The memory loss and progressive dementia caused by Alzheimer's disease can be halted by drugs that curb inflammation in the brain, according to a new approach to treating the most common form of dementia.
The study points out that inflammation in the brain can drive the development of the disease and suggests that by reducing this inflammation, the growth of the disease can be curtailed.
Dr Diego Gomez-Nicola, lead study author, 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. In addition, the activity of the molecules regulating the numbers of microglia correlated with the severity of the disease.
The researchers then studied these same immune cells in mice that had been bred to develop features of Alzheimer's. They found that Alzheimer's brains had more immune cells, known as microglia, than healthy brains.
Diagram of the brain of a person with Alzheimer's Disease.
"With an ageing population and no new dementia drugs in over a decade, the need to find treatments that can slow or stop disease progression is greater than ever", said Doug Brown, director of research at the Alzheimer's Society. They wanted to find out whether blocking the receptor responsible for regulating microglia, known as CSF1R, could improve cognitive skills.
"The next step is to work closely with our partners in the industry to find a safe and suitable drug that can be tested to see if it works in humans".
"Excitingly, it does however highlight new avenues for researchers to exploit and strengthens the case for targeting other cell types within the brain in the fight against Alzheimer's", he added.
In the study, mice which were given a drug to block a receptor - called CSF1R - responsible for the rise in microglia in their brains, had fewer memory and behavioural problems.
Another important finding was that the inhibitor did not reduce microglia levels below the number needed for healthy immune function, suggesting blocking CSF1R only eliminates excessive numbers of cells. The treatment did not, however, stop the build up of characteristic amyloid plaques in the animals' brains.
He added: "While this basic science research provides strong evidence, the challenge will now be to develop medicines for people with dementia, so we await the development of clinical treatments with interest". The researchers say this supports evidence from other studies that suggest several factors may be involved in disease progression.
Alzheimer's treatment closer as brain inflammation shown to be key
