Millions blinded by conditions such as glaucoma will one day be able to see again as scientists discover a way to regenerate a damaged optic nerves.

Hope for  Glaucoma suffers

Hope for Glaucoma suffers

Researchers found a therapy named high contrast visual stimulation which involves making sufferers stare at changing patterns of black lines actualy helped the nerve cells grow back.

This combined with gene therapy,which increased the amount of a protein known to promote optic nerve regeneration triggered an even greater improvement in sight.

The National Institutes of Health's National Eye Institute, President which carried out the study was quoted as saying: 'Reconnecting neurons in the visual system is one of the biggest challenges to developing regenerative therapies for blinding eye diseases like glaucoma.

'This research shows that mammals have a greater capacity for central nervous system regeneration than previously known.'

The optic nerve is the data cable for the eye, carrying visual information from the light-sensing cells in the retina in the back of the eye, tthen onto the brain.

Like a bundle of computer wires, it consists of around a million of a type of nerve cells called ganglion.

Each ganglion has an axon - a long, thread-like protrusion extending out of it, along which impulses are conducted from ganglion to ganglion.

A variety of diseases or damage to the optic nerve, such as glaucoma, cause vision loss and blindness when they destroy or damage these axons.

In adults, the axons in the cells in the retina fail to regrow on their own, which is why vision loss from diseases of the optic nerve is usually permanent.

As part of the study, researchers took mice and crushed the optic nerve in one of their eyes using forceps.

The rodents were then placed in a chamber several hours a day for three weeks where they viewed high-contrast images - essentially changing patterns of black lines.

Compared to mice that did not receive the high-contrast visual stimulation, the mice that did had 'significant' re-growth of the axons in their retinas, researchers said.

Prior studies by scientists showed that increasing activity of protein called mTOR could also promote optic nerve regeneration and by combining visual stimulation with increased mTOR activity might have an even greater effect.

Two weeks prior to crushing the mice's optic nerves nerve crush, the scientists used gene therapy to cause the ganglion cells in the retina to overexpress mTOR.

After the optic nerves were crushed, these mice were given high-contrast visual stimulation daily.

After three weeks, the scientists saw more extensive regeneration of their axons - growing around 6mm, they reported

They carried out gene therapy on more mice to overexpress mTOR even more, and up'd the high-contrast visual stimulation by sewing their other working eye shut. This caused axons along the entire optic nerve and into the various visual centres of the brain grew back.

In three weeks, the axons grew as much as 12 millimetres, a rate about 500 times faster than untreated axons.

Lead author Dr Andrew Huberman, associate professor at Stanford University School of Medicine, said: 'We saw the most remarkable growth when we closed the good eye, forcing the mice to look through the injured eye.

The animals's sight was partially restored after they received the treatment, he concluded.

'This study's striking finding that activity promotes nerve regrowth holds great promise for therapies aimed at degenerative retinal diseases,' said Thomas Greenwell, National Eye Institute program director.

Dr Dolores M Conroy, Director of Research at the UK's main eye research charity Fight for Sight said: 'The potential to regenerate retinal ganglion cell axons that make the correct brain connections is a fantastic breakthrough in the fight to restore sight lost due to glaucoma and other optic nerve conditions.

'Fight for Sight's research programme in glaucoma includes understanding how the brain reorganises itself in humans with the condition and strategies to protect the nerve cells from damage.'

The research was published online in Nature Neuroscience.

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