Hoon Ryu, PhD

Associate Professor of Neurology


Phone: 857.364.5910
Fax: 857.364.4540
Email: hoonryu@bu.edu
Location: VA Boston Healthcare System, 150 South Huntington Avenue, Boston, MA 02130



Dr. Hoon Ryu earned his doctoral degree from Chonbuk National University, South Korea. He completed a postdoctoral research fellowship and was appointed Instructor of Neurology at Beth Israel Deaconess Medical Center and Harvard Medical School in 1999. He joined the Boston University School of Medicine’s Department of Neurology in 2004 as an Assistant Professor. Now he is an Associate Professor and an investigator with the Boston University Alzheimer’s Disease Center and VA Boston Healthcare System. He is a director of the laboratory for Neuronal Gene Regulation and Epigenetics. He works on the identification of biomarkers, the determination of molecular genetic, epigenetic mechanisms, and the development of therapeutics using cell culture systems and animal models of neurodegeneration. He has published over 70 original reports.

Research Interests

Epigenetic changes encompass an array of molecular modifications including DNA methylation and changes to the chromatin packaging of DNA by post-translational histone modifications. The structure, dynamics, and chemical properties of chromatin almost completely determines how, when, and which genes are turned on and off. Chromatin remodeling and transcription regulation are tightly controlled under physiological conditions. Deregulation of chromatin remodeling is linked to the pathogenesis of neurodegenerative disorders but the mechanism is elusive. In order to identify how genomes are deregulated by heterochromatin, Dr. Ryu is performing ChIP genome-wide sequencing combined with RNA-sequencing followed by platform integration analysis. He has found that altered chromatin plasticity is closely linked to the pathogenesis of Huntington’s disease via an expression of ESET (ERG-associated protein with a SET domain), a histone H3K9-specific methyltransferase. Currently, he is conducting research about mechanisms of ESET gene induction and neuronal heterochromatin condensation in Alzheimer’s disease.

ADC Role

Dr. Ryu is a basic scientist collaborating with ADC investigators on the molecular pathological mechanism of Alzheimer’s disease.

Awards and Memberships


Dr. Ryu is currently the recipient of the NIH R01 Awards. He has awarded CHDI Grant, American Parkinson Disease Association (APDA) Pilot Study Award from the Boston University APDA Center of Excellence, National Center for Drug Discovery in Neurodegeneration (NCDDN) Fellowship Award from Harvard Medical School. He is a member of the Society for Neuroscience and New England Biological Society.


Selected Publications

1.  Lee J, Kosaras B, Del Signore SJ, Cormier K, McKee A, Ratan RR, Kowall NW, Ryu H. (2011) Modulation of lipid peroxidation and mitochondrial function improves neuropathology in Huntington’s disease mice. Acta Neuropathol. 121:487-498.

2.  J Lee, Hwang YJ , Boo JH, Han D, Kwon OK, Todorova K , Kowall NW, Kim Y and Ryu H. (2011) Dysregulation of upstream binding factor-1 acetylation at K352 is linked to impaired ribosomal DNA transcription in Huntington’s disease. Cell Death & Differ. 18:1726–1735.

3.  Lee J, Ryu H. (2010) Epigenetic modification is linked to Alzheimer’s disease: is it a maker or a marker? BMB Rep. 43:649-655.

4.  Lee, J., Kannagi, M., Ferrante, R.J., Kowall, W.N., and Ryu, H. (2009) Activation of Ets-2 by oxidative stress induces Bcl-xL expression and accounts for glial survival in amyotrophic lateral sclerosis. FASEB Journal. 23:1739-1749.

5.  Lee J, Boo JH, Ryu H. (2009) The Failure of Mitochondria Leads to Neurodegeneration: Do Mitochondria Need A Jump Start? Adv. Drug Deliv. Rev. 61:1316-1323.

6.  Liu, M.L., Liu, M.J., Shen, Y.F., Ryu, H., Kim, H.J., Klupsch, K., Downward, J., and Hong, S.T. (2009) Omi is a mammalian heat-shock protein that selectively binds and detoxifies oligomeric amyloid-beta. J. Cell Sci. 122:1917-1926.

Lee, J., Hagerty, S., Cormier, K.A., Ferrante, R.J., Andrew L. Kung, A.L., and Ryu, H. (2008) Monoallele deletion of CBP leads to pericentromeric heterochromatin condensation through ESET expression and histone H3 (K9) methylation. Hum. Mol. Genet. 17:1774-1782.

Lee, J., Kosaras, B., Aleyasin, H., Han, J. A., Park, D. S., Ratan, R. R., Kowall, N., Ferrante, R. J., Lee, S. W., and Ryu, H. (2006) Role of cyclooxygenase-2 induction by transcription factor Sp1 and Sp3 in neuronal oxidative and DNA damage response. FASEB Journal. 20:2375-2387.

Ryu H, Lee J, Hagerty SW, Soh BY, McAlpin SE, Cormier KA, Smith KM, Ferrante RJ. (2006) ESET/SETDB1 gene expression and histone H3 (K9) trimethylation in Huntington’s disease. Proc Natl Acad Sci U S A . 2006 Dec 12; 103(50): 19176-81. [PDF]

Ryu H, Lee J, Impey S, Ratan RR, Ferrante RJ. Antioxidants modulate mitochondrial protein kinase A and increase CREB binding to D-Loop DNA of the mitochondrial genome in neurons. Proc Natl Acad Sci USA.2005 Sep 27; 102(39): 13915-20. [PDF]

Lee J, Kim CH, Simon D, Aminova L, Andreyev A, Kushnareva Y, Murphy A, LONZE BE, Kim KS, Ginty DD, Ferrante RJ, Ryu H, Ratan RR. Mitochondrial CREB regulates mitochondrial gene expression and neuronal survival. J Biol Chem. 2005 Dec 9; 280(49): 40398-401. [PDF]

Ohtsuka T,Ryu H, Minamishima YA, Aaronson S, Lee SW. (2004) ASC functions as an adaptor for Bax and regulates a p53-Bax mitochondrial pathway of apoptosis. Nat Cell Biol 2004 Feb; 6(2): 121-8. [PDF]

Lee J, Ryu H, Ferrante RJ, Morris SM Jr, Ratan RR. Translational control of inducible nitric oxide synthase expression by arginine can explain the “arginine paradox”. Proc Natl Acad Sci USA 2003 Apr 15; 100(8): 4843-8. [PDF]

Ryu H, Lee JH, Olofsson BA, Mwidau A, Deodoglu A, Escudero M, Flemington E, Azizkhan-Clifford J, Ferrante RJ, Ratan RR. Histone deacetylase inhibitors prevent oxidative neuronal death independent of expanded polyglutamine repeats via an Sp1-dependent pathway. Proc Natl Acad Sci USA. 2003 Apr 1; 100(7): 4281-6. [PDF]

Ryu H, Lee JH, Zaman K, Ross BD, Flemington E, Neve R, Ratan RR. Sp1 and Sp3 are oxidative stress-inducible, anti-death transcription factors in cortical neurons. J Neurosci. 2003 May 1; 23(9): 3597-606. [PDF]