Jungsu Kim, PhD, BS
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 (Dept. of Neuroscience) and completed his postdoctoral training at Washington University in the laboratory of Dr. David Holtzman (Dept. of Neurology). 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 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. Main research topics include the role of non-coding RNAs and lipid-regulating proteins in neurodegenerative diseases and cardiovascular diseases.
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
NB 108B MMGE
Traumatic Brain Injury
The main interest of Kim lab is to understand the pathogenic mechanisms of Alzheimer’s disease and other neurodegenerative diseases (Parkinson's disease, Frontotemporal dementia, Huntington's disease, and Amyotrophic Lateral Sclerosis) and to identify novel therapeutic targets.
Current research efforts aim to understand the roles of Apolipoprotein (ApoE) and ApoE-regulating proteins, such as ABCA1 and LDLR, in Alzheimer’s disease. We are also interested in studying the role of microRNAs and other non-coding RNAs (e.g. lncRNAs) in Alzheimer’s disease, other neurodegenerative diseases, and brain aging.
In addition, we are investigating whether microRNAs of our interest affect cardiovascular diseases, obesity, and diabetes.
Desc: Outstanding Young Investigator Award
Org: Charleston Conference on Alzheimer’s disease
Desc: The New Vision Award
Org: The Association of Korean Neuroscientists
Desc: Outstanding Junior Faculty Award