“…A decrease in parkin function leads to toxic accumulation of unwanted proteins and has been implicated in the etiology of various neurodegenerative disorders, including PD (Buneeva and Medvedev, 2006, Lim, 2007, Olzmann, et al, 2008). Conversely, overexpression of parkin protects DA neurons against a variety of cellular insults in vitro and in vivo , most importantly against those involved in mediating METH neurotoxicity, such as DA-induced oxidative stress, inhibition of mitochondrial function, and impairment of the proteasome (Darios, et al, 2003, Jiang, et al, 2012, Jiang, et al, 2004, Kirik and Bjorklund, 2005, Lo Bianco, et al, 2004, Oluwatosin-Chigbu, et al, 2003, Petrucelli, et al, 2002, Yang, et al, 2005, Yang, et al, 2011). These findings suggest the importance of parkin in the functioning and maintenance of DA neurons.…”