A NYU medical research team has uncovered a mechanism hat instigates inflammation Alzheimer’s atherosclerosis and type-2 diabetes. Published in Nature Immunology, the findings suggest that there is a shared biochemical thread between the two diseases and that new methods of therapy could successfully manage the chronic inflammation in these diseases without damaging the body’s immune system.
Normally, when the human body encounters a pathogen, it responds with a burst of chemicals called cytokines, which attract immune cells to the infection, which leads to inflammation. The amyloid plaques that form within the brain and lead to Alzheimer’s as well as crystalline cholesterol that is often affiliated with vascular diseases also cause inflammation, however the mechanism of inflammation in these cases is unclear. Scientists previously believed that these plaques and crystals would accumulate outside cells and macrophages then induce inflammation in an attempt to clear the cell walls.
"We've discovered that the mechanism causing chronic inflammation in these diseases is actually very different," stated Dr. Kathryn Moore, NYU professor and study author.
The research team discovered that this matter does not actually exist outside the cells as previously thought. Rather, a receptor known as CD36 that exists on macrophages actually attracts the soluble forms of the lingering particles inside the cell, where they are then transformed into matter that triggers the inflammation.
Dr. Moore comments, "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 and amyloid damage the macrophage and trigger a powerful cytokine, called interleukin-1B, linked to a chronic inflammatory response."
This discovery has exciting implications clinically and in general for Alzheimer's support. When the team successfully blocked the CD36 receptor in mice with atherosclerosis, the cytokine reaction failed, because of this significantly fewer crystals formed into plaques and naturally, inflammation diminished.
"Our findings identify CD36 as a central regulator of the immune response in these conditions and suggest that blocking CD36 might be a common therapeutic option for all three diseases," stated Dr. Moore.