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

Slowing of axonal transport is a very early event in the toxicity of ALS-linked SOD1 mutants to motor neurons.

Nature neuroscience - 1 Jan 1999

Williamson T L, Cleveland D W

Abstract excerpt

Mutations in copper/zinc superoxide dismutase 1 (SOD1), primary causes of human amyotrophic lateral sclerosis (ALS), provoke motor neuron death through an unidentified toxic property. The known neurofilament-dependent slowing of axonal transport, combined with the prominent misaccumulation of neurofilaments in ALS, suggests that an important aspect of toxicity may arise from damage to transport. Here we verify...

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 Axonal Transport
Share to Axons

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mice, Transgenic

Share to Motor Neurons

Share to Nerve Degeneration

Share to Superoxide Dismutase

Share to Superoxide Dismutase-1

Source

Identifiers

PMID: 10195180
DOI: 10.1038/4553

Genes

SOD1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Slowing of axonal transport is a very early event in the toxicity of ALS-linked SOD1 mutants to motor neurons.PMID 10195180Read ↗

Retrograde axonal transport and motor neuron disease.Semantic proximity Read ↗

Familial amyotrophic lateral sclerosis-linked SOD1 mutants perturb fast axonal transport to reduce axonal mitochondria content.Semantic proximity Read ↗

Axonal transport defects: a common theme in neurodegenerative diseases.Semantic proximity Read ↗

Familial amyotrophic lateral sclerosis-linked mutant SOD1 aberrantly interacts with tubulin.Semantic proximity Read ↗

Deficits in axonal transport precede ALS symptoms in vivo.Semantic proximity Read ↗

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

Amyotrophic lateral sclerosis associated with mutations in the CuZn superoxide dismutase gene.Semantic proximity Read ↗

A mutation in dynein rescues axonal transport defects and extends the life span of ALS mice.Semantic proximity Read ↗

Slow component of axonal transport is impaired in the proximal axon of transgenic mice with a G93A mutant SOD1 gene.Semantic proximity Read ↗

Axonal transport of mutant superoxide dismutase 1 and focal axonal abnormalities in the proximal axons of transgenic mice.Semantic proximity Read ↗

Mutant SOD1 inhibits ER-Golgi transport in amyotrophic lateral sclerosis.Semantic proximity Read ↗

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

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