Dr. Junghee Lee is Assistant Professor of Neurology at Boston University (BU) Chobanian & Avedisian School of Medicine and Principal Investigator at BU Alzheimer’s Disease Research Center (ADRC). As a postdoctoral fellow in the Department of Neurology at Harvard Medical School and Beth Israel Deaconess Medical Center, Dr. Lee carried out intensive research projects related to oxidative stress and neuronal gene regulation using cell lines, primary cortical neurons, and astrocytes from rodent animal models of various neurodegenerative disorders. As a junior faculty at Boston University, she established translational studies that focus on in vivo mechanisms and therapeutic applications in animal models of neurodegenerative diseases such as Alzheimer’s Disease (AD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS). Dr. Lee joined VA Bedford as a research scientist in 2003 and moved to VA Boston Healthcare System in 2008 where she has been managing an active research laboratory as the PI of NIH R01 grant. Dr. Lee’s research lab, Laboratory for Neuronal Injury and Inflammation has established various advanced skills and resources for studying cellular and molecular neurodegenerative mechanisms including neuronal gene regulation and epigenetic modifications in pre-existing cell lines and animal models of neurodegeneration as well as in human postmortem brains and spinal cords.

Research Interests:
Epigenetic mechanisms of neurodegeneration in HD, ALS, and AD: Epigenetic mechanisms are associated with the pathogenesis of neurodegenerative disorders. The identification of new epigenetic mechanisms and markers will lead to the development of novel therapeutics for the treatment of neurodegenerative disorders. Epigenetics is one of Dr. Lee’s major research interests. Her lab has investigated the association of epigenetic mechanisms with HD, ALS, and AD. Her previous and recent findings provide fundamental components that can be translated into epigenetic therapy to treat neurodegenerative disorders. In addition, she found that deregulation of SIRT3, a mitochondrial histone deacetylase, is linked to mitochondrial dysfunction in AD via mitochondrial p53 and mitochondrial transcription-dependent manner.