ArticleNeurotoxicity research2010
Restoration of nigrostriatal dopamine neurons in post-MPTP treatment by the novel multifunctional brain-permeable iron chelator-monoamine oxidase inhibitor drug, M30.
Article in Neurotoxicity research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed.
- Monoamine Oxidase Inhibitors in Drug Discovery Against Parkinson's Disease: An Update.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Exploring the role of HIF-1α in pathogenesis of parkinson's disease and its potential as a therapeutic target.Molecular biology reports · 2025Review
- Monoamine Oxidase Inhibitors in Toxic Models of Parkinsonism.International journal of molecular sciences · 2025Review
- Therapeutic Potential Effect of Glycogen Synthase Kinase 3 Beta (GSK-3β) Inhibitors in Parkinson Disease: Exploring an Overlooked Avenue.Molecular neurobiology · 2024Review
- Targeting Biometals in Alzheimer's Disease with Metal Chelating Agents Including Coumarin Derivatives.CNS drugs · 2024Review
- The Role of Oxygen Homeostasis and the HIF-1 Factor in the Development of Neurodegeneration.International journal of molecular sciences · 2024Review
- Alterations in iron content, iron-regulatory proteins and behaviour without tau pathology at one year following repetitive mild traumatic brain injury.Acta neuropathologica communications · 2023Article
- Review
- A brief history of brain iron accumulation in Parkinson disease and related disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Emerging Therapeutic Strategies for Parkinson's Disease and Future Prospects: A 2021 Update.Biomedicines · 2022Review
- Review
- Parkinson's disease and iron.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- Conservative iron chelation for neurodegenerative diseases such as Parkinson's disease and amyotrophic lateral sclerosis.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- Article
- A review on iron chelators as potential therapeutic agents for the treatment of Alzheimer's and Parkinson's diseases.Molecular diversity · 2019Review
- Monoamine oxidase inhibitors, and iron chelators in depressive illness and neurodegenerative diseases.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Synthesis and Cytoprotective Characterization of 8-Hydroxyquinoline Betti Products.Molecules (Basel, Switzerland) · 2018Article
- Understanding the Role of Hypoxia Inducible Factor During Neurodegeneration for New Therapeutics Opportunities.Current neuropharmacology · 2018Review
- Neuroprotective effects of multifaceted hybrid agents targeting MAO, cholinesterase, iron and β-amyloid in ageing and Alzheimer's disease.British journal of pharmacology · 2016Review
- Gene dysregulation is restored in the Parkinson's disease MPTP neurotoxic mice model upon treatment of the therapeutic drug Cu(II)(atsm).Scientific reports · 2016Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The anti-Parkinson iron chelator-monoamine oxidase inhibitor M30 [5-(N-methyl-N-propargyaminomethyl)-8-hydroxyquinoline] was shown to possess neuroprotective activities in vitro and in vivo, against several insults applicable to several neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and ALS. In the present study we sought to examine the effect of M30 on a pre-existing lesion induced by the parkinsonism-inducing toxin, MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine). In this neurorescue paradigm, M30 orally administered to mice for 14 days (2.5 mg/kg/day) following MPTP was shown to significantly elevate striatal dopamine levels, reduce its metabolism, and elevate tyrosine-hydroxylase protein levels (from 25.86 +/- 5.10 to 68.35 +/- 10.67% of control) and activity (from 7.52 +/- 0.98 to 16.33 +/- 2.92 pmol/mg protein/min). Importantly, M30 elevated MPTP-reduced dopaminergic (from 62.8 +/- 4.1 to 84.2 +/- 5.9% of control) and transferrin receptor (from 31.3 +/- 2.6 to 80.4 +/- 7.6% of control) cell count in the SNpc. Finally, M30 was shown to decrease mitosis, thus providing additional protection. These findings suggest that brain-permeable M30 may clearly be of clinical importance for the treatment of PD.
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