ArticleScientific reports2016
Gene dysregulation is restored in the Parkinson's disease MPTP neurotoxic mice model upon treatment of the therapeutic drug Cu(II)(atsm).
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Site-specific metabolic and hypoxia-associated profiles in metastatic melanoma.Journal for immunotherapy of cancer · 2026Article
- Review
- Neuroprotective Potential of Synaptamide in MPTP-Induced Parkinson's Disease.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Article
- Comparative Analysis of T-Cell Signatures and Astroglial Reactivity in Parkinson's Pathology Across Animal Models with Distinct Regenerative Capacities.International journal of molecular sciences · 2026Article
- Article
- Chrysin for Neurotrophic and Neurotransmitter Balance in Parkinson's Disease.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Copper homeostasis and the ubiquitin proteasome system.Metallomics : integrated biometal science · 2023Review
- Mechanistic Insights Expatiating the Redox-Active-Metal-Mediated Neuronal Degeneration in Parkinson's Disease.International journal of molecular sciences · 2022Review
- Small molecules to perform big roles: The search for Parkinson's and Huntington's disease therapeutics.Frontiers in neuroscience · 2022Review
- Copper-ATSM as a Treatment for ALS: Support from Mutant SOD1 Models and Beyond.Life (Basel, Switzerland) · 2020Review
- Epigenomic analysis of Parkinson's disease neurons identifies Tet2 loss as neuroprotective.Nature neuroscience · 2020Article
- Translation Imaging in Parkinson's Disease: Focus on Neuroinflammation.Frontiers in aging neuroscience · 2020Article
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7 authors.
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Abstract
The administration of MPTP selectively targets the dopaminergic system resulting in Parkinsonism-like symptoms and is commonly used as a mice model of Parkinson's disease. We previously demonstrated that the neuroprotective compound Cu(II)(atsm) rescues nigral cell loss and improves dopamine metabolism in the MPTP model. The mechanism of action of Cu(II)(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(II)(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(II)(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.
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