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Article

Deficits in axonal transport precede ALS symptoms in vivo.

Proceedings of the National Academy of Sciences of the United States of America - 23 Nov 2010

Bilsland Lynsey G, Sahai Erik, Kelly Gavin, Golding Matthew, Greensmith Linda, Schiavo Giampietro

Abstract excerpt

ALS is a fatal neurodegenerative disease characterized by selective motor neuron death resulting in muscle paralysis. Mutations in superoxide dismutase 1 (SOD1) are responsible for a subset of familial cases of ALS. Although evidence from transgenic mice expressing human mutant SOD1(G93A) suggests that axonal transport defects may contribute to ALS pathogenesis, our understanding of how these relate to disease...

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Source

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Identifiers

PMID: 21059924
DOI: 10.1073/pnas.1006869107
PMCID: PMC2996651

Genes

SOD1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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