Universidad Ana G. Mendez, Recinto Cupey
Parkinson’s disease (PD) is the second most common neurodegenerative disease in the world, with no known causes. Many studies have shown gene mutations and environmental toxins that may have a role in the onset of Parkinson’s disease. The creation of Lewy bodies, which promote the degeneration of dopaminergic neurons and contribute to dementia and slow movements, is one of the hallmarks of PD.
Lewy bodies are a-synuclein (aSyn) aggregates that build up in the brain. The involvement of soluble epoxide hydrolase (sEH) during PD has led to therapy strategies that inhibit sEH function. Some of these inhibitors are currently on the market, such as triclocarban (TCC), but their increased use as a personal care product has generated concerns. In various studies, AUDA has been shown to be a sEH inhibitor for bleomycin-induced lung damage and fibrosis. Our goal is to use AUDA to reverse the effects of aSyninduced neurotoxicity. We hypothesize that supplementing with AUDA will help the NL 5901 worms recover from their PD phenotype. The wild type N2 dopaminergic neurons with GFP tags were compared to the C. elegans strain NL5901, which has aSyn overexpression and is tagged with YFP. We generated agesynchronized plates with the strains first, then examine their thrashing with a 10-day thrashing test. The worms will then be given AUDA to see if it has helped them recover from the aSyn-induced neurotoxicity.