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Our lab studies the pathogenesis and mechanisms underlying Huntington's Disease (HD). Previous research has indicated that neuronal iron levels are elevated in the brains of HD patients. Currently, I am investigating the role of amyloid precursor protein (APP), an iron export protein, in disease phenotype and neurodegeneration.
Huntington's disease affects about 30000 people in the USA and is caused by a CAG repeat expansion in the huntingtin gene. Oligomers are soluble protein species and there is evidence that they have an important role in disease progression. Therefore, mutant huntingtin protein oligomers are considered as a therapeutic target in Huntington's disease. My research project is centered on an approach to target oligomers of mutant protein. I am seeking and studying genes that decrease levels of these oligomers using cell and mouse disease models.