nitric oxide (NO) likely plays a critical role in this age-related cascade. NO is a major signaling molecule produced in the central nervous system to modulate neurological activity through stimulating cyclic GMP synthesis. However, the same physiological concentrations of NO, relevant in cellular signaling, may also initiate and amplify oxidative damage by diffusion-limited reactions with superoxide (O(2)(•-)) to produce peroxynitrite (ONOO(-)). This is perhaps best illustrated in ALS where physiological levels of NO promote survival of motor neurons, but the same concentrations can stimulate motor neuron apoptosis and glial cell activation under pathological conditions. While these changes represent a complex mechanism involving multiple cell types in the pathogenesis of ALS, they also reveal general processes underlying neurodegeneration.

Indexed as

Amyotrophic Lateral SclerosisAnimalsApoptosisHumansModels, BiologicalMotor NeuronsNitric OxideOxidative StressSuperoxide DismutaseSuperoxide Dismutase-1Nitric OxideSOD1 protein, humanSuperoxide DismutaseSuperoxide Dismutase-1

Identifiers

PMID22488161
PMCPMC4145402
OpenAlexW2077072979

What OpenQuestion holds

Textmetadata
LicenceTDM
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.