An immune system protein could offer a potential new target for Alzheimer’s disease treatments, according to research published today.
Findings from the research, carried out by scientists at the University of Glasgow and the Hong Kong University of Science and Technology, suggest that an immune system protein could help to reverse some of the physical and cognitive changes seen in Alzheimer’s disease.
The research, published in Proceedings of the National Academy of Sciences (PNAS), showed that the protein IL-33 reduced the amount of amyloid in the brains of mice that showed symptoms similar to Alzheimer’s. Improvements in memory were also recorded in the mice.
IL-33 is a protein that acts as a chemical signal for immune cells and the scientists found that it appears to work by activating immune cells to find and destroy amyloid plaques, the clumps of sticky protein that cause damage in the brains of people with Alzheimer’s disease.
Some genetic studies have suggested a link between this protein and the development of Alzheimer’s. Inflammation is also known to play a key role in the development of dementia.
Dr James Pickett, Head of Research at Alzheimer’s Society, said: “The researchers have shown that the protein can lead to short-term improvements in memory and reductions in the amount of amyloid in the brains of mice with symptoms similar to Alzheimer’s disease. They suggest that the protein can switch the function of the immune cells in the brain.
Instead of causing harmful inflammation, the immune cells seek out and destroy the toxic amyloid plaques caused by 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.”
Dr Pickett went on to say that clinical trials that target inflammation “may be a promising approach” in the race to find new treatments that can slow or halt Alzheimer’s disease progression.