One of the great mysteries of medicine is why one person can reach the age of 100 and still have an incredibly sharp mind, be articulate, and have excellent memory, while another loses all of these faculties early in life. In my book, “Excitotoxins: The Taste That Kills,” I theorized that excitotoxicity was playing a major role in memory loss. I have since modified my hypothesis to include a process in which the immune system goes wild. I call the process immunoexcitotoxicity, which describes interplay between the brain’s immune system and excitotoxicity. The evidence supporting my hypothesis continues to mount as major pieces of the puzzle are discovered. It is now agreed that with Alzheimer’s dementia, the brain is chronically inflamed, as one sees intense microglial activation (activation of the brain’s main immune cell). These immune cells, the microglia, can assume several modes of behavior — some very beneficial and some quite destructive. The big question is: Why do the microglia get stuck in a destructive mode of activity? A series of new studies have found something that may have shed some light on this critical question. Researchers discovered that a special protein called TREM2 signals the microglia to remove harmful debris and to cool down inflammation — processes that protect and repair the brain. People with mutated TREM2 protein lose control of their microglia, so that these cells become stuck in a very destructive behavior. This mutation is much more common in people with Alzheimer’s disease. It may be the case that chronic inflammation explains why the gene becomes mutated in the first place. If so, following an anti-inflammatory diet and using anti-inflammatory supplements can help protect the brain against this process.
Ref: Russell Blaylock, MD