Abstract

The prevalence of Parkinson's Disease (PD) has doubled in the last 25 years, making it the second most common neurodegenerative disease in the US. Central to PD pathology is the degeneration of dopaminergic neurons within the substantia nigra pars compacta. Levodopa, a primary therapeutic agent, aids in dopamine production to alleviate symptoms of PD. However, it has side effects due to premature conversion of L-dopa into dopamine before passing the blood-brain barrier. Compounds such as sinapic acid, characterized by their methoxy and hydroxyl groups, possess antioxidant properties that can mitigate oxidative stress damaging mitochondrial DNA. This study aimed to mitigate parkinsonism effects from ɑ-synuclein mutation using sinapic acid (10, 20, 30 µM), levodopa 30µM, and sinapic acid 30µM + levodopa 30µM, assessing its impact on lifespan, dopamine concentration, movement speed, and memory, comparing it with Levodopa. 30125, 8848, and 8146 strained drosophila were crossed to obtain Mutant ɑ-synuclein Drosophila expressing GFP in dopaminergic neurons. Drosophila (wild and PD) were exposed to treatments, with assessments at 5 and 35 days old. Two-way ANOVA and post hoc Tukey/Scheffe analyses revealed that all 30µM treatment groups significantly reduced PD symptoms of PD strain drosophila (p<0.05). Sinapic acid 30µM + Levodopa 30µM exhibited the best results, attributed to sinapic acid's antioxidant abilities. It had a 43.7% increase in movement speed, a 56% increase in lifespan, and a 62.5% increase in memory. Long-term Levodopa showed increased detrimental effects due to its adverse impacts during consumption. Limitations included the absence of various chemicals (carbidopa and paraquat), suggesting the need for future studies with these chemicals and other model organisms (rats and C.elegans).