Restore Eyesight By Turning Back Epigenetic Clock

Restore Eye Sight By Turning Back Epigenetic Clock placard | Feature | Restore Eye Sight By Turning Back Epigenetic Clock

A recent study published on Nature.com claims that scientists can restore eyesight to a youthful state. Read on to learn more.

RELATED: Epigenetic Clock May Predict Brain Aging and Dementia

In this article:

  1. Background
  2. Studies & Findings
  3. Summary Points

Can Science Really Restore Eyesight?

Background

Throughout our lifetime, DNA methylation and other epigenetic changes effectively switch genes on or off in specific tissues.

As we age, there are negative consequences for the cells in our bodies as our DNA accumulates epigenetic “noise”. Excess amounts of DNA Methylation interrupts normal gene expression, and results in deterioration of cells and tissues. Cells can lose their identity or stop working. The patterns of gene expression that promote youthful toughness and strength aren’t read and translated as clearly anymore.
This makes it harder for tissues to regenerate or repair itself, which is why it’s so much harder for older people to “bounce back” from injuries.

Whether we can restore our Methylation completely to its previous state of youthful strength and restore tissue function and healing is still unknown.
The Fountain Of Youth is still a myth… but we’re not giving up the search – just redirecting our focus to look closer.

Retinal ganglion cells (RGCs) are brain neurons connected to our eyes. Together with Axons, they form the optic nerve. If damaged in youth, these specialized cells can recover from injury and regenerate. However, as we get older, they have a much harder time regenerating.

Many studies have taken place to identify precisely how RGCs survive or regenerate, and some success has been made but never enough to completely restore vision after optic nerve damage.

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Study & Findings

Human eyesight | Findings | Restore Eye Sight By Turning Back Epigenetic Clock

Lu et al. took a different approach in their study and looked at reverting RGCs to a younger ‘age.’ They tried turning the epigenetic clock far back enough for cells to regenerate on their own, after they’d already reached the point of aging where that function had stopped.

Mice were infected with adeno-associated viruses, which were engineered to induce an expression of transcription factors (Oct4, Sox2, and Klf4 – together called OSK) that can trigger an immature state in mature cells.

Their team was able to reprogram the targeted neurons so that those neurons reverted to a more youthful state.

The researchers looked at the mice’s ability to regenerate cells if axons were crushed. They found that the OSK expression triggered RGC regeneration and axon extension, all with no harmful repercussions after the alteration.
Essentially they could restore eyesight in mice.

The studies also tested whether vision could be restored in old mice even when areas of DNA methylation were removed. Using TET enzymes that catalyze the removal of DNA methylation, when reducing the enzyme production, the effects of OSK were blocked. Thus it seems the changes in DNA methylation are necessary for the effects of OSK.

Previous studies were predominantly done prior to optic nerve damage, but Lu et al. could compare the technique at different stages before and after axon injury. They were still able to improve RGC survival and regeneration.

The injury was not just limited to nerve damage. Vision loss from a mouse variant of glaucoma was also reversed in their study.

Additional research in human neurons in vitro showed that OSK expression also enhanced axon regrowth and cell survival.

Human subjects remain to be tested, but this does suggest that people with permanent optic nerve damage could be one step closer to restoring their eyesight. There’s also promising implications that this research could be used in other neuron-regeneration studies, potentially even treatments for other brain or spinal cord injuries.

Summary Points

  • In mice studies, axons that connect the eyes with brain neurons and form part of the optic nerve can recover from injury and regenerate.
  • Research in human neurons in vitro showed that OSK expression also enhanced axon regrowth and cell survival.
  • Changes in DNA methylation are necessary for the effects of OSK.
  • Human studies are needed, but people with permanent optic nerve damage could be one step closer to restored eyesight.

If you’re interested in learning more about epigenetics, visit the TruDiagnostic website or get more involved at the TruDiagnostic forum.

Please share your thoughts about methylation expression to restore eyesight with us in the comments section below.

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