Science Illustrated

THE END OF BLINDNESS

Amazing new technologi­es and therapies are slowly winning the war against blindness. From artificial retinas to full eye transplant­s!

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Moreover, a person is officially blind, if the light sensitivit­y of his eyes is limited, i.e. it takes very powerful light to be able to see anything, or if he cannot distinguis­h between contrasts and grey tones, causing the field of vision to lose its contours.

Cataract causes about half of all cases of blindness in the world, although the disease can easily be cured by replacing the lens of the eye. Other common eye diseases affect the retina, and so far, doctors have not been able to treat those. That is true for age-related macular degenerati­on (AMD) and diabetic retinopath­y, which are responsibl­e for 13+ % of all cases of blindness. Hereditary diseases such as retinitis pigmentosa can also make the light-sensitive cells of the retina die. These patients with damaged retinas can now get some of their vision back with the Alpha AMS chip.

Chip uses healthy cells

The implant is a developmen­t of another electronic retina called Argus II, which was introduced in 2011. The predecesso­r functioned by a video camera mounted on a pair of glasses recording the surroundin­gs and sending the data to the electronic retina and from there onto the brain.

Alpha AMS has no camera and only uses the eye’s own lens to activate the electronic retina. Moreover, the chip has a much higher resolution of 1,600 pixels – i.e. the points that make up the image – as compared to only 60 pixels in Argus II, providing the blind person with a much more detailed image of the world. And as the crowning touch, the chip uses the nerve cell layers which still function.

The retina consists of three layers with different types of nerve cells. The backmost layer, which is the furthest away from the light, includes the light-sensitive cells known as rods and cones, and this is the layer into which the chip is implanted. When the light strikes the light-sensitive cells, they send signals to the central layer, in which they are processed by another type of nerve cells, that compare signals from light-sensitive cells nearby to each other to find contrasts and draw contours. A major part of the visual impression is produced in this layer. Only the most important data (or approximat­ely 0.06 %) are passed on to the brain via cells in the front layer of the retina.

In many blind people with damaged retinas, the cell layers responsibl­e for the processing of the light signals remain intact. The Alpha AMS chip uses the functional cells to process the signals from its light-sensitive pixels, before they are sent on to the optic nerve, just like with the signals from the retina’s own rods and cones, markedly improving the image quality. Stem cells repair the retina Though the Alpha AMS is sophistica­ted, it is still primitive as compared to the real retina. So, scientists have long been trying to transplant a piece of the retina of a deceased donor to the eye of a person who has become blind as a result of damage to his retina, but so far, the effort has been in vain.

The main problem is that the retina consists of 125 million nerve cells linked in

many ways and uniting into one million nerve links that make up the optic nerve. The many nerve links from the donor’s retina must be joined with the receiver’s optic nerve, which is an impossible task for surgeons.

So, doctors try to cure defective retinas by means of an alternativ­e strategy. Instead of transplant­ing a piece of retina from a donor, they inject stem cells into the eye, making them reconstruc­t the damaged retina from scratch. Stem cells have a unique ability to divide and develop into other specialise­d cell types, depending on what the body needs. When the stem cells enter the eye, they develop into the retina’s light-sensitive rods and cones, which develop links to the nerve cells in the retina’s two other layers.

In 2012, the method was tested for the first time on two patients who were blind due to the AMD disease, which breaks down the retina’s sharpest point, the macula. Steven Schwartz from the University of California, Los Angeles, grew embryonic stem cells in the lab under specific conditions that made them develop into the light- sensitive cells of the retina. Subsequent­ly, they were injected behind the retinas of the two patients, whose vision improved markedly during the following weeks.

Before the treatment, one patient could only just sense the motion of a hand in front of her eyes, but when the stem cells had had time to develop for one week in the eye, she could count the fingers of the hand, and after a month, she could read large letters. The stem cell therapy had enabled the blind person to see something in a few weeks.

In 2017, scientists from the RIKEN Centre for Developmen­tal Biology in Kobe, Japan, developed the method, so the stem cells can be extracted from the blind person’s skin cells and used to grow a new piece of retina.

Another promising way of curing blindness is gene therapy. The method can be used, when the blindness is due to one single gene. The defective gene is replaced by a healthy one, which is entered into the cells of the eye by means of a virus. In 2017, eye specialist Stephen Russell from the US University of Iowa published the results of a gene therapy experiment involving 20 people with a congenital error of the RPE65 gene, which makes the light-sensitive cells of the retina perish. The experiment caused such a marked improvemen­t of the participan­ts’ vision that the US health authoritie­s, FDA, approved the new treatment in December 2017, so it can now be offered to all blind Americans with defects of this particular gene.

The entire eyeball transplant­ed

Although scientists have developed an entire arsenal of electronic and biological treatments for different types of blindness, there are still many blind people who do not benefit from existing options, such as the victims of accidents that cause major physical damage to the eye or patients with glaucoma, which destroys the optical nerve. Their only way of getting their vision back is to have a new eye from a deceased donor.

Doctors already use transplant­s from donors to treat damage to the cornea, which is located on top of the pupil as the external part of the eye. The efficient surgery is carried out 100,000 times a year, meaning that almost as many corneas are transplant­ed as all other organs combined.

However, the leap to transplant­ing the entire eye is a huge one. Surgeon Kia Washington from the US University of Pittsburgh has transplant­ed eyes of research animals, and according to her, it is still impossible to transplant only the eyeball. Doctors have to include the optic nerve all the way in between the two cerebral hemisphere­s to the place in which the right and left eyes’ optical nerves cross. So, the patient needs to have a major part of his face replaced, including one eye and ear plus part of the skull.

The bold surgeon has carried out the complex surgery on 22 rats, of which 15 survived. One of the rats even kept itself and the new eye alive for two years, but studies showed that no electric nerve signals flowed from the retina through the optic nerve.

Kia Washington is, however, confident, and her research is supported by the US Ministry of Defence, which hopes that transplant­s of entire eyes can save the vision of many soldiers who have been in accidents or explosions. According to the scientist, the first transplant of an entire eye can be carried out in a matter of 10 years. By then, most blind people would probably be able to see something due to electronic implants, gene therapy, stem cells, or transplant­s.

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 ??  ?? The donor eye's optic 1 nerve must be linked with the receiver's ownoptic nerve in order for the brain to receive visual impression­s from the eye. That is extremely difficult, as the optic nerve is a bundle made up of 1+ million individual nerves.The donor eye's blood 2 vessels must be joined with the receiver'sblood circulatio­n in order for the eye to be supplied with oxygen and nutrients. In animal experiment­s, donor eyes normally only survive for a few weeks, but the blood vessels might join, if the eye survives longer.3 The donor eye'smuscles must be linked with the receiver'snervous system, allowing the eye to move. The problem should be solvable, when the eye survives long enough for the nerve links to establish themselves.
The donor eye's optic 1 nerve must be linked with the receiver's ownoptic nerve in order for the brain to receive visual impression­s from the eye. That is extremely difficult, as the optic nerve is a bundle made up of 1+ million individual nerves.The donor eye's blood 2 vessels must be joined with the receiver'sblood circulatio­n in order for the eye to be supplied with oxygen and nutrients. In animal experiment­s, donor eyes normally only survive for a few weeks, but the blood vessels might join, if the eye survives longer.3 The donor eye'smuscles must be linked with the receiver'snervous system, allowing the eye to move. The problem should be solvable, when the eye survives long enough for the nerve links to establish themselves.
 ??  ?? Today, an eye can only be transplant­ed along with half a face. So far, the surgery has only been carried out on animals.
Today, an eye can only be transplant­ed along with half a face. So far, the surgery has only been carried out on animals.
 ?? PHILIPPE PSAILA/SPL ?? The Argus II glasses provide blind people with primitive vision by means of a camera and a retina chip. CAMERA INDUCTION COIL ANTENNA
PHILIPPE PSAILA/SPL The Argus II glasses provide blind people with primitive vision by means of a camera and a retina chip. CAMERA INDUCTION COIL ANTENNA

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