Jungsu Kim

Jungsu Kim, PhD

P. Michael Conneally Professor of Medical and Molecular Genetics


Dr. Kim is the P. Michael Conneally Professor of Medical and Molecular Genetics. Dr. Kim graduated Summa Cum Laude in 2000 from Pohang University of Science & Technology in Korea with a bachelor’s degree in life science. He earned his Ph.D. from Mayo Clinic College of Medicine in 2007 under the guidance of Dr. Todd Golde and completed his postdoctoral training at Washington University in the laboratory of Dr. David Holtzman. After 3 years of postdoctoral training, he established his laboratory at Washington University, as an Assistant Professor in the Department of Neurology. In June 2013, Dr. Kim joined the Department of Neuroscience at Mayo Clinic. After 5 years of tenure as a Senior Associate Consultant I at Mayo Clinic, Dr. Kim relocated his laboratory to the Stark Neurosciences Research Institute at IU School of Medicine in 2018.

Dr. Kim’s laboratory is interested in understanding the molecular and cellular basis of neuronal and glial dysfunction in Alzheimer’s disease, other aging-associated neurodegenerative diseases, and normal brain aging. Research in our lab is aimed at developing therapeutic strategies for Alzheimer’s disease by targeting brain lipid-regulating proteins, such as apolipoprotein E (ApoE), low density lipoprotein receptor (LDLR), and ATP-binding cassette transporter A1 (ABCA1). We are also interested in the role of epigenetics and non-coding RNAs in the pathogenesis of Alzheimer’s disease and other aging-associated neurodegenerative diseases. Emerging transcriptomics technologies recently revealed that many non-coding regions actually encode functional RNAs, such as microRNAs (miRNAs) and long non-coding RNAs (lncRNAs). Using cell culture, animal models, and systems biology approaches, we study non-coding RNAs that may play critical roles in neurodegenerative diseases, brain aging and cardiovascular diseases.

Key Publications

1. H. Yoon, K. C. Belmonte, T. Kasten, R. Bateman, J. Kim, Intra- and Inter-individual Variability of microRNA Levels in Human Cerebrospinal Fluid: Critical Implications for Biomarker Discovery. Sci. Rep. 7, 12720 (2017).
2. F. Liao, H. Yoon, J. Kim, Apolipoprotein E metabolism and functions in brain and its role in Alzheimer's disease. Curr. Opin. Lipidol. 28, 60-67 (2017).
3. H. Yoon, L. F. Flores, J. Kim, MicroRNAs in brain cholesterol metabolism and their implications for Alzheimer's disease. Biochim. Biophys. Acta 1861, 2139-2147 (2016).
4. J. Kim et al., miR-186 is decreased in aged brain and suppresses BACE1 expression. J. Neurochem. 137, 436-445 (2016).
5. J. Kim et al., miR-27a and miR-27b regulate autophagic clearance of damaged mitochondria by targeting PTEN-induced putative kinase 1 (PINK1). Mol. Neurodegener. 11, 55 (2016).
6. J. Kim et al., microRNA-33 Regulates ApoE Lipidation and Amyloid-beta Metabolism in the Brain. J. Neurosci. 35, 14717-14726 (2015).
7. J. Choi et al., The E3 ubiquitin ligase Idol controls brain LDL receptor expression, ApoE clearance, and Abeta amyloidosis. Sci. Transl. Med. 7, 314ra184 (2015).
8. J. Kim et al., miR-106b impairs cholesterol efflux and increases Aβ levels by repressing ABCA1 expression. Exp. Neurol. 235, 476-483 (2012).
9. J. Kim et al., Anti-apoE immunotherapy inhibits amyloid accumulation in a transgenic mouse model of Abeta amyloidosis. J. Exp. Med. 209, 2149-2156 (2012).
10. J. Kim et al., Haploinsufficiency of human APOE reduces amyloid deposition in a mouse model of amyloid-beta amyloidosis. J. Neurosci. 31, 18007-18012 (2011).
11. J. M. Castellano et al., Human apoE Isoforms Differentially Regulate Brain Amyloid-β Peptide Clearance. Sci. Transl. Med. 3, 89ra57 (2011).
12. J. Kim, D. M. Holtzman, Prion-like behavior of amyloid-beta. Science 330, 918-919 (2010).
13. J. M. Basak, J. Kim, Differential effects of ApoE isoforms on dendritic spines in vivo: linking an Alzheimer's disease risk factor with synaptic alterations. J. Neurosci. 30, 4526-4527 (2010).
14. J. Kim et al., Overexpression of low-density lipoprotein receptor in the brain markedly inhibits amyloid deposition and increases extracellular Abeta clearance. Neuron 64, 632-644 (2009).
15. J. Kim, J. M. Basak, D. M. Holtzman, The role of apolipoprotein E in Alzheimer's disease. Neuron 63, 287-303 (2009).
16. S. E. Wahrle et al., Overexpression of ABCA1 reduces amyloid deposition in the PDAPP mouse model of Alzheimer disease. J. Clin. Invest. 118, 671-682 (2008).
17. J. Kim et al., BRI2 (ITM2b) Inhibits Abeta Deposition In Vivo. J Neurosci. 28, 6030-6036 (2008).
18. J. Kim et al., Abeta40 inhibits amyloid deposition in vivo. J. Neurosci. 27, 627-633 (2007).
19. E. McGowan et al., Abeta42 is essential for parenchymal and vascular amyloid deposition in mice. Neuron 47, 191-199 (2005).



Medical & Molecular Genetics
Indianapolis, IN


Alzheimers Disease
Diabetes Endocrinology
Personalized Medicine
Translational Research
Traumatic Brain Injury