New Research From Stanford Claims to Have Found a Cure for Alzheimer’s Disease

Alzheimer’s disease is one of the primary causes of death in the United States.  An estimated 60,000 people die from the disease every year.   The risk of developing Alzheimer’s disease increases with age.  Researchers at Stanford University have recently claimed that they have found a way to prevent and even cure Alzheimer’s disease by boosting the immune response of the brain.

The researchers at Stanford discovered that the brain’s nerve cells die due to the cessation of cells that normally clear bacteria, harmful deposits, and viruses of the brain.  These cells are known as microglia and function optimally when people are young.  With age, however, a protein called EP2 prevents the microglia from functioning efficiently.

Amyloid-beta plaques in the brain deteriorate nerve cells and are primary contributors to Alzheimer’s disease. The researchers found that by blocking the protein EP2, microglia is able to function normally again, and can continue their job of sweeping up the harmful amyloid-beta plaques.

Studies used mice to show that a drug can block EP2 and reverse memory loss, as well as a variety of other Alzheimer’s-related issues.  According to Dr. Katrin Andreasson, who is a professor of neurology and neurological sciences at Stanford University School of Medicine, “Microglia are the brain’s beat cops…Our experiments show that keeping [the mice] on the right track counters memory loss and preserves healthy brain physiology.”

About 10 to 15% of the brain’s cells consist of microglial cells. They act as a primary defense, scouting for potentially harmful activities and materials. When microglial cells detect trouble, they release chemicals that attract other microglia to the affected area to destroy and clean out any foreign invaders.

Microglial cells also function as garbage collectors, eating dead cells and molecular debris that include anyloid-beta plaques.  These plaques play a huge role in Alzheimer’s disease, acting as gummy deposits and preventing the connections between neurons, leading to a decrease in memory ability and spatial awareness.

Dr. Andreasson notes, “The microglia are supposed to be, from the get-go, constantly clearing amyloid-beta, as well as keeping a lid on inflammation. If they lose their ability to function, things get out of control. Amyloid-beta builds up in the brain, inducing toxic inflammation.”

The researchers discovered that in young mice’ brains, microglia kept amyloid-beta plaques under control, but in the brains of older mice, the EP2 protein was activated to stop the microglia from secreting enzymes that digest the plaques.

In a like manner, mice that were genetically engineered to not possess EP2 protein did not develop Alzheimer’s disease, even after being injected with a solution of amyloid-beta.  This shows that their cells were clearing the protein away naturally.

For the mice that developed Alzheimer’s disease, the blocking of EP2 reversed memory impairment.

The Stanford researchers are now working to produce a compound that will only block EP2 to avoid unnecessary side effects.