The benefit of finding a genetic association with specific genes is that we can begin to understand more about how the parasite triggers the development of ocular disease during embryogenesis and fetal development by examining what is known about the chronological expression and localization of COL2A1 and ABCA4 during development and after birth. COL2A1 encodes type II collagen which is found in the vitreous humor, cornea, sclera, lens, ciliary body, retinal pigment epithelium, and retina of the eye. During embryogenesis, type IIA procollagen is localized around cells of the developing ganglion cell layer, playing a role in guiding the Folinic acid calcium salt pentahydrate axonal processes of the developing retinal ganglion cells as they traverse the retinal surface and converge to form the optic nerve bundle. Both IIA and IIB transcripts occur in retinal pigment epithelial cells, with the protein localized around these cells during embryogenesis, acting to maintain the structural strength of the attachment area of retina and pigment epitheliuim. In the mouse eye, transcripts for types IIA and IIB mRNA have been detected during embryogenesis starting at least from day 10.5, with the relative levels of both isoforms remaining fairly constant during normal embryonic development, and with the type IIB isoform slightly predominating. The critical period for the development of major congenital eye disorders is during weeks 4 to 8 of gestation. The genetic association between ocular disease in congenital toxoplasmosis and COL2A1 might reflect differences in collagen expression in the retina and vitreous influencing migration or dissemination of the parasite within the eye, or stability of the eye structures when there are multiplying parasites in the choroid, retina or optic nerve. This would be likely to have its most profound effect on Lomitapide Mesylate pathology during early embryogenesis when the eye is forming and COL2A1 is first expressed. Since toxoplasmosis is a complex disease, multiple genes and modifiers will contribute to end stage pathology. Hence, we do not expect that end stage pathology seen in congenital toxoplasmosis will be the same as that observed in the case of a very specific genetic disorder like Stickler��s disease. Nevertheless, differences in collagen expression could contribute to similar end stage consequences of disease that occur rarely in toxoplasmosis but commonly in Sticklers disease.