Computers Search for Parkinson/AD Origins
Supercomputer analysis has helped researchers develop a model of how a particular protein can lead to cellular damage resulting in Parkinson’s, Alzheimer’s and a host of other chronic diseases.
Computer simulations allowed researchers from UC San Diego to show 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 study is published in the Federation of European Biochemical Societies (FEBS) Journal.
The researchers 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.
“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 Parkinson’s disease, and how to reverse this process.”
Igor Tsigelny, project scientist in chemistry and biochemistry at UC San Diego, said that the team’s 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.”
The complex calculations for the study were performed on Blue Gene supercomputers at SDSC and the Argonne National Labs.
Nauert PhD, R. (2007). Computers Search for Parkinson/AD Origins. Psych Central. Retrieved on February 6, 2016, from http://psychcentral.com/news/2007/03/26/computers-search-for-parkinsonad-origins/707.html