David W. Garber, PhD
Dept. of Medicine
Division of Gerontology, Geriatrics, and Palliative Care
Office Address: BDB 654
Websites: School of Medicine Faculty Profile
Pennsylvania State University, University Park, PA
BS, Biology, 1976
Milton S. Hershey Medical Center, Pennsylvania State University, Hershey, PA
PhD, Physiology, 1981
Medical College of Pennsylvania, Philadelphia, PA
Postdoctoral fellow, Dept. of Physiology/ Biochemistry, 1981-3
Coronary vascular disease, including heart disease and stroke, is the leading cause of death in the developed world. Numerous studies have shown that high levels of low density lipoprotein (LDL) cholesterol are associated with increased risk for atherosclerotic heart disease, while high levels of high density lipoprotein (HDL) are associated with reduced risk. The major protein component of HDL, apolipoprotein (apo) A-I, is considered to be primarily responsible for the atheroprotective properties of HDL. Apo E associates with chylomicrons, very low density lipoproteins (VLDL), and HDL, and mediates the clearance of triglyceride-rich lipoproteins. Both apo A-I and E have anti-inflammatory properties that contribute to atheroprotective properties.
Our group has pioneered the design of peptide mimetics of apolipoproteins that have similar structural motifs as apo A-I and apo E, and has used these mimetic peptides to study the physical properties of apo A-I and apo E. My laboratory has extended these studies into animal models with the intent to use peptide mimetics of apolipoproteins to determine what properties of apo A-I and apo E prevent atherosclerosis and inflammatory processes in vivo. We are now extending these studies into animal models of Alzheimer ’s disease and insulin resistance.
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