Has Stanford University found a cure for Alzheimer's disease?
These cells, called 'microglia' function well when people are young, but when they age, a single protein called EP2 stops them operating efficiently. (By Sarah Knapton, Science Editor) The Telegraph
Now scientists have shown that blocking the protein allows the microglia to function normally again so they can hoover up the dangerous sticky amyloid-beta plaques which damage nerve cells in Alzheimer's disease.
The researchers found that, in mice, blocking EP2 with a drug reversed memory loss and myriad other Alzheimer’s-like features in the animals.
“Microglia are the brain’s beat cops,” said Dr Katrin Andreasson, Professor of neurology and neurological sciences at Stanford University School of Medicine.
“Our experiments show that keeping them on the right track counters memory loss and preserves healthy brain physiology.”
By 2015 there will be 850,000 people with dementia in the UK, with Alzheimer's disease being the most common type. The disease kills at least 60,000 people each year.
Microglial cells make up around 10 to 15 per cent of cells in the brain. They act as a frontline defence, looking for suspicious activities and materials. When they spot trouble, they release substances that recruit other microglia to the scene which then destroy and get rid of any foreign invaders.
They also work as garbage collectors, chewing up dead cells and molecular debris strewn among living cells including clusters of amyloid-beta which aggregate as gummy deposits and break the connections between neurons, causing loss of memory and spatial awareness. These clusters are believed to play a substantial role in causing Alzheimer’s.
“The microglia are supposed to be, from the get-go, constantly clearing amyloid-beta, as well as keeping a lid on inflammation,” added Dr Andreasson. “If they lose their ability to function, things get out of control. A-beta builds up in the brain, inducing toxic inflammation.”
The scientists discovered that in young mice, the microglia kept the sticky plaques under control. But when experiments were done on older mice, the protein EP2 swung into action and stopped the microglia producing enzymes which digested the plaques.
Similarly mice which were genetically engineered not to have EP2 did not develop Alzheimer's disease, even when injected with a solution of amyloid-beta, suggesting that their cells were getting rid of the protein naturally.
And for those mice who developed Alzheimer's, blocking EP2 reversed memory decline.
Now Stanford is hoping to produce a compound which only blocks EP2 to prevent unnecessary side effects.
The study was published in the Journal of Clinical Investigation. (Article By Sarah Knapton, Science Editor) The Telegraph