Jaehong Suh, Ph.D.

Dr. Jaehong Suh is an Assistant Professor of Neurology at Massachusetts General Hospital and Harvard Medical School. His current research focuses on the genetic and molecular mechanisms of Alzheimer’s disease (AD), with the aim of identifying novel therapeutic targets for the disease. Dr. Suh investigates how AD-associated genes, including ADAM10 and Ataxin-1 and their mutations contribute to AD etiology and pathogenesis. His recent studies showed that novel ADAM10 mutations found in AD families decrease the alpha-secretase activity of ADAM10 and thus increase amyloid-beta pathology in the brain. Prior to joining MGH, Dr. Suh studied neuronal cell death mechanism and tau mRNA splicing at Ajou University School of Medicine in South Korea and completed his postdoctoral training in Dr. Rudolph Tanzi’s lab at MGH. He received both of his B.S. and Ph.D. degrees in Biological Sciences from Korea Advanced Institute of Science and Technology (KAIST). Dr. Suh’s research has been supported through awards from NIH, Cure Alzheimer’s Fund and BrightFocus Foundation.

To learn more, visit Dr. Suh’s profile page at Massachusetts General Hospital.

Funded Research

These projects were made possible from Cure Alzheimer's Fund support.

Selected Publications

These published papers resulted from Cure Alzheimer’s Fund support.

Suh, J., Romano, D. M., Nitschke, L., Herrick, S. P., DiMarzio, B. A., Dzhala, V., Bae, J. S., Oram, M. K., Zheng, Y., Hooli, B., Mullin, K., Gennarino, V. A., Wasco, W., Schmahmann, J. D., Albers, M. W., Zoghbi, H. Y., & Tanzi, R. E. Loss of Ataxin-1 Potentiates Alzheimer’s Pathogenesis by Elevating Cerebral BACE1 Transcription, Cell, August 22, 2019, Read More

Dzhala, V., Fowler, A. J., DiMarzio, B. A., Staley, K. J., & Suh, J. Analysis of brain region-specific mRNA synthesis and stability by utilizing adult mouse brain slice culture, STAR Protocols, June 17, 2022, Read More

Suh, J., Choi, S. H., Romano, D. M., Gannon, M. A., Lesinski, A. N., Kim, D. Y., & Tanzi, R. E. ADAM10 Missense Mutations Potentiate beta-amyloid accumulation by impairing pro-domain chaperone function, Neuron, September 19, 2013, Read More