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Is Our Immune System to blame for Alzheimer’s disease?

By Catherine William

alzheimers photoWith increasing amounts of evidence suggesting that our own immune system plays a large role in Alzheimer’s disease, Duke University has conducted a new study examining the issue. The study has been completed with the usage of mice, and has since been published in the Journal of Neuroscience.

The study implies that in Alzheimer’s disease, certain immune cells in the brain abnormally consume a vital nutrient named Arginine. The research team was able to come to a conclusion that by blocking this process with a small-molecule drug, it prevented the characteristic brain plaques and memory loss in a mouse model of the disease. The research has not only pointed to a new potential cause of Alzheimer’s, but a new treatment strategy.

“If indeed arginine consumption is so important to the disease process, maybe we could block it and reverse the disease,” said senior author Carol Colton, professor of neurology at the Duke University School of Medicine, and a member of the Duke Institute for Brain Sciences.

The brains of people with Alzheimer’s disease have two sections; “plaques” and “tangles.” Plaques are composed of sticky proteins called beta amyloid, and tangles are twisted strands of a protein called tau.

In the study, the scientists utilized a type of mouse, called CVN-AD, that they had created by switching out a number of important genes to make the animal’s immune system more similar to a human’s. Compared with other mice that were not injected with anything during the research, the CVN-AD mouse inherited plaques and tangles, behavior changes, and neuron loss. In addition, the gradual onset of these symptoms in the CVN-AD mouse gave researchers a chance to study its brain and to focus on how the disease forms.

The team found that most immune system components stayed the same in number, but a type of brain-resident immune cells named microglia that are known first responders to infection begin to divide and change early in the disease. The microglia express a molecule, CD11c, on their surface. The scientists found heightened expression of genes associated with suppression of the immune system. They also found dampened expression of genes that work to ramp up the immune system.

The group did find CD11c microglia and arginase, an enzyme that breaks down arginine, are highly expressed in regions of the brain involved in memory, in the same regions where neurons had died.

“It’s surprising, because [suppression of the immune system is] not what the field has been thinking is happening in [Alzheimer’s disease],” says Colton.

Instead, scientists have previously assumed that the brain releases molecules involved in ramping up the immune system, which supposedly damage the brain.

Blocking arginine using the small drug difluoromethylornithine (DFMO) before the start of symptoms in the mice, the team saw fewer CD11c microglia and plaques develop in their brains. These mice performed better on memory tests.

“All of this suggests to us that if you can block this local process of amino acid deprivation, then you can protect — the mouse, at least — from Alzheimer’s disease,” Colton says.

Several sources and medical journals as well as experts support the idea that the immune system, which guards our bodies from foreign invaders, plays a large role in Alzheimer’s disease.

But the exact role of immunity in the disease is still a mystery. Colton adds that “this study [is] opening doors to thinking about Alzheimer’s in a completely different way to break the stalemate of ideas in [Alzheimer’s].”

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