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

Mice lacking cytosolic copper/zinc superoxide dismutase display a distinctive motor axonopathy

1 Oct 1999

Abstract excerpt

OBJECTIVE: To characterize the motor neuron dysfunction in two models by performing physiologic and morphometric studies. BACKGROUND: Mutations in the gene encoding cytosolic superoxide dismutase 1 (SOD1) account for 25% of familial ALS (FALS). Transgenes with these mutations produce a pattern of lower motor neuron degeneration similar to that seen in patients with FALS. In contrast, mice lacking SOD1 develop...

Read the complete abstract on PubMed

Topics

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

Share to Amyotrophic Lateral Sclerosis Research
Share to Genetic Neurodegenerative Diseases
Share to Neurogenetic and Muscular Disorders Research

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

Source

Identifiers

PMID: 10522879
DOI: 10.1212/wnl.53.6.1239

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

Mice lacking cytosolic copper/zinc superoxide dismutase display a distinctive motor axonopathyPMID 10522879Read ↗

Neuropathological changes in two lines of mice carrying a transgene for mutant human Cu,Zn SOD, and in mice overexpressing wild type human SOD: a model of familial amyotrophic lateral sclerosis (FALS).Semantic proximity Read ↗

Massive mitochondrial degeneration in motor neurons triggers the onset of amyotrophic lateral sclerosis in mice expressing a mutant SOD1.Semantic proximity Read ↗

Late-onset motoneuron disease caused by a functionally modified AMPA receptor subunitSemantic proximity Read ↗

Mutant Cu, Zn superoxide dismutase that causes motoneuron degeneration is present in mitochondria in the CNS.Semantic proximity Read ↗

A Drosophila Model for Amyotrophic Lateral Sclerosis Reveals Motor Neuron Damage by Human SOD1Semantic proximity Read ↗

Prolonged survival and milder impairment of motor function in the SOD1 ALS mouse model devoid of fibroblast growth factor 2Semantic proximity Read ↗

Progressive impairment of CaV1.1 function in the skeletal muscle of mice expressing a mutant type 1 Cu/Zn superoxide dismutase (G93A) linked to amyotrophic lateral sclerosis.Semantic proximity Read ↗

Motor Neuron Abnormalities Correlate with Impaired Movement in Zebrafish that Express Mutant Superoxide Dismutase 1Semantic proximity Read ↗

Restricted expression of mutant SOD1 in spinal motor neurons and interneurons induces motor neuron pathology.Semantic proximity Read ↗

A comprehensive assessment of the SOD1G93A low-copy transgenic mouse, which models human amyotrophic lateral sclerosisSemantic proximity Read ↗

Delineating sex-dependent and anatomic decline of motor functions in the SOD1G93A mouse model of amyotrophic lateral sclerosisSemantic proximity Read ↗

Anatomical and functional analysis of the corticospinal tract in an FRDA mouse modelSemantic proximity Read ↗

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