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 calm preamble to announcing the onset of a zombie apocalypse – we’re talking about organ donation. Thanks to this life-saving procedure, a good number of us may literally still be pumping iron, posing and, um, pooping, long after we die.
But as smart as our scientists are, there are some parts of the body that just don’t donate well. While organs like kidneys or livers can be put on ice for hours to slow damage from lack of oxygen, tissue from the central nervous system becomes non-viable in less than four minutes after death. And frustratingly, exactly why this happens, and whether it’s reversible, has not been well understood. Until now.
“We were able to wake up 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, a postdoctoral researcher at the John A. Moran Eye Center at the University of Utah, in a statement. “In eyes obtained up to five hours after an organ donor’s death, these cells responded to bright light, colored lights, and even very dim flashes of light.”
Abbas is lead author of a new study, published this week in the journal Nature, aimed at figuring out 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 that will, they write, “enabl[e] transformative studies in the human central nervous system, rais[e] questions about the irreversibility of neuronal cell death, and provid[e] new avenues for visual rehabilitation.”
While the researchers were indeed able to revive the photoreceptor cells, initially at least, things didn’t look good. “Until now, it hasn’t been possible to get the cells in all of the different layers of the central retina to communicate with each other the way they normally do in a living retina,” explained study co-author Anne Hanneken, a retinal surgeon, and Scripps Research Associate Professor at the Department of Molecular Medicine of the Scripps Research Institute in San Diego.
The reason, they realized, was oxygen deprivation. So they set about finding a way to overcome the damage caused by lack of oxygen, with study co-author and fellow Moran Eye Center scientist Frans Vinberg designing a special transportation unit that could restore oxygenation and other nutrients to eyes taken from organ donors within 20 minutes of death.
That wasn’t the only invention Vinberg brought to the experiment. He also came up with a device that could stimulate these retinas to produce electrical activity, and measure the output. Thanks to this technique, the team were able to break 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 associated with the health of the inner layers of the retina – so to have been able to stimulate them in postmortem eyes is really important. It means that the layers of the macula were communicating again, just like they do when we’re alive, to help us see.
“We were able to make the retinal cells talk to each other, the way they do in the living eye to mediate human vision,” Vinberg explained. “Past studies have restored very limited electrical activity in organ donor eyes, but this has never been achieved in the macula, and never to the extent we have now demonstrated.”
It may be a small result – 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 neuron death, which so far has proven irreversible. If neurons can in fact be restored to living quality, perhaps it will force us to once again reconsider what counts as “dead” – and maybe we’ll see the Grim Reaper staved off even longer than we’ve already managed.
Of course, even if that is where this discovery leads eventually, there are more pressing matters at hand – as anybody who wears glasses can attest. And the team are confident their results will have big advantages for the future of vision research too: “Going forward, we’ll be able to 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 slew of new results hint at a way for future researchers to study neurodegenerative diseases throughout the body, not just in the eyes, but its importance for vision research can’t be overstated. The study has already broken ground for its revival of b waves, and the team suspect they’ve also discovered the mechanism responsible for rate-limiting the speed of human central vision; the techniques also open the door to developing visual therapies on working human eyes, saving researchers the ethical concerns of using non-human primates (and even more so for human primates) or the scientific problems that come with using lab mice (who have no macula.)
All they need now is more eyes.
“The scientific community can now study human vision in ways that just aren’t possible with laboratory animals,” said Vinberg. “We hope this will motivate organ donor societies, organ donors, and eye banks by helping them understand the exciting new possibilities this type of research offers.”
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