Newly published research from Stanford University could help steer treatment of a disease that affects 36 million people worldwide: Alzheimer’s disease.
According to the Telegraph, Stanford University researchers have discovered the cause of dying nerve cells in the brain, particularly from Alzheimer’s disease. Cells that are designated to clean up harmful bacteria, viruses, and damaging deposits stop working, which results in the Alzheimer’s symptom of brain deterioration. These clean-up cells are called “microglia” and they make up about 10 to 15 percent of all brain cells. These essential cells do their job efficiently in the brains of young people; but as humans age, a protein called EP2 can stop the microglia from functioning. This can lead to Alzheimer’s disease, a neurodegenerative ailment that causes devastating memory loss and eventually death.
The treatment for Alzheimer’s disease is simple in concept. Block the EP2 protein that inhibits the microglia. If the protein no longer keeps the microglia from functioning, it can go about its business cleaning up nerve-damaging pathogens like amyloid-beta plaques. Stanford researchers realized the concept by developing an Alzheimer’s drug to block the protein, which they then tested on mice with Alzheimer’s symptoms. The drug effectively reversed memory loss in the rodents and other harmful effects of Alzheimer’s.
The study regarding this possible cure for Alzheimer’s disease was published online in The Journal of Clinical Investigation, according to Stanford Medicine. In the study, researchers emphasized the necessity of keeping microglia fully functioning to either reduce the chances of Alzheimer’s disease or possibly cure Alzheimer’s patients.
“Microglia are the brain’s beat cops,” said the study’s senior author, Katrin Andreasson, MD, a professor of neurology and neurological science.
“Our experiments show that keeping them on the right track counters memory loss and preserves healthy brain physiology… The microglia are supposed to be, from the get-go, constantly clearing A-beta, as well as keeping a lid on inflammation. If they lose their ability to function, things get out of control. A-beta builds up in the brain, inducing toxic inflammation.”
Tests conducted for the Alzheimer’s study included measuring the ability of mice to remember where food is located in a maze and how quickly a mouse forgets objects that it has previously encountered. The mice selected were genetically predisposed to get a disease very similar to Alzheimer’s disease among mice. Control group mice with normally functioning brains and no Alzheimer’s-like symptoms were also tested. Both groups of mice were given the EP2-blocking drug and a placebo control solution. Both groups of mice experienced reliable memory whenever their microglial cells were functioning as they should–without the EP2 protein interfering–effectively reversing the damage of Alzheimer’s disease.
Although the research is just beginning, this could be great news for Alzheimer’s disease patients and the families of those suffering from Alzheimer’s. Others may not be as optimistic that a cure for Alzheimer’s disease is, indeed, on the horizon. But any step towards an Alzheimer’s cure is progress.
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