Fatal Protein Interactions May Explain Neurological Diseases
In a collaborative study at the University of California, San Diego, investigators from neurosciences, chemistry and medicine, as well as the San Diego Supercomputer Center (SDSC) have investigated how proteins involved in neurodegenerative diseases such as Alzheimer's and Parkinson's disease interact to form unique complexes. Their findings explain why Alzheimer's patients might develop Parkinson's, and vice versa.
The new and unique molecular structures they discovered can now be used to model and develop new drugs for these devastating neurological diseases. Their findings will be published in the September 3 issue of Public Library of Science (PLoS) ONE on September 4, 2008.
The team, led by Eliezer Masliah, M.D., professor of neurosciences and pathology in the UC San Diego School of Medicine, found that "fatal" or abnormal interactions among the a-synuclein protein (a-syn, involved in Parkinson's disease) and Abeta amyloid (Aß, which leads to the plaques associated with Alzheimer's disease) interact and form unique "hybrid" complexes. These hybrid abnormal protein interactions result in combined neurodegenerative diseases.