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.
|Autori:||FERRUCCI M; PASQUALI L; PAPARELLI A; RUGGIERI S; FORNAI F|
|Titolo:||Pathways of methamphetamine toxicity|
|Anno del prodotto:||2008|
|Digital Object Identifier (DOI):||10.1196/annals.1432.013|
|Appare nelle tipologie:||1.1 Articolo in rivista|