Researchers at NYU Langone Medical Center have discovered a mechanism that triggers chronic inflammation in Alzheimer's, atherosclerosis and type-2 diabetes. The results, published today in Nature Immunology, suggest a common biochemical thread to multiple diseases and point the way to a new class of therapies that could treat chronic inflammation in these non-infectious diseases without crippling the immune system. Alzheimer's, atherosclerosis and type-2 diabetesdiseases associated with aging and inflammationaffect more than 100 million Americans.
When the body encounters a pathogen, it unleashes a rush of chemicals known as cytokines that draws immune cells to the site of infection and causes inflammation. Particulate matter in the body, such as the cholesterol crystals associated with vascular disease and the amyloid plaques that form in the brain in Alzheimer's disease, can also cause inflammation but the exact mechanism of action remains unclear. Researchers previously thought that these crystals and plaques accumulate outside of cells, and that macrophagesimmune cells that scavenge debris in the bodyinduce inflammation as they attempt to clear them.
"We've discovered that the mechanism causing chronic inflammation in these diseases is actually very different," says Kathryn J. Moore, PhD, senior author of the study and associate professor of medicine and cell biology, Leon H. Charney Division of Cardiology at NYU Langone Medical Center.
The researchers found that particulate matter does not linger on the outside of cells. Instead, a receptor called CD36 present on macrophages draws the soluble forms of these particles inside the cell where they are transformed into substances that trigger an inflammatory response. Says Dr. Moore, "What we found is that CD36 binds soluble cholesterol and protein matter associated with these diseases, pulls them inside the cell, and then transforms them. The resulting insoluble crystals an
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NYU Langone Medical Center / New York University School of Medicine