Treating Ocular Diseases at the Cell Level
A therapeutic modality for treating ocular disease by using preserved (frozen) mitochondrial transplantation.
Mitochondrial dysfunction is a major contributor to the pathogenesis of many ocular diseases. Among them are common sight-threatening retinal ischemic insults, such as Central Retinal Artery Occlusion, Acute Angle Closure Glaucoma and Non-arthritic Anterior Ischemic Optic Neuropathy (NAION). A hallmark of these pathologies is the death of retinal ganglion cells (RGCs), a type of neuronal cells located near the inner surface of the retina that are responsible for transmission of visual signals from the retina to the brain.
Inventors
Dr. Ziv Rotfogel, Kaplan Medical Center
Dr. Avital Eisenberg, Kaplan Medical Center
Contact info
Sari Prutchi Sagiv PhD. Director of Pharma and Diagnostics
For further information please contact:
sari@mor-research.comWe developed a protocol for the preservation of highly functional, ready-to-use mitochondria for transplantation, and to establish its beneficial effect in NAION disease. Our preliminary results show that mitochondria injected to the vitreous cavity are internalized by retinal ganglion cells and protect them from ischemia-induced death in-vivo. Furthermore, we show novel preservation protocols that retain mitochondrial function and most importantly, also retain their protective effect against cell death.
NAION is the leading cause of sudden optic nerve-related vision loss, predominantly in the population over 50 years of age (2.3 to 10.2 per 100,000 for persons over the age of 50).
Pre-clinical studies