Niacin interacts with a highly-selective receptor, HCAR2, present in immune cells physically associated with amyloid plaques
US-based Indiana University School of Medicine researchers found that niacin or vitamin B3 limits Alzheimer’s disease progression when used in models in the lab, a discovery that could potentially pave the way toward therapeutic approaches to the disease.
The study, recently published in Science Translational Medicine, investigates how niacin modulates microglia response to amyloid plaques in an Alzheimer’s disease animal model.
Niacin, which sustains metabolism throughout the body, is mainly obtained through a typical diet; it also can be taken in supplements and cholesterol-lowering drugs. The brain, however, uses niacin differently.
In the brain, niacin interacts with a highly-selective receptor, HCAR2, present in immune cells physically associated with amyloid plaques. When niacin—used in this project as the FDA-approved Niaspan drug—activates the receptor, it stimulates beneficial actions from these immune cells, said the researchers.
Past epidemiology studies of niacin and Alzheimer’s disease showed that people who had higher levels of niacin in their diet had diminished risk of the disease. Niacin is also currently being used in clinical trials in Parkinson’s disease and glioblastoma.