Saturday, January 10, 2015

Has Stanford Found a Cure for Alzheimer’s?

It is with optimistic caution that I share the latest good news regarding Alzheimer’s research from Stanford University. They may have found the elusive and overdue cure for Alzheimer’s disease. Over the past fifteen years, I’ve heard exciting news about Alzheimer’s research that fizzled out after sailing through preliminary testing.

Is the Stanford University research going to be exception to past experience? I hope so!

I’ve always heard that you can’t keep doing the same thing and expect a different outcome. That is one reason that grants are often awarded to researchers who try a new approach to the same problem:  What causes Alzheimer’s and how can it be cured?

The hallmarks of Alzheimer’s disease are deposits of beta-amyloid plaques between nerve cells and tangles of the protein tau that build up inside cells. Aging is the number one risk factor for developing the disease, but it is not a normal part of aging.

Alzheimer’s is a destructive and always fatal brain disease, currently the sixth leading cause of death in the United States. Alzheimer’s relentlessly progresses from mild symptoms to the final stages requiring constant care. People with the disease live an average of eight years, but some live twenty years or longer.

Stanford’s approach is to boost the brains’ own immune response to prevent and cure Alzheimer’s. Researchers at Stanford University School of Medicine discovered that by blocking the protein EP2, microglia cells will continue to cleanse the brain of dangerous beta-amyloid deposits.

“The microglia are supposed to be, from the get-go, constantly clearing amyloid-beta, as well as keeping a lid on inflammation,” Dr. Katrin Andreasson, professor of neurology and neurological sciences at Stanford, said.

Microglia cells are your own personal defense system. Their function is to search and destroy dead cells and other debris in the brain such as the gummy deposits Alzheimer’s disease leaves in the wake of its destructive path.

Experiments on mice have been encouraging. Microglia goes about its business of protecting the brains of young mice. In older mice, the presence of EP2 proteins stopped the microglia cells from doing their job of destroying the dead cells. Another group of mice were genetically engineered to never develop EP2, and even when injected with beta-amyloid did not develop Alzheimer’s. Even more exciting news for people with Alzheimer’s—blocking EP2 in older mice reversed the memory loss!

Of course, a great distance separates animal testing and drug development. Stanford has hopes of developing a drug to block EP2. They believe a compound that only blocks EP2 would not have unnecessary side effects.

Have researchers finally found the key to unlock the mystery of Alzheimer’s disease? Time will tell if the Stanford study is the long-awaited breakthrough and the end of Alzheimer’s.

Copyright © January 2015 by L.S. Fisher
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