The study, recently published in Science Translational Medicine, investigates how niacin modulates microglia response to amyloid plaques in an Alzheimer's disease animal model.
The study’s principal investigators were Miguel Moutinho, PhD, a postdoctoral researcher in anatomy, cell biology, and physiology, and Gary Landreth, PhD, the Martin Professor of Alzheimer’s Research.
“This study identifies a potential novel therapeutic target for Alzheimer’s disease, which can be modulated by FDA-approved drugs,” Moutinho said. “The translational potential of this strategy to clinical use is high.”
The majority of niacin, which supports metabolism throughout the body, comes from a conventional diet, however it can also be found in supplements and medications that lower cholesterol. However, Moutinho discovered that niacin is utilised differently by the brain. Niacin interacts with the highly-selective HCAR2 receptor in immune cells that are physically linked to amyloid plaques in the brain. Niacin, the FDA-approved Niaspan medicine utilised in this experiment, activates the receptor, stimulating positive immune cell responses, according to Landreth.
“After the Alzheimer’s disease animal models received niacin, they ended up with fewer plaques and they have improved cognition,” Landreth said, “and we directly showed that these actions were due to the HCAR2 receptor.”
Higher dietary niacin intake was associated with a lower incidence of Alzheimer’s disease, according to previous epidemiology studies on the subject, according to Landreth. Additionally, niacin is currently being tested in clinical studies for Parkinson’s and glioblastoma.
To further their research into niacin and the brain, Landreth and Moutinho are collaborating with Jared Brosch, MD, associate professor of clinical neurology, who is applying for a clinical pilot trial to study the affects of niacin and the human brain.