Breakthrough treatment for AMD blindness trialled - A new treatment for the most common form of blindness in Britain has been developed by scientists.
Researchers discovered that sufferers of AMD (dry age related macular degeneration) have a lack of protective enzyme in the eye that could be why it leads to reduction in eye sight.
Drugs that boost this chemical in the eye are to be tested on patients within a year, it was reported in the journal Nature.
More than 500,000 people in Britain suffer from AMD which is caused by the deterioration and death of the cells in the macula, a part of the retina used to see straight ahead.
The disease robs sufferers of their sight by creating a black spot in the centre of their vision which slowly gets bigger.
With numbers of AMD sufferers expected to treble in the next 25 years as the population ages, there is an urgent need for a breakthrough.
Scientists at the University of Kentucky found the activity of the enzyme called DICER1 was dramatically reduced in the retina of human donor eyes with the condition.
Laboratory experiments on mice also showed this reduced expression was associated with a build-up of a poisonous molecule called Alu RNA that kills cells in the retina.
Dr Jayakrishna Ambati, of the University of Kentucky, and colleagues found DICER1 can shield the retina against the destructive effects of Alu RNA.
"When the levels of Dicer decline, the control system is short-circuited and too much Alu RNA accumulates.
"This leads to death of the retina."
In developed countries it is estimated that one in fifty people over fifty years of age, and up to one in five people over the age of 85, have AMD.
Currently, there is no reliably proven medical treatment for dry AMD. But not smoking and eating a healthy diet may help to slow the rate of deterioration.
Dr Ambati has created two treatments that could potentially halt the march of the disease. One works by boosting levels of Dicer, the other breaks down the toxic Alu RNA
The University of Kentucky has applied to patent the techniques and the first trials on people could start by the end of this year. ( telegraph.co.uk )
Researchers discovered that sufferers of AMD (dry age related macular degeneration) have a lack of protective enzyme in the eye that could be why it leads to reduction in eye sight.
Drugs that boost this chemical in the eye are to be tested on patients within a year, it was reported in the journal Nature.
More than 500,000 people in Britain suffer from AMD which is caused by the deterioration and death of the cells in the macula, a part of the retina used to see straight ahead.
The disease robs sufferers of their sight by creating a black spot in the centre of their vision which slowly gets bigger.
With numbers of AMD sufferers expected to treble in the next 25 years as the population ages, there is an urgent need for a breakthrough.
Scientists at the University of Kentucky found the activity of the enzyme called DICER1 was dramatically reduced in the retina of human donor eyes with the condition.
Laboratory experiments on mice also showed this reduced expression was associated with a build-up of a poisonous molecule called Alu RNA that kills cells in the retina.
Dr Jayakrishna Ambati, of the University of Kentucky, and colleagues found DICER1 can shield the retina against the destructive effects of Alu RNA.
"When the levels of Dicer decline, the control system is short-circuited and too much Alu RNA accumulates.
"This leads to death of the retina."
In developed countries it is estimated that one in fifty people over fifty years of age, and up to one in five people over the age of 85, have AMD.
Currently, there is no reliably proven medical treatment for dry AMD. But not smoking and eating a healthy diet may help to slow the rate of deterioration.
Dr Ambati has created two treatments that could potentially halt the march of the disease. One works by boosting levels of Dicer, the other breaks down the toxic Alu RNA
The University of Kentucky has applied to patent the techniques and the first trials on people could start by the end of this year. ( telegraph.co.uk )
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