As the largest resource of information specific to women's brain health, we are sure you will find what you are looking for, and promise that you will discover new information.
Published on: December 9, 2014
by Sarah Knapton for The Telegraph:
Alzheimer’s could be prevented and even cured by boosting the brain’s own immune response, scientists at Stanford University believe.
Researchers discovered that nerve cells die because cells which are supposed to clear the brain of bacteria, viruses and dangerous deposits, stop working.
These cells, called ‘microglia’ function well when people are young, but when they age, a single protein called EP2 stops them operating efficiently.
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.”
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.
Recent findings suggested the serotonin system may be an effective target for prevention and treatment of mild cognitive impairment. “Now that we have more evidence that serotonin is a chemical that appears affected early in...
By the time you start losing your memory, it’s almost too late. That’s because the damage to your brain associated with Alzheimer’s disease (AD) may already have been going on for as long as twenty years....
For decades, the only way to officially diagnose Alzheimer’s disease was by analysing a patient’s brain during a postmortem. More recently, physicians have been able to use positron emission tomography scans of the brains of living people...
The material presented through the Think Tank feature on this website is in no way intended to replace professional medical care or attention by a qualified practitioner. WBHI strongly advises all questioners and viewers using this feature with health problems to consult a qualified physician, especially before starting any treatment. The materials provided on this website cannot and should not be used as a basis for diagnosis or choice of treatment. The materials are not exhaustive and cannot always respect all the most recent research in all areas of medicine.