Philip L. De Jager

Philip L. De Jager
Brigham & Women’s Hospital
Boston, MA, United States

Speaker of Workshop 3

Will talk about: Why we need disruptive innovation to accelerate MS research

Bio sketch:

Philip L. De Jager is the Steven R. and Kathleen P. Haley Distinguished Chair for the Neurosciences at the Brigham & Women’s Hospital and is an associate professor of neurology at Harvard Medical School. He is the director for basic and translational research at the Institute for the Neurosciences at the Brigham & Women’s Hospital and is an associate member of the Broad Institute of Harvard University and the Massachusetts Institute of Technology. He continues to practice clinical neurology, seeing patients within the Partners Multiple Sclerosis Center that is affiliated with the Brigham & Women’s Hospital and Massachusetts General Hospital in Boston. In 2008, Philip received the prestigious Harry Weaver Neuroscience Scholar Award from the National Multiple Sclerosis Society. His work focuses on understanding the genomic, epigenomic, and neuroimmunologic architecture of neurodegenerative diseases such as multiple sclerosis, Alzheimer’s disease, and age-related cognitive decline.

Philip received his BS (summa cum laude) in molecular biophysics & biochemistry and French literature from Yale University. He received his PhD in neurogenetics from The Rockefeller University and his MD from Cornell University Medical College. He also completed an MMSc program in clinical investigation at Harvard Medical School and the Massachusetts Institute of Technology. In addition, he completed subspecialty training in neuroimmunology at the Brigham and Women’s Hospital and in human genetics at the Broad Institute.

Talk abstract:

Multiple sclerosis (MS) is a disease of the brain and spinal cord that has two components: inflammation, with recurring episodes of acute damage, and slowly progressive neuronal loss, which manifests as a gradual decline in cognitive and other functions. Although we know much about the inflammatory component of MS, our treatment options are imperfect and we currently have no tools with which to predict individual disease course. There is a tremendous heterogeneity among individuals with a syndromic diagnosis of MS.

Biomarker studies to date have identified modest associations with different aspects of the disease, but no single biomarker is informative. Further, we currently do not understand the pathophysiology of the neurodegenerative component of the disease. Thus, to address the issue of personalizing MS care and gain insights into disease progression that could lead to novel therapeutics, we need a new paradigm for MS investigation and analytics that is capable of considering multiple dimensions of information.