Alzheimer's May Be Linked To Arginine Deprivation, But Supplements Won't Help

Alzheimer's
Immune cells in the brain may be abnormally consuming the nutrient arginine, and this may be a cause of Alzheimer's disease: new study. Photo courtesy of Shutterstock.

Within the brains of Alzheimer's patients, plaques and tangles of proteins accumulate and generally clog the neuronal flow. Now, a new Duke University study has an original and unusual take on this well-known problem. Certain immune cells may be abnormally consuming the nutrient arginine, the researchers propose, since the characteristic brain plaques and resulting memory loss did not occur when this process was blocked.

“We see this study opening the doors to thinking about Alzheimer's in a completely different way, to break the stalemate of ideas,” Dr. Carol Colton, senior author and professor of neurology at the Duke University School of Medicine, stated in a press release.

L-arginine is an amino acid, a chemical building block necessary for the body to make proteins, commonly obtained from food. It’s found in red meat, poultry, fish, and dairy products. Now, before we go any further, let’s answer the question you are doubtlessly asking: Does this study mean anyone living in fear of Alzheimer’s needs to eat more arginine-rich foods or pop a supplement or two?

No. Unforunately, eating more arginine would not enrich the brain, since much of the nutrient would be blocked by the blood brain barrier and never make it to the regions of the brain that need it.

First, A Little Genetic Engineering

For the study, the scientists used a mouse model that they had genetically engineered several years ago. The immune system of the CVN-AD mouse is more similar to a human's plus its brain contains plaques and tangles and neuron loss (resulting in rodent memory loss) similar to an Alzheimer’s patient. Most importantly, the scientists engineered the CVN-AD mouse so that there is a gradual onset of symptoms, allowing researchers time to study its brain and see how the disease begins.

Observing the lifespan of a group of these CVN-AD mice, the research team found that most immune system components remained the same in number, while one type of brain immune cells, the microglia, began to divide and change early in the disease. Notably, microglia are known to be first responders to infection.

Analyzing patterns of activity in the brains of the mice, the scientists discovered increased expression of genes linked to suppression of the immune system. At the same time, they found less expression of genes that ramp up the immune system. (Commonly, most researchers assume Alzheimer’s is an inflammatory disease, where too much immune activity is taking place.)

The group also found both microglia and arginase, an enzyme that breaks down arginine, to be highly expressed in regions of the brain involved in memory. Experimentally, they used the drug difluoromethylornithine (DFMO) to block arginase before symptoms of Alzheimer’s began in the mice.

Not only did fewer plaques develop, but the mice performed better on memory tests. Now, the research group has begun to investigate DFMO, a cancer drug which has not yet been approved by the Food and Drug Administration, to see if it can cure or modify features of Alzheimer's after they appear.

Source: Kan MJ, Lee JE, Wilson JG, et al. Arginine Deprivation and Immune Suppression in a Mouse Model of Alzheimer’s Disease. The Journal of Neuroscience. 2015.

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