Neuroscience Ph.D. candidate Saumya Keremane has been awarded a National Institutes of Health (NIH) Individual Predoctoral Fellowship (F31) to support her research on mechanisms and treatments for inherited blindness.

This competitive fellowship recognizes early-stage researchers whose work shows strong potential to advance science and improve human health.

Keremane's research, conducted in the labs of Richard Taylor, a professor and head of the Department of Physics, and Dr. Bala Ambati, an ophthalmologist and research professor in the Department of Bioengineering, focuses on understanding and preventing neuron degradation to treat inherited blindness.

Vision begins when light-sensing cells in the back of the eye, called photoreceptors, detect light and pass that information through a chain of cells, including interneurons and others, which send the signal to the brain. In a hereditary eye disease called retinitis pigmentosa, the photoreceptors gradually break down, and the interneurons connected to them begin to deteriorate as well. This leads to night blindness, loss of peripheral vision, and eventually total blindness.

Some treatments have attempted to restore vision by transplanting new photoreceptors, but these often fail to restore vision because the transplanted cells can't properly connect with the damaged interneurons to relay signals to the brain. Other treatments which implant an electrode to replace the photoreceptors experience similar issues, where the interneurons remain deteriorated. 

Keremane hopes to address interneuron deterioration by first understanding how the cell morphology changes during eye disease and then apply gene therapies to protect and restore them to a healthy state.

"Once the photoreceptors begin to die, their connections also suffer, leading to photoreceptor replacement therapies failing" said Keremane. "If transplant therapies are ever going to work, we need to keep the rest of the circuitry intact so new cells can integrate properly. Without that, there won't be vision."

To do this, Keremane plans to recreate the most common genetic mutation behind retinitis pigmentosa and investigate a protein known to influence interneuron growth. The goal is to pinpoint when the interneurons start to decline, identify windows of time when treatment could intervene, and uncover the specific molecules that could be targeted by future therapies.

"The outcomes of this project will inform strategies for optimizing retinal prostheses, improving photoreceptor transplantation, and developing targeted therapies," said Taylor.

Retinitis pigmentosa affects more than two million people worldwide, and currently has no cure, though low vision aids and rehabilitation programs can help people make the most of their remaining sight. Understanding how interneuron damage unfolds, and how gene therapies could prevent it, could open new doors for future treatments.

"We're hopeful that these studies will deepen our understanding of retinal diseases like retinitis pigmentosa, and contribute to transformative therapies that restore vision for millions of affected individuals," said Ambati.

"The NIH F31 fellowship is a prestigious award for doctoral students, recognizing both the strength of research and the rigor required to develop a competitive application,” Taylor said. "Keremane’s proposal demonstrated an innovative approach and the creative pairing of fractal analysis of retinal cells from our lab with cell biology and gene therapy research in the Ambati lab."

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May 15, 2026

Rachel Bedford