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What’s Happening with Arginine and Alzheimer’s?

News June 26th, 2015

A new study from Duke University School of Medicine finds an integral part of the Alzheimer’s riddle. The amino acid, arginine, is being consumed by the brain’s immune system and is actually weakening our defenses. If “arginine consumption is so important to [the process of Alzheimer’s] disease… maybe we could block it and reverse the disease,” said Carol Colton, senior author of the study and professor of neurology.

If you understood that, great; if not, the rest is going to be in layman’s terms. Let’s start with microglia.

What is Microglia?

Microglia are essentially scavengers (like crabs or hyenas), but good for you. They eat up (or remove) all dead cells, bacteria, and viruses in the brain. Without them, our brains would literally swell and inflame – something our brains do as Alzheimer’s progresses due to the tangles and plaques that form.

What the Duke University study is showing is that, the immune system is failing because the microglia are consuming arginine.

What is Arginine?

Arginine is an amino acid that helps protect nerve cells from damage. Arginine increases blood flow from the brain to the body, helping with immune responses and keeping the gateways of communication open between cells.

Arginine and Alzheimer’s

According to Duke University’s findings, microglia are eating up arginine and this is why plaques and tangles are forming. In mice specifically engineered to mimic our human immune system, they found that by blocking the arginase before symptoms of Alzheimer’s occur, fewer plaques developed in fewer mice.

Now as with all Alzheimer’s research, take this with a grain of salt. After all, it’s unknown whether or not this will impact people who are already diagnosed with Alzheimer’s. Additionally, Colton (lead author of the study) cautions those who think eating arginine supplements will help. As it is, unless the arginase is blocked, it’ll simply devour the arginine.

Further Reading

What’s interesting with this study is that it shares some parallels to the Stanford study published earlier this year. Stanford found that a receptor protein inside the microglia (called EP2) was reacting adversely to Alzheimer’s hotspots in the brain, causing the microglia to inflame rather than suppress inflammation.

Both studies are linking the immune system to the reason behind Alzheimer’s, which does make sense. Both studies are also finding problems in the microglia, our brains’ defense system that makes up less than 15% of the brain cells. And both studies have found that if you block the EP2 protein and the arginase enzyme then you can promote healthier brain function.

Why are the microglia – defenders of the brain – causing such problems as we age? Consider Gregg Easterbrook’s article again, What Happens When We All Live to 100?, from The Atlantic, in which he compiles numerous resources and first-hand accounts on aging. He poses the question “why do some people develop heart disease while others with the same habits don’t?” and the potential answer is “aging is the prime cause of many chronic diseases,” or in other words, aging may be the disease and what we know as disease are merely symptoms.

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