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Neuroprotection pathways explored to slow RPE atrophy
CHICAGO — After anti-VEGF therapy is used to treat neovascular age-related macular degeneration, 90% of patients’ conditions stabilize but only 40% of patients gain three or more lines of visual improvement, according to a presentation here. In addition, there is no effective treatment for dry AMD.
“The vision in both these cases ultimately continues to worsen as the [retinal pigment epithelium] atrophy progresses,” David N. Zacks, MD, PhD, told colleagues at Retina Subspecialty Day preceding the joint meeting of the American Academy of Ophthalmology and Asia-Pacific Academy of Ophthalmology. The reason for the decline, he said, is that photoreceptors die.
By blocking apoptosis, however, photoreceptor cell death can be prevented, both by upstream blockade of the Fas receptor and downstream blockade of caspases, he said.
Studies have aimed to define the specific molecular pathways that control photoreceptor death and develop therapeutic interventions, or identify targets for such interventions, that will delay or prevent photoreceptor cell death and preserve retinal function. For example, loss of IL-6 function results in significantly increased death of photoreceptors, and the addition of IL-6 prevents photoreceptor death, Zacks said.
“We can modulate the pathways to shift the balance of power,” he said.
Disclosure: Zacks has equity in ONL Therapeutics and patents through University of Michigan and Massachusetts Eye and Ear Infirmary.