Center faculty member Robert Vassar, PhD, was part of a large collaborative study that identified a protein called interferon induced transmembrane protein 3 (IFITM3) that modulates the γ-secretase enzyme which produces amyloid — the major component of Alzheimer’s-associated amyloid plaques.
The study found that brain inflammation causes the level of IFITM3 to increase, which in turn causes γ-secretase to make more amyloid. Aging also increases IFITM3, which may explain why age is the primary risk factor for Alzheimer’s disease, at least in part. Additionally, they found that brain tissue from late-onset Alzheimer’s disease patients have increased levels of IFITM3, which may contribute to the disease process.
The work suggests that lowering the level or activity of IFITM3 in the brain may represent a viable therapeutic approach for the prevention of Alzheimer’s disease.
