Cdk5 sinks into ALS

Trends Neurosci. 2002 Jan;25(1):8-10. doi: 10.1016/s0166-2236(00)02000-2.

Abstract

Recent research points to an involvement of deregulated cdk5 activity in the pathogenesis of mutant SOD1-mediated disease. In addition, inhibition of this activity might promote motor neuron survival. These observations have opened the door to further research into the role of cdk5 in ALS and other neurodegenerative diseases.

Publication types

  • Review

MeSH terms

  • Amyotrophic Lateral Sclerosis / genetics
  • Amyotrophic Lateral Sclerosis / metabolism*
  • Amyotrophic Lateral Sclerosis / physiopathology
  • Animals
  • Cell Death / physiology*
  • Central Nervous System / metabolism*
  • Central Nervous System / pathology
  • Central Nervous System / physiopathology
  • Cyclin-Dependent Kinase 5
  • Cyclin-Dependent Kinases / metabolism*
  • Cytoskeleton / metabolism
  • Cytoskeleton / pathology
  • Disease Models, Animal
  • Humans
  • Mice
  • Motor Neurons / metabolism*
  • Motor Neurons / pathology
  • Nerve Tissue Proteins / metabolism
  • Superoxide Dismutase / metabolism*
  • Superoxide Dismutase-1

Substances

  • Nerve Tissue Proteins
  • SOD1 protein, human
  • neuronal Cdk5 activator (p25-p35)
  • Sod1 protein, mouse
  • Superoxide Dismutase
  • Superoxide Dismutase-1
  • Cyclin-Dependent Kinase 5
  • CDK5 protein, human
  • Cdk5 protein, mouse
  • Cyclin-Dependent Kinases