For many of us today, death will not be the end. We don’t mean that in a metaphysical sense – and this isn’t a weirdly quiet preamble to heralding the start of a zombie apocalypse – we’re talking about organ donation. Thanks to this life-saving procedure, quite a few of us can literally still pump iron, pose, and, uh, poop, long after we’re dead.
But as smart as our scientists are, there are some parts of the body that just don’t do well. While organs like the kidneys or liver can be put on ice for hours to slow damage from lack of oxygen, central nervous system tissue becomes nonviable within four minutes of death. And frustratingly, exactly why this happens, and if it’s reversible, hasn’t been fully understood. Until now.
“We were able to awaken photoreceptor cells in the human macula, which is the part of the retina responsible for our central vision and our ability to see fine detail and color,” explained Fatima Abbas, postdoctoral fellow at the John A. Moran. University of Utah Eye Center, in a statement. “In eyes obtained up to five hours after the death of an organ donor, these cells responded to bright light, colored lights, and even very faint flashes of light.”
Abbas is the lead author of a new study, published this week in the journal Nature, aimed at understanding how neurons die – and potential ways to revive them. Using human retinas as a model for the central nervous system, the team made a series of discoveries which, they write, “will allow[e] transformative studies in the human central nervous system, rais[e] questions about the irreversibility of neuronal cell death, and provide[e] new avenues for visual rehabilitation.
While the researchers were indeed successful in reviving the photoreceptor cells, at least initially things weren’t going well. “So far, it has not been possible to get the cells of all the different layers of the central retina to communicate with each other as they normally do in a living retina,” explained the co-author of the study. , Anne Hanneken, retina specialist. surgeon and Scripps Research Associate Professor in the Department of Molecular Medicine at the Scripps Research Institute in San Diego.
The reason, they realized, was oxygen deprivation. So they set out to find a way to overcome the damage caused by the lack of oxygen, with study co-author and fellow Moran Eye Center scientist Frans Vinberg designing a special transport unit that could restore oxygenation and other nutrients to eyes taken from organ donors within 20 years. moment of death.
That wasn’t the only invention Vinberg brought to the experiment. He also developed a device that could stimulate these retinas to produce electrical activity and measure the output. Thanks to this technique, the team was able to overcome another barrier: the first-ever recording of a “b-wave” signal from the central retina of post-mortem human eyes.
In living eyes, b waves are a type of electrical signal associated with the health of the inner layers of the retina – so it is very important to have been able to stimulate them in post-mortem eyes. This means that the layers of the macula were communicating again, as they do in our lifetime, to help us see.
“We were able to get the retinal cells to talk to each other, like they do in the living eye to mediate human vision,” Vinberg explained. “Previous studies have restored very limited electrical activity in the eyes of organ donors, but this has never been achieved in the macula, and never to the extent that we have now demonstrated.”
It may be a small finding – the macula is only about 5 millimeters (0.2 inches) in diameter, after all – but it has huge implications. As it stands, death is a state partially defined by the death of neurons, which so far has been shown to be irreversible. If neurons can in fact regain their quality of life, it may force us to reconsider once again what is considered “dead” – and perhaps we will see the Grim Reaper shunned even longer than we have. we’ve already done that.
Of course, while this is where this discovery ultimately leads, there are more pressing questions at hand – as anyone who wears glasses can attest. And the team is confident that their findings will also have great benefits for the future of vision research: “In the future, we can use this approach to develop treatments to improve vision and light signaling in eyes with macular diseases, such as age. -related macular degeneration,” Hanneken pointed out.
The multitude of new findings hint at a way for future researchers to study neurodegenerative diseases throughout the body, not just in the eyes, but its importance to vision research cannot be overstated. The study has already paved the way for its b-wave revival, and the team suspects they have also uncovered the mechanism responsible for limiting the speed of human central vision; the techniques also open the door to developing visual therapies on working human eyes, sparing researchers the ethical concerns of using non-human primates (and even more so for human primates) or the scientific issues of the use of laboratory mice (which do not have a macula.)
All they need now is more eyes.
“The scientific community can now study human vision in a way that is simply not possible with laboratory animals,” Vinberg said. “We hope this will motivate organ donor societies, organ donors and eye banks by helping them understand the exciting new possibilities that this type of research offers.”