Blind mice had their eyesight restored by the activation of proteins which rolled back a sort of genetic scarring that occurs overtime, promising that at least some of the worst and seemingly inevitable affects of aging are avoidable through modern medicine.
The retinal ganglion neurons of mice were restored to a youthful state in cases of glaucoma, as well as when the optic nerve had been damaged. Both were achieved through expressing certain transcription factors — proteins that turn genes on and off.
“The study sheds light on the mechanisms of ageing, and identifies new potential therapeutic targets for age-related neuronal diseases such as glaucoma,” reads a press release from Nature.
The new study, published in Nature, was conducted by Dr. David Sinclair, of the world’s foremost experts on ageing-related research in mice.
He has made a career of rolling back different biological clocks in mice through the use of various compounds like resveratrol and Metformin, and his book, Lifespan: Why We Age and Why We Don’t Have To, is a New York Times best-seller.
A dusty old book
The science behind his new paper involves the curious process of methylation. Governed by epigenetics, changes in the genetic expression of the cell over time, methylation in mammalian tissues, the authors found, prevents the cells from replicating proteins properly while simultaneously encoding a kind of genetic history.
In his book, Sinclair details the modern theory of aging, which is that changes in epigenetics and damage to cells and tissues prevent the body from properly reading protein-encoding genes, resulting in either faulty, less-functional, i.e. older genes being transcribed, or the proteins not being replaced at all.
Here the authors found that when the mouse neurons were recovering, the methyl groups which built up over time left, resulting in demethylation. Demethylation was associated with younger genetic expression, in other words, the mouse’s genes remembered how to be young again, only after demethylation had occurred.
“These data indicate that mammalian tissues retain a record of youthful epigenetic information—encoded in part by DNA methylation—that can be accessed to improve tissue function and promote regeneration in vivo,” write the authors in their summary.
It remains to be seen whether records of youthful genetic expression are contained within other mammalian tissues through methylation, and whether or not they can be accessed through demethylation.
If it’s true that simply altering some transcription factors is enough to clear the dust off the rule book for how to build young proteins, Sinclair stands to make a major breakthrough.
Earlier in the year, World at Large reported on another study which demonstrated the ability to reprogram skin fibroblasts into replacement photoreceptors which also restored vision in blind mice.
Speaking with World at Large, study author Sai Chavala, Ph.D. hoped to move his method on to the exact thing Sinclair’s new glaucoma study is working to fix.
“ We […] believe this can be a game changer in the field of regenerative ophthalmology. We also believe this is a platform technology and have already started establishing protocols to generate retinal ganglion cells valuable for patients suffering from glaucoma,” says Chavala.
The work of the two men are noteworthy for many reasons, not least of all due to the simplicity of the treatments. If they can be successfully trialed in humans, blindness might soon be a thing of past.
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Editor’s note: We changed the featured image as someone alerted us that it was not in fact a mouse but a guinea pig.