Protein aggregation is a typical trait of a number of neurodegenerative diseases associated with aging. The genes responsible for modulating the aggregation are not completely known. There is an inverse correlation between the number of the CAG triplets within the huntingtin gene, and the age of onset of symptoms in patients of Huntington’s disease (HD). However, there is high variation at the age of onset of the disease, among carriers of short but pathologic CAG tandems, which suggests that the genetic background of the patients strongly influences the severity of the disease.

We use C. elegans models of polyglutamine (polyQ) toxicity to find and characterize potential druggable targets that modify the progression of the disease. We also use mammalian models, to validate the results obtained in worms. We also are doing preclinical studies using mice models of Huntington’s disease, a condition that is a paradigm of polyQ-causing diseases.