MR-5 3133
​MR-5 3237
Gelfand Laboratory


Dr. Gelfand graduated with a degree in Biomedical Engineering from the University of Iowa (Iowa City). He next attended the University of Virginia (Charlottesville) where he earned his Ph.D. also in Biomedical Engineering. Brad next joined the Ambati Laboratory at the University of Kentucky in 2010 as a Postdoc and joined the faculty in 2012. In 2016, Brad returned to UVA as an Assistant Professor in the Department of Ophthalmology. When he's not in the lab, he enjoys spending time with his lovely wife Christen, daughters Morgan and Stella and his dogs Yoda and Luke.


B.S. ​University of Iowa, 2004

Ph.D. ​University of Virginia, 2010

Post-Doc ​University of Kentucky, Department of Ophthalmology and Visual Sciences 2012

We study the blinding disease age-related macular degeneration, utilizing the tools of immunology,molecular biology, and engineering.

Bradley D. Gelfand Assistant Professor

Research Interests

Medical and Molecular Imaging
Signal and Image Processing
Biomechanics/Injury Biomechanics or Biomechanics and Mechanobiology
Cardiovascular Engineering
Fluid Mechanics

Selected Publications

A Revised Hemodynamic Theory of Age-Related Macular Degeneration. Trends in Molecular Medicine 2016 Aug;22(8):656-70. Bradley D. Gelfand and Jayakrishna Ambati
Iron Toxicity in the Retina Requires Alu RNA and the NLRP3 Inflammasome. Cell Reports 2015 Jun 23;11(11):1686-93. Bradley D. Gelfand Et Al.
Nucleoside reverse transcriptase inhibitors possess intrinsic anti-inflammatory activity. Science. 2014 Nov 21;346(6212):1000-3. Benjamin J Fowler, Bradley D. Gelfand, Et Al.
DICER1 loss and Alu RNA induce age-related macular degeneration via the NLRP3 inflammasome and MyD88. Cell. 2012 May 11;149(4):847-59. Valeria Tarallo, Yoshio Hirano, Bradley D. Gelfand Et Al.
Human haemodynamic frequency harmonics regulate the inflammatory phenotype of vascular endothelial cells. Nat Commun. 2013;4:1525 Ryan E. Feaver, Bradley D. Gelfand, Brett R. Blackman

Featured Grants & Projects

Cellular and Molecular Consequences of the Blood Supply in the Eye One major focus of our work is to study the cellular and molecular consequences of the blood supply in the eye. Specifically, we are interested in quantifying the biomechanical changes that occur in the choroidal vasculature in healthy and diseased eyes, and how these micro-environmental cues affect the biology and pathology of the eye. To accomplish this, we perform high-resolution 3-D microscopy to generate accurate maps of the human choroidal anatomy in health and in disease which is utilized for computational fluid dynamic modeling. To study the influence of choroidal hemodynamics on ocular health, we employ a sophisticated cell culture system which is capable of reproducing the hemodynamic environment of the human eye. In a related project, our research analyzes the molecular mechanisms which underlie development of age-related macular degeneration. One such pathway involves deficiency of the RNA processing enzyme DICER1. Specifically, we seek to determine how DICER1 deficiency promotes death of retinal cells and the consequences of DICER1 deficiency on aberrant blood vessel growth.