Manoj Mohan Kulkarni, Ph.D receives $65,000 grant to study Retinitis Pigmentosa and Leber Congenital Amaurosis

Grand Commandery officers from the Grand Commandery of California traveled to the University of California, located in Berkeley to make a $65,000 check presentation to Manoj Mohan Kulkarni, Ph.D. The Sir Knights presenting the check were: David Stud…

Grand Commandery officers from the Grand Commandery of California traveled to the University of California, located in Berkeley to make a $65,000 check presentation to Manoj Mohan Kulkarni, Ph.D. The Sir Knights presenting the check were: David Studley, Grand Generalissimo and Trustee of the Knights Templar Eye Foundation; Howard Ramsey, Past Grand Commander; Gregg Hall, Past Grand Commander; Brandon Duenas, Past Commander, San Jose #10; Walter Crossley, Past Commander, San Jose #10

Inherited forms of retinal degenerations such as retinitis pigmentosa (RP) & Leber Congenital Amaurosis (LCA) are a leading cause of blindness with a worldwide prevalence of 1:3000-4000. RP and LCA are typically diagnosed early in childhood.

The affected pediatric population quickly loses the ability to see in dim light. This stage is followed by loss of daylight vision resulting in complete blindness around adolescence. Current treatments either slow vision loss or attempt to restore vision by making residual neurons in the retina artificially light-sensitive. Recent studies in mouse models of RP have demonstrated that such therapies are compromised by the appearance of abnormal spontaneous neural activity, or “neural noise”, then can mask and thus degrade the important visual signals. Identifying neural origins of this noise is a critical next step to finding ways to reduce it and thus improve the efficacy of therapies.

Previous studies have demonstrated that a particular interneuron, the AII amacrine cell, may generate and spread the abnormal activity to other neurons in the diseased retina. Dr. Kulkarni hypothesizes that the neural circuits activating the AII amacrine cells become abnormal during disease progression. These studies aim to identify the abnormal changes in the neural circuits, and thus reveal potential pharmacological targets that may allow them to silence aberrant activity while preserving the signals essential for vision. Knowledge from these studies is expected to inform the development of therapies for treating affected children.

Brandon Mullins