Yoon Ha, MD, PhD received his medical degree and PhD from Yonsei University. He completed his internship and neurosurgery residency at Severance hospital, Yonsei University in 1999. In 2015, Dr. Ha was appointed Professor of Neurological Surgery in Yonsei Univ. Dr. Ha is board certified in the fields of Neurological Surgery.
Dr. Ha has an active research interest in spinal surgery and basic research, particularly in numerous multicenter outcome research studies of spinal deformities, cervical OPLL, spinal cord injury, spinal trauma and tumors involving the spinal column. He has served as an Editor in Chief of “The Neurospine” and editor on the Editorial Boards of Neurosurgery (2016), Neurosurgery Focus (2017), and Asian spine journal (2017 ~).
During his career in medicine, Dr. Ha has won numerous awards for medicine. He has won the Synthes Award for Research in Spinal cord injury and spinal column injury at Congress of Neuyrological Surgeons in 2004 (San Francisco). He received basic science research award in Cervical Spine Research Societies in 2004 (Boston) and 2009 (Salt Lake City).
Dr.Ha’s clinical fields of interest are Adult Spinal Deformity Surgery, Cervical Deformity and Correction Surgery, Cervical OPLL and spondylotic myelopathy, Endoscopic spine surgery for lumbar degenerative disease, Robotic spinal surgery for spine tumor resection and Biologic therapy for Malignant Spinal cord tumor.
Control of Reactive astrocytes for spinal cord regeneration
Neuroregeneration and remyelination after central nervous system (CNS) injury rarely occur in adult mammalian brain and spinal cord. It has been proposed that the main cause of this failure in CNS repair system originates from the glial scar which includes scar-forming reactive astrocytes. However, the molecular and cellular mechanisms of how glial scar impedes CNS repair system is unknown. Here we report that CNS repair system is strongly suppressed by the monoamine oxidase B (MAOB)-dependent excessive GABA production and release from reactive astrocytes in a severe spinal cord injury (SCI) model. A genetic or pharmacological inhibition of MAOB effectively converts the GABA-containing reactive astrocytes to proBDNF-expressing active astrocytes which facilitate neuroregeneration, remyelination and functional recovery after SCI. Particularly, a treatment with KDS2010, a newly-developed, reversible MAOB inhibitor, results in not only a marked increase in astrocytic and neuronal proBDNF, but also a significant increase in astrocytic, neuronal, and oligodendrocytic TrkB, the receptor for mature BDNF (mBDNF). Our findings propose MAOB as a highly effective therapeutic target for SCI and KDS2010 as a next-generation drug candidate for SCI.