By D. Virgil Alfaro III et al.
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Extra resources for Age-Related Macular Degeneration, 2nd Edition
However, though there is an association between CFH and AMD, the CFH knockout mice do not display many of the hallmark AMD features. Contrary to other models of AMD, almost 30% of these animals showed a substantial thinning of their BM. Plus, since CFH itself is a main component of drusen, the loss of this protein may reduce the volume of sub-RPE deposits. Transgenic CFH Y402H Mice Recent studies have shown an increase risk of AMD in individuals with the Y402H polymorphism in the complement factor H gene (132).
However, further work is required to assess the molecular mechanisms underneath this neovascularization. (c) 2015 Wolters Kluwer. All Rights Reserved. 28 SECTION 1 ANATOMY, PHYSIOLOGY, AND PATHOLOGY OF THE MACULA VLDLR-Targeted Mutant Homozygous strains of mice with targeted mutations for VLDLR gene developed new blood vessels in the area of the outer plexiform layer of the retina and choroidal anastomoses by 3 months (51). ApoE Overexpression Eyes in hypercholesterolemic mice displayed AMD-like changes in the BM/RPE complex (35).
Young ApoB100 mice developed basal laminar deposits when fed with a HF diet and exposed to oxidative blue-green light (47). At older ages, ApoB100 mice exposed to normal diets (c) 2015 Wolters Kluwer. All Rights Reserved. Chapter 2 Animal Models for Age-Related Macular Degeneration 19 exhibited BM thickening, loss of the basal infoldings of the RPE, and basal laminar deposits (48,49). When these animals were additionally fed HF diets, more basal linear deposits were observed. Lipoprotein Receptors LDL receptor (LDLR) knockout mice are incapable of importing cholesterol, leading to increased plasma cholesterol levels and development of atheromatosis.