Dr. Carol Hall, Alcoa Professor of chemical engineering at NC State and Hung D. Nguyen, a graduate student in Hall's lab, used a computer simulation technique, discontinuous molecular dynamics, to visualize the meanderings of small proteins called peptides. Movies of the simulation show that 96 randomly placed peptides spontaneously aggregate into what Hall calls a "sandwich" of layered protein sheets, similar to the amyloid fibrils discovered in diseased people and animals. Hall says that understanding how fibrils form in human or animal organs may lead to discoveries of how to slow or halt fibril formation.
The research was published in the Nov. 16 edition of Proceedings of the National Academy of Sciences.
It is not known whether fibrils cause Alzheimer's, Parkinson's and the other so-called amyloid diseases, or whether they are just associated symptoms. In any event, the fibrils form plaques in human and animal organs, often the brain. Although it's not clear if these plaques cause memory loss in Alzheimer's patients, for instance, scientists are interested in finding out the mechanisms behind the formation of fibrils.
"All of these diseases Alzheimer's, Parkinson's, ALS, Huntington's have the same unusual phenomena. Proteins completely different proteins in each disease assemble into ordered aggregates, amyloid fibrils, so that a vital organ, usually the brain, is crisscrossed by these structures," Hall said. "This tells us that the problem has something to do with the general nature of proteins rather than with the specifics of the particular disease-associated proteins."