Patrice Fort

Patrice Fort, PhD

Associate Professor of Ophthalmology and Visual Sciences, Director of the Vision Research Training Program (NEI-T32) of the UM Kellogg Eye Center
Accepting new students?
Trainings and Identities
MORE Mentor Training, Implicit Bias Training
Research Interests
Intrinsic retinal neuron survival mechanisms; retinal glial cells implications in pathological and normal retinal functions; crystallin protein functions in the retina; signaling pathways regulation

Our laboratory fosters collaboration, communication, and involvement of each lab members without distinctions relative to level of training or origin. It is the expectation that everyone participates in the lab's life to the extent they can and it is recognized that everyone has a different perspective that adds value to the discussion. Through my role in recruitment committees and course and training program director, I am particularly sensitive to the philosophy of holistic review process.

Identifying and understanding mechanisms of retinal cell death that occur in neurodegenerative disorders such as diabetes.
Our research focuses on studying retinal diseases and their mechanisms, in order to develop new treatments to prevent or reverse associated vision loss.
A major focus in our lab is the development of strategies to treat retinal neurodegenerations, including diabetic retinopathy. One of our objectives is to investigate the function and regulation of crystallin proteins in the adaptive responses of retinal cells during chronic disease states such as diabetes. Using whole proteome analysis, we have demonstrated that the expression of retinal crystallin proteins undergoes dramatic alteration. Studies in animal models and in humans have shown that diabetic retinopathy is a complex disease characterized by vascular alterations, inflammation, and neuronal cell death, processes which involve crystallin proteins. We have also demonstrated that alpha-crystallins, a subset of crystallin proteins, have intrinsic neuroprotective properties in retinal neurons and that those properties are impaired during diabetes. We are currently developing different cellular and integrated approaches to determine the mechanisms and pathways responsible for the loss of neuroprotective function of crystallin.
It has been demonstrated that crystallins are expressed in the human eye; however, their expression and regulation in human diabetic retina has not been studied. Another one of our projects uses proteomic and immunohistochemical analysis to evaluate the impact of diabetes on the expression of retinal crystallins in humans. Our goal in this project is to confirm the potential of crystallins for developing novel therapies to prevent neurodegeneration under stress conditions.