Retrograde axonal transport and motor neuron disease

Anna Lena Ström, Jozsef Gal, Ping Shi, Edward J. Kasarskis, Lawrence J. Hayward, Haining Zhu

Research output: Contribution to journalReview articlepeer-review

61 Scopus citations


Transport of material between extensive neuronal processes and the cell body is crucial for neuronal function and survival. Growing evidence shows that deficits in axonal transport contribute to the pathogenesis of multiple neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). Here we review recent data indicating that defects in dynein-medi- ated retrograde axonal transport are involved in ALS etiology. We discuss how mutant copper-zinc superoxide dismutase (SOD1) and an aberrant interaction between mutant SOD1 and dynein could perturb retrograde transport of neurotrophic factors and mitochondria. A possible contribution of axonal transport to the aggregation and degradation processes of mutant SOD1 is also reviewed. We further consider how the interference with axonal transport and protein turnover by mutant SOD1 could influence the function and viability of motor neurons in ALS.

Original languageEnglish
Pages (from-to)495-505
Number of pages11
JournalJournal of Neurochemistry
Issue number2
StatePublished - Jul 2008


  • Amyotrophic lateral sclerosis
  • Axonal transport
  • Dynein
  • Motor neuron
  • Superoxide dismutase

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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