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

Partial deficiency of manganese superoxide dismutase exacerbates a transgenic mouse model of amyotrophic lateral sclerosis.

Annals of neurology - 1 Apr 2000

Andreassen O A, Ferrante R J, Klivenyi P, Klein A M, Shinobu L A, Epstein C J, Beal M F

Abstract excerpt

The pathogenesis of neuronal cell death as a consequence of mutations in copper/zinc superoxide dismutase (SOD1) associated with familial amyotrophic lateral sclerosis may involve oxidative damage and mitochondrial dysfunction. We examined whether crossing transgenic mice with the G93A SOD1 mutat...

Read the complete abstract on PubMed

Topics

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

Share to Amyotrophic Lateral Sclerosis
Share to Cell Death
Share to Mice, Mutant Strains

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Motor Neurons

Share to Oxidative Stress

Share to Point Mutation

Share to Substantia Nigra

Share to Superoxide Dismutase

Source

Identifiers

PMID: 10762155

Genes

SOD1
SOD2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-10762155-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Partial deficiency of manganese superoxide dismutase exacerbates a transgenic mouse model of amyotrophic lateral sclerosis.PMID 10762155Read ↗

Transgenic mouse model for familial amyotrophic lateral sclerosis with superoxide dismutase-1 mutationSemantic proximity Read ↗

Transgenic mouse models of amyotrophic lateral sclerosis.Semantic proximity Read ↗

Unraveling the Complexity of Amyotrophic Lateral Sclerosis: Recent Advances from the Transgenic Mutant SOD1 MiceSemantic proximity Read ↗

Disease progression in a transgenic model of familial amyotrophic lateral sclerosis is dependent on both neuronal and non-neuronal zinc binding proteins.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 ↗

Pathogenic mechanisms in familial amyotrophic lateral sclerosis due to mutation of Cu, Zn superoxide dismutase.Semantic proximity Read ↗

Motor neuron disease caused by mutations in superoxide dismutase 1.Semantic proximity Read ↗

Amyotrophic lateral sclerosis associated with mutations in superoxide dismutase: a putative mechanism of degeneration.Semantic proximity Read ↗

Amyotrophic lateral sclerosis: from current developments in the laboratory to clinical implications.Semantic proximity Read ↗

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

Mitochondrial defects in transgenic mice expressing Cu,Zn superoxide dismutase mutations: the role of copper chaperone for SOD1.Semantic proximity Read ↗

Transgenic models of amyotrophic lateral sclerosis.Semantic proximity Read ↗

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