Immune system retargeted to remove toxic protein

From the Summer 2016 edition of Care and cure magazine, injections of an immune system protein can trigger the fight against the signs of Alzheimer's disease in mice.

The role of the immune system in Alzheimer’s disease is receiving more attention as researchers try to reduce the harmful inflammation that creates stress and damage for brain cells. New results in mice suggest that an injection of the protein IL-33 can stop the immune system from creating inflammation and instead begin clearing away the toxic amyloid plaques that are a hallmark of Alzheimer's disease.

Inflammation is a natural response to damage or infection that helps the body to cope, however it can cause damage itself if it lasts for a long time. When the sticky amyloid plaques form in the brain, the immune system triggers inflammation which worsens the damage to the brain cells.

By injecting the protein IL-33 into mice with signs of Alzheimer's disease, researchers in Hong Kong were able to reduce the amount of inflammation and switch the immune system to a more targeted approach to clear the plaques.

The mice injected with the protein showed improvements in memory within a week, but it is not known what the long-term effects were.

Professor Eddy Liew, who led the work, cautioned, 'Exciting as it is, there is some distance between laboratory findings and clinical applications. 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.'

There are clinical trials ongoing that are testing drugs to reduce the level of inflammation in the brain, including the antibiotic minocycline and arthritis drug etanercept.

Dr James Pickett, Head of Research at Alzheimer's Society, said, 'We know that inflammation plays a key role in the development of dementia and some genetic studies have suggested a link between this protein and the development of Alzheimer's disease. 

'It's still early days for this line of research and we will need to see if similar mechanisms occur in people as in mice. 

'With an ageing population and no new dementia drugs in over a decade, the need to find treatments that can slow or stop the disease progression is greater than ever. There are already some clinical trials looking at inflammation – this latest finding adds to our understanding of why targeting inflammation may be a promising approach.'

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