Steve Hyman returns to the lab after a decade as Harvard provost
During his ten years as Harvard’s provost, Steven E. Hyman, MD, reshaped the University’s research landscape, driving the creation of interdisciplinary, cross-school research collaborations quite foreign to an institution best know for its very strong, but very independent science departments and schools. He supported the establishment of what are now the Harvard Global Health Institute, the Origins of Life Initiative, the Department of Stem Cell and Regenerative Biology (SCRB) — the first Harvard department based in two schools — and he was instrumental in the creation of HSCI.
And when Hyman stepped down from his administrative post in 2012, Hyman joined both SCRB and HSCI, returning to the lab in hopes of applying new stem cell and genomic science to the treatment of mental disorders.
Hyman’s goal is to understand the role genes play in the causation of schizophrenia, bipolar disorder, and autism. When he returned to Harvard in 2001, having served for five years as the director of the National Institute of Mental Health, there were very few molecular clues about what cause these conditions. But over the past decade, technological advances have revealed hundreds of genes related to mental disorders, each variant adding a slight percentage of risk.
“We had no chance of identifying myriad genes of small effect with the methods available a decade ago,” said Hyman, who also serves as the director of the Stanley Center, at the Broad Institute of Harvard and MIT. “What is most exciting is that these genes are beginning to coalesce into recognizable biochemical pathways.”
Hyman is working with fellow HSCI Principle Faculty members Kevin Eggan, PhD, and Paola Arlotta, PhD, to generate neurons thought to be abnormal in schizophrenia. They will then study how different genes change these cells’ molecular activity.
“Having a list of genes that create disease risk is only a first step,” Hyman said. “It is critical to understand what they do and how subtle variations in their DNA sequences might contribute to illness,” which could open new avenues in the pharmaceutical treatment of