Using the massive computer-simulation power of the San Diego Supercomputer Center (SDSC) at UC San Diego, researchers are zeroing in on the causes of Parkinsons disease, Alzheimers disease, rheumatoid arthritis and other diseases.
A study published in this weeks Federation of European Biochemical Societies (FEBS) Journal offers for the first time a model for the complex process of aggregation of a protein known as alpha-synuclein, which in turn leads to harmful ring-like or pore-like structures in human membranes, the kind of damage found in Parkinsons and Alzheimers patients.
The researchers at SDSC and UC San Diego also found that the destructive properties of alpha-synuclein can be blocked by beta-synuclein a finding that could lead to treatments for many debilitating diseases.
The current journals cover features an image from the research that helps illustrate the scientists work.
This is one of the first studies to use supercomputers to model how alpha-synuclein complexes damage the cells, and how that could be blocked, said Eliezer Masliah, professor of neurosciences and pathology at UC San Diego. We believe that these ring- or pore-like structures might be deleterious to the cells, and we have a unique opportunity to better understand how alpha-synuclein is involved in the pathogenesis of Parkinsons disease, and how to reverse this process.
Igor Tsigelny, project scientist in chemistry and biochemistry at UC San Diego and a researcher at SDSC, said that the teams research helped confirm what researchers had suspected. The present study using molecular modeling and molecular dynamics simulations in combination with biochemical and ultrastructural analysis shows that alpha-synuclein can lead to the formation of pore-like structures on membranes.
In contrast, he said, beta-synuclein appears to block the propagation of alpha-synucleins into harmful structures.