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Malia Michelle Edwards, Ph.D.

Assistant Professor of Ophthalmology

Research Interests

retinal glia; particularly their role in vascular development and disease ...read more

Background

Dr. Malia Edwards is a researcher at the Wilmer Eye Institute with a particular focus on retinal gila and their roles in vascular development and disease.

Dr. Edwards’ interest in glia began during graduate school studying the effect oxidative stress and inflammation exert on astrocytes. As a post-doctoral fellow at The Jackson Laboratory, Dr. Edwards cloned and characterized a mouse mutant, Lama1, with abnormal retinal vasculature and astrocyte development. She joined Dr. Lutty’s lab to expand her knowledge of retinal vascular development and has since continued studying vascular development in the Lama1 mice and in a mouse which lacks ganglion cells, Math5.

Titles

Assistant Professor of Ophthalmology

Departments / Divisions

Ophthalmology

Education

Degrees

Ph.D.; Monash University (Victoria) (Australia) (2003)
B.S.; University of Michigan (Michigan) (1996)

Research & Publications

Research Summary

Dr. Edwards and her lab are currently investigating how early in the disease process Müller cell changes occur, and how their activation and remodeling affects AMD disease progression by influencing blood vessels, neurons and retinal pigment epithelial cells.

As an independent investigator, Dr. Edwards plans to continue investigating the role astrocytes and Müller cells play in retinal vascular development and also how these interactions affect retinal disease. Her most recent work has been investigating glial changes in aged human retinas with and without age-related macular degeneration (AMD). She has observed glial membranes on both the vitreoretinal surface and external to the ELM in eyes with advanced stages of AMD.

Furthermore, Müller cells are activated and disorganized within AMD retinas. Together, these findings suggest that Müller cells are remodeling in AMD. Such remodeling could affect the normal function of these glial cells, having detrimental consequences for other retinal cells.

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