Paroxetine Retards Disease Onset and Progression in Huntingtin Mutant Mice

Ann Neurol. 2004 Apr;55(4):590-4. doi: 10.1002/ana.20075.

Abstract

We report that administration of paroxetine, a widely prescribed antidepressant drug that acts by inhibiting reuptake of the neurotransmitter serotonin, suppresses the neurodegenerative process and increases the survival of huntingtin mutant mice, an animal model of Huntington's disease (HD). Paroxetine attenuated motor dysfunction and body weight loss and improved glucose metabolism in the HD mice. Paroxetine was beneficial when treatment was initiated before or after the onset of motor dysfunction, suggesting a potential for such antidepressant drugs in the treatment of presymptomatic and symptomatic HD patients.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Disease Progression
  • Female
  • Humans
  • Huntingtin Protein
  • Huntington Disease / drug therapy*
  • Huntington Disease / genetics*
  • Huntington Disease / metabolism
  • Male
  • Mice
  • Mice, Mutant Strains
  • Mice, Transgenic
  • Mutation*
  • Nerve Tissue Proteins / genetics*
  • Neuroprotective Agents / pharmacology
  • Neuroprotective Agents / therapeutic use*
  • Nuclear Proteins / genetics*
  • Paroxetine / pharmacology
  • Paroxetine / therapeutic use*

Substances

  • HTT protein, human
  • Htt protein, mouse
  • Huntingtin Protein
  • Nerve Tissue Proteins
  • Neuroprotective Agents
  • Nuclear Proteins
  • Paroxetine