About Our Lab
The overarching goal of our research is to define key molecular pathways in the pathogenesis of neurodegeneration. We have focused on pathogenic mechanisms that occur across neurodegenerative disorders such as accumulation and deficient degradation of aggregation-prone proteins and mitochondrial dysfunction. As a general strategy, our lab is studying rare genetic diseases, such as Huntington’s and genetic forms for Parkinson’s, in particular those with mutations in genes that play a role in these common pathogenic pathways (e.g. PINK1, LRRK2, Parkin, ATP13A2, DJ-1, Gaucher) with a goal of identifying converging pathways and specific targets for therapeutic development in neurodegeneration. Learn more about the Krainc Lab
Song P, Trajkovic K, Tsunemi T, Krainc D. Parkin Modulates Endosomal Organization and Function of the Endo-Lysosomal Pathway. Journal of Neuroscience. 2016 Feb 24;36(8):2425-37.
Mazzulli JR, Zunke F, Isacson O, Studer L, Krainc D. α-Synuclein-induced lysosomal dysfunction occurs through disruptions in protein trafficking in human midbrain synucleinopathy models. Proc Natl Acad Sci U S A. 2016 Feb 16; 113(7):1931-6.