SCIENTISTS have hailed a "potential breakthrough" in the treatment of Alzheimer's disease after a protein therapy was shown to completely reverse symptoms within a week during a trial on genetically-engineered mice.

The study, co-led by researchers at Glasgow University and the Hong Kong University of Science and Technology (HKUST), could lead to human clinical trials on Alzheimer's patients as early as next year, although the scientists behind the project warn that there is "a long distance" to go to turn the success in the mouse study into an effective treatment in humans.

The trial tested the effects of a protein called IL-33 on a strain of mice genetically-engineered to mimic the development of Alzheimer's disease in humans.

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The IL-33 protein occurs naturally in the human brain and spinal cord, but previous studies have shown that it exists in much lower concentrations in the brains of people suffering from Alzheimer's disease compared to healthy individuals.

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The study, published today [tue] in the PNAS scientific journal, demonstrates that mice given injections of this protein via their stomach lining restored their memory and cognitive functions back to the level of a healthy mouse of the same age within one week.

The scientists believe that IL-33 works by mobilising immune cells in the brain to destroy amyloid plaque deposits - one of the markers of Alzheimer's disease. The IL-33 protein triggers the production of an enzyme known as neprilysin in the brain's immune cells, which breaks down the harmful amyloid deposits.

Previous research has shown that the progression of Alzheimer's disease is characterised by the build up of amyloid plaques and neurofibrillary tangles in the brain which gradually erode the connections between nerve cells, eventually leading to nerve cell death and loss of brain tissue.

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The findings of the new Glasgow-Hong Kong research suggest that IL-33 may hold the key to a drug which could reverse the progress of Alzheimer's disease in humans.

Professor Eddy Liew, an expert in immunology at Glasgow University who co-directed of the study, said he was "cautiously optimistic" about the prospects for a protein-based treatment in the future.

Prof Liew said: "On the one hand I think it's very exciting, but on the other hand, intellectually, as a scientist, I know that there is a long distance between a mouse and a human, but we can hope.

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"It is such a desperate disease and, at the moment, there is no treatment at all."

Prof Liew said that patients may be able to self-administer injections of IL-33, as diabetics do with insulin, to first reverse the symptoms and then prevent them returning.

He said he expected the treatment would be most effective for patients in the relatively early stages of the disease "before the brain has disintegrated".

Alzheimer’s disease is the most common form of dementia, accounting for around half of all cases. In Scotland, there are around 45,000 people living with Alzheimer's disease, but this has been forecast to increase more than tenfold over the next 40 years as the population ages.

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The first step towards a potential treatment will be Phase One clinical trials later this year on healthy human volunteers, to establish the safe threshold for IL-33 doses.

If successful, this will pave the way to Phase Two clinical trials in 2017 when the therapy can be tested for the first time on around 50-100 Alzheimer's patients.

“Exciting as it is, there is some distance between laboratory findings and clinical applications," said Prof Liew. "There have been enough false ‘breakthroughs’ in the medical field to caution us not to hold our breath until rigorous clinical trials have been done.

"We are just about entering Phase One clinical trial to test the toxicity of IL-33 at the doses used. Nevertheless, this is a good start.”

Jim Pearson, director of policy & research for charity Alzheimer Scotland, said: "While the initial findings may be promising, this is still the very early phase of the research and we look forward to hearing more from the clinical trials."