Chen and his colleagues report their findings in the Jan. 9 issue of Science.
The findings are based solely on a series of neural cell experiments, focused on the retinal health of live mice, that were designed to assess the impact of both under-expression and overexpression of the HDAC4 protein.
Subsequent lab work led the researchers to determine that in sufficient quantities the protein indeed displays a protective effect against eye cell death and thereby has an "essential role in neuronal survival," they wrote.
Yet despite expressing enthusiasm for his current work, Chen emphasized the ongoing nature of the effort.
"Even though the genetics are the same in mice and humans, at this stage it's really very experimental," he stressed. "And much more work needs to be done before we know this will be efficacious in humans."
Nevertheless, Dr. Robert Cykiert, a clinical associate professor of ophthalmology at New York University Langone Medical Center in New York City, described the current work as an "impressive" effort.
"Clearly a lot of people go blind from retinal diseases," he said, noting that glaucoma and macular degeneration are two serious conditions that result from retinal cell death. "And this protein they worked with appears to be what we call neuro-protective, in that it has protective benefits on both the photoreceptor layer that gets damaged in macular degeneration as well as on the ganglion cell layer which is damaged by glaucoma. So this finding could actually turn out to be a major accomplishment, affecting a lot of patients down the road."
However, Rando Allikmets, an associate professor of ophthalmology, pathology and cell biology at Columbia University in New York City, took Chen's cue in cautioning that the true measure of the current work awaits human clinical trials.
"It's a very good study, an interesting observation and a very encouraging finding that
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