About Our Lab
The overarching goal of our research is to define the key molecular pathways in the pathogenesis of neurodegenerative diseases including Parkinson’s and Huntington’s disease. Using patient-derived induced pluripotent stem cells (iPSCs) differentiated into neurons, we study cellular dysfunction of endolysosomal and mitochondrial pathways in genetic models of Parkinson’s (α-synuclein, LRRK2, VPS35, ATP13A2, PINK1, parkin, DJ-1 and GBA1), as well as the cellular mechanisms involved in Huntington’s disease and Frontotemporal Dementia (FTD) pathogenesis. We aim to advance patient-specific approaches to therapeutic development, including development of new technologies for iPSCs to examine selective neuronal vulnerability. We focus on identification of converging pathogenic pathways to identify key targets for therapeutic development in neurodegenerative diseases such as Parkinson's. 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.