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Pathways of Methamphetamine Toxicity
Author(s) -
Ferrucci Michela,
Pasquali Livia,
Paparelli Antonio,
Ruggieri Stefano,
Fornai Francesco
Publication year - 2008
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1432.013
Subject(s) - methamphetamine , toxicity , pharmacology , medicine
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.