NICO-Webinar: "Ionic-liquid Nox1 inhibitor to be used as a therapeutic solution to delay the progression of Parkinson's disease." 25/10/2023 @ 14.00
Published: Saturday, October 21, 2023 by Giovanna Gambarotta
NeuroWebinar & Seminar
**Hybrid seminar: both in presence (max 25 people in Seminar room) and on webex
Wednesday 25/10/23 h. 2:00 pm - Hybrid Seminar
Ana C. Cristóvão, CICS-UBI Health Sciences Research Centre, University of Beira Interior; NeuroSoV-Fastprinciple-Lda, UBIMedical - Covilhã, Portugal
Ionic-liquid Nox1 inhibitor to be used as a therapeutic solution to delay the progression of Parkinson's disease.
Parkinson's Disease (PD) is a chronic neurodegenerative disorder affecting up to 10 million people worldwide. Despite the efforts to develop a cure for PD, current therapeutic approaches can only target the symptoms. As symptomatic therapies lose effectiveness over time, patients end up with no therapeutic options. Therefore, delaying the disease progression became a promising solution to deal with this disorder. PD pathogenesis is highly influenced by oxidative stress, and we have previously shown that ROS generated by NADPH oxidase 1 (Nox1) has detrimental impacts on dopaminergic neurons, being a valuable target for therapeutic developments. Inline, we have tested a chemical inhibitor ionic liquid for Nox1 inhibitor (N1inh-IL) capable of preventing neurodegeneration in experimental PD models. In vitro studies showed that N1inh-IL has no cytotoxic effect on N27 neurons, while it significantly prevents the neurotoxic effect of two specific neurotoxins 6-hydroxydopamine (6OHDA) and 1-methyl-4-phenylpyridinium (MPP+). In vivo, the dopaminergic neuroprotective capacity of N1inh-IL, was evaluated in two animal models of PD, one induced by intrastriatal injection of 6OHDA and the other by chronic exposure to paraquat (PQ). The infusion of the N1inh-IL into the right ventricle did not cause neuronal toxicity, while it could prevent 6OHDA-induced neurodegeneration in the substantia nigra (SN) of mice. Moreover, four weeks after been exposed to PQ, the brain intraventricle diffusion or the intranasal delivery of N1inh-IL in rats was capable to prevent the motor dysfunction induced by the toxin and the accumulation of alpha-synuclein in the SN.
These results highlight that N1inh-IL can be an innovative therapy to reduce the speed of the progression of PD.
Host: Marina Boido, Serena Bovetti, Serena Stanga | webex link