A relatively new study conducted at the Stanford University School of Medicine (led by Dr. Jenny Johansson) appears to have made a breakthrough in the fight to cure Alzheimer’s Disease.
Microglia and Alzheimers
When analyzing the brain, researchers discovered that roughly 15 percent of the cells in the brain are Microglia. Microglia are, as the study’s senior author, Katrin Andreasson puts it, “the brain’s beat cops.” They clean up dead cells, fight against bacteria and viruses, and put a lid on inflammation in the brain. Obviously, these are very important for keeping a healthy brain.
One of the reasons microglia became so important to monitor however was due to the fact that they clean up clusters of A-beta proteins as well. If you or someone close to you has suffered Alzheimers, then you’re probably already familiar with A-beta as clumps with others to form Alzheimers plaques and cause toxic inflammation. So, if the microglia are fighting against these plaques, then why aren’t they in Alzheimers patients?
Microglia and EP2
The interesting part is that the microglia don’t die off as we age, but are inhibited due to a “blocking receptor protein” within each microglial called EP2. They’ve noticed that when EP2 comes into contact with prostaglandin E2 or PGE2 (common locales for the effects of Alzheimers to take place), the microglia inflame rather than fight back.
Of course, the researchers found that EP2 is much more active and the microglia is thereby less effective in older people. In one of the experiments conducted on mice. The young mice had no problem sending the microglia to ward of inflammation, but the older mice suffered a lot more inflammation and the microglia were even slower at recruiting others (due to the EP2 protein).
So the hypothesis became, “What if we blocked the blocking EP2 protein in microglia? Would the microglia continue to fight the toxic inflammation and clear out the molecular clusters?”
The answer (as we currently know it with mice)? Yes.
The researchers removed the EP2 receptor protein from bioengineered mice and the result was a MASSIVE reduction in inflammation. They even introduced the A-beta protein in young and old mice and, sure enough, when the mice didn’t have the EP2 protein, the mice didn’t suffer the memory loss effects of Alzheimers.
In addition, the study found that aspirin (and other nonsteroidal anti-inflammatory drugs) can also block the EP2 protein. Although apparently this doesn’t help once Alzheimers has been diagnosed. That’s not saying take one aspirin a day, but – what I think they’re trying to say is – if over-the-counter medicines already exist to promote microglia function, then the cure can attainable; maybe even right around the corner.
The study was published on December 8th, 2014 and has been backed by the National Institutes of Health (NIH), the Alzheimer’s Association, Swedish Research Council and National Science Foundation.