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Overview

Moore Laboratory

Molecular Neurodegeneration

The Moore Laboratory investigates the molecular pathophysiology of Parkinson’s disease, a chronic progressive neurodegenerative movement disorder. The majority of Parkinson’s disease cases occur in a sporadic manner although 5 to 10 percent of cases are inherited, with causative mutations identified in at least eight genes. The Moore Laboratory studies the normal biology and pathobiology of gene products that cause inherited Parkinson’s disease, including the common leucine-rich repeat kinase 2 (LRRK2, PARK8), the retromer component VPS35 (PARK17), the E3 ubiquitin ligase parkin (PARK2), and the lysosomal P5-type ATPase ATP13A2 (PARK9).

The laboratory’s goal is to elucidate the normal biological function of these proteins in the mammalian brain and the molecular mechanism(s) through which disease-associated variants in these proteins induce neuronal dysfunction and eventual neurodegeneration in inherited forms of Parkinson’s disease. Through a clear understanding of the physiological function and pathological dysfunction of these proteins, the Moore Laboratory hopes to gain important insight into the molecular mechanisms and cellular pathways underlying neurodegeneration in inherited and idiopathic forms of Parkinson’s disease.

The laboratory adopts a translational approach to identify and validate novel therapeutic strategies that may slow or halt progressive neurodegeneration in Parkinson’s disease. To achieve these goals, the lab uses a multidisciplinary approach employing molecular, cellular and biochemical experimental techniques in a number of model systems including human cell lines, primary neuronal cultures, the baker’s yeast Saccharomyces cerevisiae, transgenic, knockout and viral-mediated gene transfer rodent models, and human brain tissue. The Moore Laboratory’s mission is to understand the molecular pathogenesis of Parkinson’s disease in order to develop novel targeted therapies and neuroprotective strategies to treat or prevent this devastating disease.