Dr. Willard 'Bill' Freeman's research in aging is focused on identifying the molecular mechanisms within the brain that result in cognitive decline with age
Dr. Willard Freeman's research program is centered on systems neurobiology related to cognitive decline with aging, diabetic retinopathy and substance abuse. Dr. Freeman received both his BA and his PhD from Wake Forest University. He completed post-doctoral training at the Vollum Institute at the University of Oregon Health Sciences Center and Yerkes National Primate Research Center at Emory University. Prior to coming to the University of Oklahoma in 2013 he was an Assistant and Associate Professor in the Department of Pharmacology at Penn State University. Dr. Freeman is in the Department of Physiology and is a member of the Reynolds Oklahoma Center on Aging, Harold Hamm Diabetes Center, and Stephensen Cancer Center.
Dr. Freeman's research in aging are focused on identifying the molecular mechanisms within the brain that result in cognitive decline with age. In a series of proteomic studies, Dr. Freeman identified the myelin-associated inhibitor signaling cascade (Nogo, MAG, OMGP through NgR1) as a potential therapeutic target for preventing or reversing cognitive decline with age. Additionally his group is investigating neuroimmune alterations, specifically in the MHCI pathway, with aging and their potential contribution to synaptic dysfunction. As part of the Reynolds Oklahoma Center on Aging his group is bringing advanced epigenomic, transcriptomic, and proteomic technologies to a variety of collaborative projects with other Center investigators.
Much of Dr. Freeman's group is currently examining epigenetic mechanisms in aging, diabetic retinopathy, cancer, and substance abuse. These share a common fundamental question: is the epigenome persistently altered by environmental factors (diet, stress, infection, drugs) that can cause disease and dysfunction years later. In their aging studies, the laboratory has identified that the changes to the epigenome with aging are sexually divergent. In other words, males and females respond differently. In the diabetes studies, Dr. Freeman is testing the hypothesis that persistent retinal cellular and molecular changes during a period of poor glycemic control persist long after re-establishment of normal glycemic control and contribute to the pathogenesis of diabetic retinopathy. This phenomenon, called metabolic memory, may be perpetuated by epigenetic mechanisms, both histone modifications and DNA methylation. His group develops next generation sequencing approaches to quantify epigenetic modifications for these studies.
Dr. Freeman’s bibliography
University of Oklahoma Health Science Center
975 NE 10th Street, SLY-BRC 1370
Oklahoma City OK 73104
Phone: (405) 271-8000 (x30729)
BA Wake Forest University
PhD 2001 Wake Forest University
Post-doctoral training at the Vollum Institute at the University of Oregon Health Sciences Center and Yerkes National Primate Research Center at Emory University Research Interests
Molecular Biology of Aging
Epigenetics and Aging