Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Survival in transgenic ALS mice does not vary with CNS glutathione peroxidase activity.

Neurology - 10 Sept 2002

Cudkowicz M E, Pastusza K A, Sapp P C, Mathews R K, Leahy J, Pasinelli P, Francis J W, Jiang D, Andersen J K, Brown R H

Abstract excerpt

OBJECTIVE: Transgenic mice that overexpress a human gene encoding mutant cytosolic superoxide dismutase (SOD1) develop a progressive motor neuron loss that resembles human ALS. Why mutant SOD1 initiates motor neuron death is unknown. One hypothesis proposes that the mutant molecule has enhanced peroxidase activity, reducing hydrogen peroxide (H2O2) to form toxic hydroxyl adducts on critical targets. To test this...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Age of Onset
Share to Amyotrophic Lateral Sclerosis

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Glutathione Peroxidase

Share to Mice, Transgenic

Share to Superoxide Dismutase

Share to Superoxide Dismutase-1

Share to Survival Analysis

Source

Identifiers

PMID: 12221165
DOI: 10.1212/wnl.59.5.729

Genes

SOD1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Survival in transgenic ALS mice does not vary with CNS glutathione peroxidase activity.PMID 12221165Read ↗

Neuron-specific expression of mutant superoxide dismutase 1 in transgenic mice does not lead to motor impairment.Semantic proximity Read ↗

Wild-type SOD1 overexpression accelerates disease onset of a G85R SOD1 mouseSemantic proximity Read ↗

Tempol moderately extends survival in a hSOD1(G93A) ALS rat model by inhibiting neuronal cell loss, oxidative damage and levels of non-native hSOD1(G93A) forms.Semantic proximity Read ↗

Phenotype of transgenic mice carrying a very low copy number of the mutant human G93A superoxide dismutase-1 gene associated with amyotrophic lateral sclerosis.Semantic proximity Read ↗

Transgenic mice expressing an altered murine superoxide dismutase gene provide an animal model of amyotrophic lateral sclerosis.Semantic proximity Read ↗

Brain beta-amyloid accumulation in transgenic mice expressing mutant superoxide dismutase 1.Semantic proximity Read ↗

Elevated free nitrotyrosine levels, but not protein-bound nitrotyrosine or hydroxyl radicals, throughout amyotrophic lateral sclerosis (ALS)-like disease implicate tyrosine nitration as an aberrant in vivo property of one familial ALS-linked superoxide dismutase 1 mutant.Semantic proximity Read ↗

Vascular endothelial growth factor prolongs survival in a transgenic mouse model of ALS.Semantic proximity Read ↗

Overexpression of ferroptosis defense enzyme Gpx4 retards motor neuron disease of SOD1G93A mice.Semantic proximity Read ↗

Extension of Drosophila lifespan by overexpression of human SOD1 in motorneurons.Semantic proximity Read ↗

Motor neuron disease in mice expressing the wild type-like D90A mutant superoxide dismutase-1.Semantic proximity Read ↗

Over-expression of Hsp27 does not influence disease in the mutant SOD1(G93A) mouse model of amyotrophic lateral sclerosis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.