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Blind Mice with Glaucoma See Again Through Simple Technique that Promotes Youthful Gene Expression

Some of the following were reprinted with permission from World in general, a news outlet focused on space, health, conservation, foreign and environmental policy and travel.

Researchers at Harvard Medical School have successfully restored vision loss and reversed glaucoma-induced damage in mice.

In mice, ganglion cells in the retina, a main cell that enables vision, were restored to a youthful state in glaucoma, as well as when the optic nerve, another key component of sight, had been damaged. Both were achieved through the expression of certain transcription factors, proteins that turn genes on and off.

“The study sheds light on the mechanisms of aging and identifies potential new therapeutic targets for age-related neural diseases, such as glaucoma.” read a statement Researchers from Harvard Medical School.

The new study, published in Nature, was conducted by Dr. David Sinclair, one of the world’s leading experts on aging-related research in mice.

Along with genetic research, Sinclair has also looked at how compounds prepared for supplements like resveratrol and Metformin affect aging, and his book, Lifespan: why we age and why we don’t have to, is a New York Times bestseller.

Repairing a scratched CD

The science behind Sinclair’s new paper it involves the curious process of methylation. Governed by epigenetics, that is, changes in the cell’s gene expression over time, the researchers found that methylation in mammalian tissues prevents cells from replicating proteins appropriately and at the same time encoding a kind of genetic history.

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One can imagine this as scratches on the bottom of a CD. If the scratches can be removed, the proper function record is still there and could still be read by the laser on a CD player.

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 reading protein-encoding genes correctly, resulting in faulty gene transcription, less functional, that is, older, or the proteins are not replaced at all.

Here, the authors found that when mouse neurons recovered from glaucoma-related damage, the methyl groups that accumulated over time disappeared, like scratches being removed from a disk.

This resulted in a process called demethylation. Demethylation was associated with younger gene expression, in other words, the mouse genes remembered how to become young again, only after demethylation had occurred.

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“These data indicate that mammalian tissues retain a record of juvenile epigenetic information, encoded in part by DNA methylation, that can be accessed to enhance tissue function and promote regeneration in vivo,” the authors write in your summary.

It remains to be seen whether the juvenile gene expression records are contained in other mammalian tissues, the liver for a random example, through methylation, and whether or not they can be accessed by demethylation.

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If it’s true that simply altering a few transcription factors is enough to clear the dust from the rulebook on how to build young proteins, Sinclair can make a breakthrough.

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