By combining thousands of simulations, Shirinifard was able to produce maps that related defects in each type of adhesion to the risk of each type of invasion. In turn, he could show that cell adhesion is key to keeping blood vessels out of the retina and that combination defects in the different types of adhesion are sufficient to determine the probability, pattern and rate of progression of CNV.
The full results of one of the most complex tissue evolution models ever deployed were published today in PLoS Computational Biology, and while the team has yet to move toward developing new CNV therapies, the work should have great significance in the search for better therapies, according to Biocomplexity Institute Director James Alexander Glazier, a co-author on the paper and professor in the IU Bloomington College of Arts and Sciences' Department of Physics.
"Hundreds of millions of dollars are spent annually to develop drugs and treatment approaches based on the two commonly hypothesized CNV initiation and progression mechanisms," he said. "Because the current work shows that neither hypothesized mechanism is an important cause of CNV, that money and effort are extremely unlikely to improve outcomes for patients. Scientists have been barking up the wrong tree. Instead, a search for therapies which restore normal adhesion in the eye is much more likely to produce effective treatments. In addition, the detailed agreement between simulation and clinical observations suggests that new approaches to measuring adhesion in patients would allow much more accurate predictions of the prognosis for individual patients."
The researchers believe these results will also have a much broader impact, as they apply to any tissue -- like the gut and the lung -- in which a basement membrane separates a capillary network from a nearby epithelium.
"The relationships between specific class
|Contact: Steve Chaplin|