Mitochondrial dysfunction in C. elegans model of Parkinson's disease
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Parkinson’s disease (PD) is a devastating neurodegenerative disease and the second most prevalent after Alzheimer’s disease. The most characteristic hallmark of Parkinson’s is the presence of Lewy Bodies, clumps of aggregated α-synuclein protein, in the Substantia Nigra. While much has been said and theorized about α-synuclein, mitochondrial dysregulation in neurons of Parkinson’s patients is an equally important consideration due to the role that the mitochondria plays in supplying neurons with their energy needs through ATP. C. elegans is a non-vertebrate animal often used to study aging and neurodegenerative disease due to its simple, well characterized genome. This literature review aims to outline the genetic and some environmental factors that cause mitochondrial dysregulation leading to the progressive neurodegeneration witnessed in Parkinson’s, as modeled in C. elegans. Through a select review of studies done on C. elegans homolog of genes associated with mitochondrial function, this review aims to elucidate the mechanism by which each mutation not only causes the deficits seen in PD on its own but also how it interacts with other genes to worsen or alleviate symptoms. Ultimately, understanding these pathways and mechanism will be crucial to discovering and creating new therapeutic treatments and targets.