By 2050, an estimated 15 million people will be diagnosed with Alzheimer’s disease…unless a cure is found. Stanford researchers have advanced the search for a cure considerably with their latest research. It turns out that that an Alzheimer’s cure might not be found in the nerve cells of the brain as experts have previously believed, but instead in preserving the immune-like cells that keep the brain functioning in tip-top shape.
Ten to fifteen percent of all brain cells are specialized cells called microglia. Microglia act as sentinels that seek out and destroy bacteria, viruses, and toxic debris that invade the brain. For example, microglia gobble up A-beta protein clusters that clump together and form Alzheimer’s plaques. Microglia also help keep inflammation subdued and produce nurturing substances that keep nerve cells healthy. However, as we age, microglia activity declines, leaving us vulnerable to memory loss and other degenerative symptoms.
According to Katrin Andreasson, MD, professor of neurology and neurological sciences and the study’s senior author, “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.”
What causes microglia function to cool down? A receptor protein called EP2. Stanford neuroscientists determined that by inhibiting EP2, microglia activity increased and resumed destroying nerve-damaging toxins. Subsequently, when EP2 decreased, the IQ of Alzheimer’s-infected mice increased.
The study—published online in The Journal of Clinical Investigation—was conducted on mice, not humans, so there’s a way to go before we can declare an Alzheimer’s cure, but the study definitely signals the potential for a specific immune-boosting drug that serves to block the EP2 receptor protein and diminish Alzheimer-related symptoms.