WEDNESDAY, Feb. 25, 2009 (HealthDay News) -- Yale University researchers believe they've filled in an important missing link in understanding the development of Alzheimer's disease.
They found that cellular proteins called prions activate the process by which amyloid-beta peptides impair brain function in people with the disease.
"It's been a black box. We have known that amyloid beta is bad for the brain, but we have not known exactly how amyloid-beta does bad things to neurons," the study's senior author, Stephen M. Strittmatter, a professor of neurology and director of Cellular Neuroscience, Neurodegeneration and Repair at Yale School of Medicine, explained in a university news release.
The researchers looked at hundreds of thousands of candidates for potential disease-mediating receptors for the specific form of amyloid-beta linked to Alzheimer's and identified cellular prion proteins as the most likely culprit. It appears, they said, that amyloid-beta peptides attach to cellular prion proteins, resulting in damage to brain cells.
"They start the cascade that makes neurons sick," Strittmatter said.
Cellular prion proteins are normally harmless and exist in all cells, but they can change shape and cause disease. And because the proteins are involved in the early stage of disease development, they're a promising target for the development of new Alzheimer's treatments, he said.
The study does not suggest that these proteins convert to an infectious agent in Alzheimer's disease, but the findings do suggest that the role of these normally harmless proteins in common neurodegenerative diseases warrants further study, Strittmatter said.
The study appears in the Feb. 26 issue of the journal Nature.
The U.S. National Institute on Aging has more about Alzheimer's disease.