Scientists have fresh hopes for an Alzheimer’s treatment after experiments to reduce inflammation in diseased mice brains prevented memory and behavioural problems in the animals.
The study, at the University of Southampton, adds weight to evidence that inflammation in the brain is what drives the disease.
Researchers used post-mortem brain tissue samples to show that the numbers of an immune cell, called microglia, increase in the brains of people with Alzheimer’s disease relative to healthy brains.
Using mice that develop features of Alzheimer’s disease, the researchers blocked the production of microglia in the brain and were able to reduce the development of memory problems.
This was done in an attempt to find out whether blocking the receptor responsible for regulating microglia – CSF1R – could improve cognitive skills.
Dr Doug Brown, Director of Research at Alzheimer’s Society, said: “We know brain inflammation occurs in Alzheimer’s disease, but researchers are still working out what impact this has on the progression of the disease.
“This study shows that the production of new immune cells in the Alzheimer’s brain contributes to the development of memory impairments – and that by blocking this immune reaction memory loss can be reduced.”
Dr Diego Gomez-Nicola, lead study author from the university, said: “These findings are as close to evidence as we can get to show that this particular pathway is active in the development of Alzheimer’s disease.
“The next step is to work closely with our partners in industry to find a safe and suitable drug that can be tested to see if it works in humans.”
Dr Simon Ridley, director of research at Alzheimer’s Research UK, said: “Research like this is vital as there are currently no treatments that can stop or slow the progression of Alzheimer’s in the brain.
“We desperately need to see greater investment in research, if we are to find new ways to help the tens of thousands of people who develop Alzheimer’s in this country every year.”
The study was published in the journal Brain.