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

Skeletal Muscle-Restricted Expression of Human SOD1 in Transgenic Mice Causes a Fatal ALS-Like Syndrome

14 Dec 2020

Abstract excerpt

Amyotrophic lateral sclerosis (ALS) is a fatal heterogeneous neurodegenerative disease that causes motor neuron (MN) loss and skeletal muscle paralysis. It is uncertain whether this degeneration of MNs is triggered intrinsically and is autonomous, or if the disease initiating mechanisms are extrinsic to MNs. We hypothesized that skeletal muscle is a primary site of pathogenesis in ALS that triggers MN...

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 Neurogenetic and Muscular Disorders Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 33381076
DOI: 10.3389/fneur.2020.592851

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Skeletal Muscle-Restricted Expression of Human SOD1 in Transgenic Mice Causes a Fatal ALS-Like SyndromePMID 33381076Read ↗

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

Pathological Sequelae Associated with Skeletal Muscle Atrophy and Histopathology in G93A*SOD1 MiceSemantic proximity Read ↗

Skeletal Muscle Satellite Cells, Mitochondria, and MicroRNAs: Their Involvement in the Pathogenesis of ALSSemantic proximity Read ↗

Skeletal muscle is a primary target of SOD1G93A-mediated toxicity.Semantic proximity Read ↗

Mutant SOD1 in neuronal mitochondria causes toxicity and mitochondrial dynamics abnormalities.Semantic proximity Read ↗

Nuclear Localization of Human SOD1 in Motor Neurons in Mouse Model and Patient Amyotrophic Lateral Sclerosis: Possible Links to Cholinergic Phenotype, NADPH Oxidase, Oxidative Stress, and DNA Damage.Semantic proximity Read ↗

Dysregulated FOXO1 activity drives skeletal muscle intrinsic dysfunction in amyotrophic lateral sclerosisSemantic proximity Read ↗

Skeletal muscle dysfunction in amyotrophic lateral sclerosis: a mitochondrial perspective and therapeutic approachesSemantic proximity Read ↗

In vivo pathogenic role of mutant SOD1 localized in the mitochondrial intermembrane space.Semantic proximity Read ↗

Skeletal muscle TDP-43 aggregation drives progressive motor dysfunction and neurodegeneration with potential for functional recovery after clearanceSemantic proximity Read ↗

Drosophila expressing human SOD1 successfully recapitulates mitochondrial phenotypic features of familial amyotrophic lateral sclerosis.Semantic proximity Read ↗

Mutated human SOD1 causes dysfunction of oxidative phosphorylation in mitochondria of transgenic mice.Semantic proximity Read ↗

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