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

Presymptomatic biochemical changes in hindlimb muscle of G93A human Cu/Zn superoxide dismutase 1 transgenic mouse model of amyotrophic lateral sclerosis.

Biochimica et biophysica acta - 1 Jan 2000

Park Kevin H J, Vincent Inez

Abstract excerpt

Amyotrophic lateral sclerosis (ALS) is primarily a motor neuron disorder. Intriguingly, early muscle denervation preceding motor neuron loss is observed in mouse models of ALS. Enhanced muscle vulnerability to denervation process has been suggested by accelerated muscle deterioration following peripheral nerve injury in an ALS mouse model. Here we provide evidence of biochemical changes in the hindlimb muscle of...

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 Cyclin D

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cyclin-Dependent Kinase 5

Share to Cyclins

Share to Hindlimb

Share to Muscle, Skeletal

Share to MyoD Protein

Share to Superoxide Dismutase

Source

Open in PubMed Open full text

Identifiers

PMID: 18485920
DOI: 10.1016/j.bbadis.2008.04.001
PMCID: PMC2517142

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Presymptomatic biochemical changes in hindlimb muscle of G93A human Cu/Zn superoxide dismutase 1 transgenic mouse model of amyotrophic lateral sclerosis.PMID 18485920Read ↗

Skeletal muscle-restricted expression of human SOD1 causes motor neuron degeneration in transgenic miceSemantic proximity Read ↗

Deregulation of Cdk5 in a mouse model of ALS: toxicity alleviated by perikaryal neurofilament inclusions.Semantic proximity Read ↗

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

Optimised and Rapid Pre-clinical Screening in the SOD1G93A Transgenic Mouse Model of Amyotrophic Lateral Sclerosis (ALS)Semantic proximity Read ↗

A large number of protein expression changes occur early in life and precede phenotype onset in a mouse model for huntington disease.Semantic proximity Read ↗

Age-dependent penetrance of disease in a transgenic mouse model of familial amyotrophic lateral sclerosis.Semantic proximity Read ↗

Characterization of early pathogenesis in the <scp>SOD1</scp> <sup>G93A</sup> mouse model of <scp>ALS</scp> : part I, background and methodsSemantic proximity Read ↗

Overexpression of the Cdk5 inhibitory peptide in motor neurons rescue of amyotrophic lateral sclerosis phenotype in a mouse modelSemantic proximity Read ↗

The effect of peripheral nerve injury on disease progression in the SOD1(G93A) mouse model of amyotrophic lateral sclerosis.Semantic proximity Read ↗

Slow development of ALS-like spinal cord pathology in mutant valosin-containing protein gene knock-in mice.Semantic proximity Read ↗

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

Characterisation of the pathogenic effects of the in vivo expression of an ALS-linked mutation in D-amino acid oxidase: Phenotype and loss of spinal cord motor neurons.Semantic proximity Read ↗

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