  Age-related macular degeneration (AMD) may cause severe loss of vision or
blindness particularly in elderly people. Exudative AMD is characterized by
angiogenesis of blood vessels growing from underneath the macula, crossing the
blood-retina barrier (that comprise Bruch's membrane, BM, and the retinal
pigmentation epithelium RPE), leaking blood and fluid into the retina and
knocking off photoreceptors. Here, we simulate a computational model of
angiogenesis from the choroid blood vessels via a cellular Potts model, as well
as BM, RPE cells, drusen deposits and photoreceptors. Our results indicate that
improving AMD may require fixing the impaired lateral adhesion between RPE
cells and with BM, as well as diminishing Vessel Endothelial Growth Factor
(VEGF) and Jagged proteins that affect the Notch signaling pathway. Our
numerical simulations suggest that anti-VEGF and anti-Jagged therapies could
temporarily halt exudative AMD while addressing impaired cellular adhesion
could be more effective on a longer time span.
