Pathways of methamphetamine toxicity: Effects of autophagy and SOD alteration in the spinal cord

Michela Ferrucci, Livia Pasquali, Antonio Paparelli, Stefano Ruggieri, Francesco Fornai

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Abstract

Methamphetamine (METH) is a drug of abuse which is neurotoxic for the nigrostriatal system. METH-induced neurodegeneration involves production of reactive oxygen species, triggering autophagic vacuoles within nigral neurons of chronic abusers of METH. In fact, Cu,Zn-superoxide dismutase 1 (SOD1) is a critical protein for the neurotoxic effects of METH on DA neurons. Moreover, mutations in the SOD1 gene cause amyotrophic lateral sclerosis, a dramatic neurodegenerative disorder. In the present paper we demonstrate that in G93A transgenic mice, overexpressing the ALS-linked mutant form of SOD1, surviving motor neurons share common intracellular alterations with METH-exposed DA neurons. We hypothesize that in mutant SOD1 transgenic mice, a defective autophagy might be responsible for the neurotoxic effects seen with in nigral neurons during METH toxicity.

Original languageEnglish
Title of host publicationAnnals of the New York Academy of Sciences
Pages177-185
Number of pages9
Volume1139
DOIs
Publication statusPublished - Oct 2008

Publication series

NameAnnals of the New York Academy of Sciences
Volume1139
ISSN (Print)00778923
ISSN (Electronic)17496632

Keywords

  • Autophagy
  • G93A mice
  • Methamphetamine
  • Motor neurons
  • Neurodegeneration
  • Spinal cord

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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