Amyloid precursor protein (APP), a key protein implicated in the development Alzheimer's disease, may play an important role in eye and muscle health. In a new report published in the June 2015 issue of The FASEB Journal, scientists have discovered that when proteins that bind to the APP, called FE65 and FE65L1, are deleted, they cause cataracts and muscle weakness in mice. Additionally, this study demonstrates that the expression of laminin, a protein pivotal for the interaction between lens epithelial cells and the lens capsule, is severely altered in mice lenses missing both FE65 and FE65L1 genes. If confirmed in human studies, the FE65 and FE65L1 proteins may become a therapeutic target for cataracts, muscular dystrophy and Alzheimer's disease.
"We hope the discoveries in this study would help to expand our understanding of the normal function of FE65 and APP," said Jaehong Suh, Ph.D., a researcher involved in the work from the Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease at Massachusetts General Hospital in Boston, MA. "From this kind of very basic research, we may be able to find more clues for the causes of, and ultimately to discover effective treatments for related human diseases such as cataract, congenital muscular dystrophies and Alzheimer's disease."