For many of us, death will not be the end. We don’t mean that in a metaphysical sense — and this isn’t an oddly calm prelude to heralding the onset of a zombie apocalypse — we’re talking about organ donation. Thanks to this life-saving procedure, a good number of us can still literally pump iron, pose and defecate long after we’ve died.
But as smart as our scientists are, there are parts of the body that just don’t donate properly. While organs such as kidneys or livers can be put on ice for hours to delay damage from oxygen starvation, central nervous system tissues become unviable in less than four minutes after death. And frustratingly, exactly why this happens and whether it is reversible is not well understood. Until now.
“We were able to wake up photoreceptor cells in the human macula, the part of the retina responsible for our central vision and ability to see fine details and colors,” explains Fatima Abbas, a postdoctoral researcher at the Johns. A. Moran Eye Center of the University of Utah, in a statement. “In eyes obtained up to five hours after the death of an organ donor, these cells responded to bright light, colored light 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 figuring out how neurons die — and possible ways to revive them. Using the human retina as a model for the central nervous system, the team made a series of discoveries that, they write, “will enable[e] transformative studies in the human central nervous system, Rais[e] questions about the irreversibility of neuronal cell death, and[e] new avenues for visual rehabilitation.”
While the researchers were indeed able to revive the photoreceptor cells, at least things didn’t look right at first. “Until now, it has not been possible to get the cells in all the different layers of the central retina to communicate with each other as they normally do in a living retina,” said study co-author Anne Hanneken, a retinal surgeon and Scripps Research Associate Professor. the Molecular Medicine Department at the Scripps Research Institute in San Diego.
The reason, they realized, was lack of oxygen. So they set out to find a way to overcome the damage caused by oxygen starvation, with study co-author and fellow scientist Frans Vinberg of the Moran Eye Center designing a special transport unit that would deliver oxygen and other nutrients to the eyes of organ donors. could recover within 20 years. minutes of death.
That wasn’t the only invention Vinberg brought into the experiment. He also came up with a device that could stimulate these retinas to produce electrical activity and measure output. This technique allowed the team to break through another barrier: the first-ever recording of a “b-wave” signal from the central retina of postmortem human eyes.
In living eyes, b-waves are a type of electrical signal related to the health of the inner layers of the retina – so it’s very important to have them stimulated in post-mortem eyes. It means that the layers of the macula were communicating with each other again, just like when we are alive, 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 explains. “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 result — after all, the macula is only about 5 millimeters (0.2 inches) in diameter — but it has huge implications. As it stands, death is a condition determined in part by the death of neurons, which has so far been shown to be irreversible. If neurons can, in fact, be restored to living quality, perhaps it will force us to rethink what counts as “dead” – and perhaps we’ll see the Grim Reaper warded off even longer than we already have.
Of course, even if that’s where this discovery ultimately leads, there are more pressing matters at stake — as anyone who wears glasses can attest. And the team is confident that their results will also have major benefits for the future of vision research: “In the future, we will be able to use this approach to develop treatments to improve vision and light signaling in eyes with macular disorders, such as age. -related macular degeneration,” noted Hanneken.
The many new results point to a way for future researchers to study neurodegenerative diseases throughout the body, not just in the eyes, but its importance for vision research cannot be overstated. The study has already pioneered the revival of b-waves, and the team suspects they may have also discovered the mechanism responsible for limiting the speed of humans’ central vision; the techniques also open the door to the development of visual therapies for working human eyes, raising the ethical concerns of using non-human primates (and even more so for human primates) or the scientific problems associated with using laboratory mice. (who do not have a macula) are saved. †
All they need now are more eyes.
“The scientific community can now study human vision in ways that are simply not possible with laboratory animals,” Vinberg said. “We hope this will motivate organ donor associations, organ donors and eye banks by helping them understand the exciting new possibilities that this type of research offers.”