Researchers in a new study have found new hints that could explain how Alzheimer's disease spreads in human brains. Case Western Reserve University researchers who were studying prions —the misfolded proteins that cause lethal, incurable diseases — have identified for the first time surface features of human prions responsible for their replication in the brain. Alzheimer's disease affects more than 6 million people in the United States. Scientists have not yet discovered the exact cause of Alzheimer's disease. The Alzheimer's Association estimates its treatment will cost an estimated $ 355 billion. The ultimate goal of the research is to develop a strategy to stop prion disease in humans and ultimately implement new approaches to work on Alzheimer's and other neurodegenerative diseases. Prions were first discovered in the late 1980s as a protein-containing biological agent that could replicate in living cells without nucleic acid. Prion diseases as well as animal transmissions of bovine spongiform encephalopathy (BSE, mad cow disease), dramatically accelerated the development of a new scientific concept of self-replicating proteins.
Human prions can bind to neighboring normal proteins in the brain and cause microscopic holes. Essentially, they turn brains into spongy structures and lead to dementia and death. "These discoveries sparked an ongoing scientific debate about whether prion mechanisms might be involved in the development and spread of other neurodegenerative diseases in humans more heterogeneous neurodegenerative diseases, and a growing body of research suggests that they are caused by different strains of human prions" Safar said. However, structural studies in human prions have delayed recent advances in laboratory rodent prions, in part because of their complex molecular properties prohibitive biosafety requirements necessary to study a disease that is invariably fatal and has no treatment.
