Krainc, Dimitri, MD, PhD



Krainc, Dimitri, MD, PhD


Aaron Montgomery Professor and Chairman


Office Phone

(312) 503-3936

Office Fax

(312) 503-0872




Ward 12-140

Areas of Research

Cell Biology, Molecular Neuroscience, Neurobiology of Disease

Training Grants

Mechanisms of Aging and Demential Training Program (M.A.D), General Motor Control Mechanisms and Disease Training Program

NU Scholar Profile

Current Research

Current Research

The overarching goal of my laboratory has been to define key molecular pathways in the pathogenesis of neurodegeneration. We have focused on pathogenic mechanisms that commonly occur in neurodegenerative disorders such as accumulation and deficient degradation of aggregation-prone proteins and mitochondrial dysfunction. As a general strategy, we are studying rare genetic diseases, in particular those with mutations in genes that play a role in these common pathogenic pathways (e.g. PINK1, Parkin, ATP13A2, Gaucher) with a goal of identifying specific targets for therapeutic development in neurodegeneration. To validate and study these mechanisms in patient-specific human neurons, we are developing new tools to generate purified population of specific neuronal subtypes from reprogrammed patient fibroblasts (iPS).

Selected Publications

Selected Publications

1. Burbulla, L.F., Song, P., Mazzulli, J.R., Zampese, E., Wong, Y.C., Jeon, S., Santos, D.P., Blanz, J., Obermaier, C., Strojny, C., Savas, J., Kiskinis, E., Zhuang, X., Krüger, R., Surmeier, J.D., Krainc, D. Dopamine oxidation mediates mitochondrial and lysosomal dysfunction in Parkinson's disease. Science, 2017(highlighted in various research and popular outlets)
2. Wong Y.C., Ysselstein, D. and Krainc, D. Mitochondria-lysosome contacts regulate mitochondrial fission via Rab7 hydrolysis. Nature, 2018

3. Burbulla, L., Jeon, S., Zheng, J, Song, P, Silverman, R.B. and Krainc, D. Direct targeting of wild type glucocerebrosidase improves pathogenic phenotypes in multiple forms of Parkinson’s disease. Science Translational Medicine, 2019.

4. Zheng, J., Chen, L., Skinner, O., Ysselstein, D., Remis, J., Lansbury, P., Skerlj, R., Mrosek, M. Heunisch, U., Krapp, S., Charrow, J., Schwake, M., Kelleher, N., Silverman, R.B., Krainc, D., β-Glucocerebrosidase modulators promote dimerization of β-glucocerebrosidase and reveal an allosteric binding site. Journal of American Chemical Society, 2018.

5. Mazzulli, J.R., Sun, Y., Knight, A.L., McLean, P.J., Caldwell, G, Sidransky, E, Grabowski, G.A. and Krainc, D. Gaucher’s Disease Glucocerebrosidase and alpha-synuclein form a bidirectional pathogenic loop in synucleinopathies. Cell, 2011 (Accompanied by the Perspective in Cell, Science Translational Medicine, and Editors’ Choice in Science).

6. 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. PNAS, See comment in PubMed Commons below2016.

7. Nyugen, M. and Krainc, D. LRRK2 phosphorylation of auxilin mediates synaptic defects in dopaminergic neurons from patients with Parkinson’s disease. PNAS, 2018.