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

Selective loss of neurofilament expression in Cu/Zn superoxide dismutase (SOD1) linked amyotrophic lateral sclerosis

1 Sept 2002

Abstract excerpt

Neurofilament pathology is a hallmark of sporadic and familial amyotrophic lateral sclerosis (SALS and FALS). The disease mechanisms underlying this pathology are presently unclear, but recent evidence in SALS patients suggest that reductions in neurofilament light subunit (NFL) mRNA may contribute to the death of motor neurones. Mutations in the gene encoding Cu-Zn superoxide dismutase (SOD1) represent the...

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
Share to Neurological diseases and metabolism

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 12358759
DOI: 10.1046/j.1471-4159.2002.01045.x

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Selective loss of neurofilament expression in Cu/Zn superoxide dismutase (SOD1) linked amyotrophic lateral sclerosisPMID 12358759Read ↗

Absence of neurofilaments reduces the selective vulnerability of motor neurons and slows disease caused by a familial amyotrophic lateral sclerosis-linked superoxide dismutase 1 mutant.Semantic proximity Read ↗

A mutant neurofilament subunit causes massive, selective motor neuron death: implications for the pathogenesis of human motor neuron disease.Semantic proximity Read ↗

Sequence variants in human neurofilament proteins: Absence of linkage to familial amyotrophic lateral sclerosisSemantic proximity Read ↗

Mutations in neurofilament genes are not a significant primary cause of non-SOD1-mediated amyotrophic lateral sclerosis.Semantic proximity Read ↗

UNRAVELING THE MECHANISMS INVOLVED IN MOTOR NEURON DEGENERATION IN ALSSemantic proximity Read ↗

Modeling ALS with iPSCs reveals that mutant SOD1 misregulates neurofilament balance in motor neurons.Semantic proximity Read ↗

SOD1 mutation is assosiated with accumulation of neurofilaments in amyotrophic lateral scelariesSemantic proximity Read ↗

Dysregulation of human NEFM and NEFH mRNA stability by ALS-linked miRNAsSemantic proximity Read ↗

Transgenic mice carrying a human mutant superoxide dismutase transgene develop neuronal cytoskeletal pathology resembling human amyotrophic lateral sclerosis lesions.Semantic proximity Read ↗

Overexpression of neurofilament subunit NF-L and NF-H extends survival of a mouse model for amyotrophic lateral sclerosis.Semantic proximity Read ↗

Protective effect of neurofilament heavy gene overexpression in motor neuron disease induced by mutant superoxide dismutase.Semantic proximity Read ↗

Transcriptional profiling in the lumbar spinal cord of a mouse model of amyotrophic lateral sclerosis: a role for wild-type superoxide dismutase 1 in sporadic disease?Semantic proximity Read ↗

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