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We previously demonstrated that the neuroprotective compound Cu<jats:sup>II<\/jats:sup>(atsm) rescues nigral cell loss and improves dopamine metabolism in the MPTP model. The mechanism of action of Cu<jats:sup>II<\/jats:sup>(atsm) needs to be further defined to understand how the compound promotes neuronal survival. Whole genome transcriptomic profiling has become a popular method to examine the relationship between gene expression and function. Substantia nigra samples from MPTP-lesioned mice were evaluated using whole transcriptome sequencing to investigate the genes altered upon Cu<jats:sup>II<\/jats:sup>(atsm) treatment. We identified 143 genes affected by MPTP lesioning that are associated with biological processes related to brain and cognitive development, dopamine synthesis and perturbed synaptic neurotransmission. Upon Cu<jats:sup>II<\/jats:sup>(atsm) treatment, the expression of 40 genes involved in promoting dopamine synthesis, calcium signaling and synaptic plasticity were restored which were validated by qRT-PCR. The study provides the first detailed whole transcriptomic analysis of pathways involved in MPTP-induced Parkinsonism. In addition, we identify key therapeutic pathways targeted by a potentially new class of neuroprotective agents which may provide therapeutic benefits for other neurodegenerative disorders.<\/jats:p>","DOI":"10.1038\/srep22398","type":"journal-article","created":{"date-parts":[[2016,3,1]],"date-time":"2016-03-01T11:49:30Z","timestamp":1456832970000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Gene dysregulation is restored in the Parkinson\u2019s disease MPTP neurotoxic mice model upon treatment of the therapeutic drug CuII(atsm)"],"prefix":"10.1038","volume":"6","author":[{"given":"Lesley","family":"Cheng","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Camelia Y. 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