ArticleNeuroscience letters2013
Diapocynin prevents early Parkinson's disease symptoms in the leucine-rich repeat kinase 2 (LRRK2R¹⁴⁴¹G) transgenic mouse.
Article in Neuroscience letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 42 citations in OpenAlex.
- Strategies for Optimizing Genetic Mouse Models to Enhance the Understanding of Parkinson's Disease.Biomedicines · 2026Review
- Role of LRRK2 in physiological activities, diseases, and therapy.Chinese medical journal · 2026Review
- Targeting NOX inhibitors in neurodegeneration: a therapeutic perspective.Metabolic brain disease · 2025Review
- Algal and Fungal Antioxidants Alleviate Oxidative Stress-Induced Reproductive Defects.Food science & nutrition · 2025Review
- Modeling Parkinson's disease in LRRK2 rodents.Neuronal signaling · 2023Review
- Novel NADPH Oxidase-2 Inhibitors as Potential Anti-Inflammatory and Neuroprotective Agents.Antioxidants (Basel, Switzerland) · 2023Article
- Contributions and Limitations of Mitochondria-Targeted and Non-Targeted Antioxidants in the Treatment of Parkinsonism: an Updated Review.Neurotoxicity research · 2022Review
- Effects of a NanoencapsulatedAntioxidants (Basel, Switzerland) · 2021Article
- Diapocynin, an NADPH oxidase inhibitor, counteracts diisopropylfluorophosphate-induced long-term neurotoxicity in the rat model.Annals of the New York Academy of Sciences · 2020Article
- A Critical LRRK at the Synapse? The Neurobiological Function and Pathophysiological Dysfunction of LRRK2.Frontiers in molecular neuroscience · 2020Review
- Progress inFrontiers in neuroscience · 2020Review
- HDAC Inhibition by Valproic Acid Induces Neuroprotection and Improvement of PD-like Behaviors in LRRK2 R1441G Transgenic Mice.Experimental neurobiology · 2019Article
- Mito-Apocynin Prevents Mitochondrial Dysfunction, Microglial Activation, Oxidative Damage, and Progressive Neurodegeneration in MitoPark Transgenic Mice.Antioxidants & redox signaling · 2017Article
- Mitochondria-Targeted Triphenylphosphonium-Based Compounds: Syntheses, Mechanisms of Action, and Therapeutic and Diagnostic Applications.Chemical reviews · 2017Review
- Redox-based therapeutics in neurodegenerative disease.British journal of pharmacology · 2017Review
- Recombinant Adeno-Associated Virus-mediated rescue of function in a mouse model of Dopamine Transporter Deficiency Syndrome.Scientific reports · 2017Article
- NADPH oxidase in brain injury and neurodegenerative disorders.Molecular neurodegeneration · 2017Review
- Article
- A Critical Review of Methodologies to Detect Reactive Oxygen and Nitrogen Species Stimulated by NADPH Oxidase Enzymes: Implications in Pesticide Toxicity.Current pharmacology reports · 2016Article
- Mitoapocynin Treatment Protects Against Neuroinflammation and Dopaminergic Neurodegeneration in a Preclinical Animal Model of Parkinson's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The most prominent mechanism proposed for death of dopaminergic neurons in Parkinson's disease (PD) is elevated generation of reactive oxygen/nitrogen species (ROS/RNS). Recent studies suggest that ROS produced during PD pathogenesis may contribute to cytotoxicity in cell culture models of PD. We hypothesized that inhibition of ROS production would prevent PD symptoms in the LRRK2(R1441G) transgenic (tg) mouse model of PD. These mice overexpress a mutant form of leucine-rich repeat kinase 2 (LRRK2) and are reported to develop PD-like symptoms at approximately 10 months of age. Despite similar expression of the transgene, our colony did not recapitulate the same type of motor dysfunction originally reported. However, tests of motor coordination (pole test, Rotor-Rod) revealed a significant defect in LRRK2(R1441G) mice by 16 months of age. LRRK2(R1441G) tg mice, or wild type littermates, were given diapocynin (200mg/kg, a proposed NADPH oxidase inhibitor) three times per week by oral gavage starting at 12 weeks of age. Decreased performance on the pole test and Rotor-Rod in the LRRK2(R1441G) mice was prevented with diapocynin treatment. No loss in open field movement or rearing was found. As expected, tyrosine hydroxylase staining was similar in both the substantia nigra and striatum in all treatment groups. Together these data demonstrate that diapocynin is a viable agent for protection of neurobehavioral function.
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