Abstract
Background
Parkinson’s Disease (PD) is a progressive neurodegenerative disease that affects ~1% of seniors and leads to shaking, stiffness and coordination issues. Mitochondrial defects characterize sporadic and hereditary forms of PD. Involvement of mitochondrial genome (mtDNA) variants in PD etiology is still debated. While most PD cases are sporadic, genes responsible for familial PD give insight into underlying biology. Crosstalk between mitochondrial and lysosomal dysfunction underlies a common mechanism of PD etiology.
Research Questions
Are mtDNA alterations involved in PD etiology?
Are mtDNA variants modifiers of PD phenotype in familial PD?
Are autophagy/lysosomal biogenesis pathways involved in cell-and mitochondrial health in PD models?
Can genetic or pharmacological manipulation of autophagy-lysosomal pathway improve PD phenotypes?