Work in Progress

  1. Does the H402 variant of Cfh predispose to increased risk for choroidal neovascularization (CNV) and/or resistance to anti-VEGF therapy?
    • Frequency and size of CNV induced by laser in H402 vs. Y 402 Cfh transgenic mice
    • Response to anti-VEGF agents
  2. Does H402 Cfh change the subretinal microenvironment predisposing to an altered activation of the immune system?
    • Use high-throughput techniques (proteomics and custom-made qPCR array) to screen the
    • subretinal tissues for levels of protein and mRNA of molecules of interest.  Important
    • molecules include: cytokines, chemokines and other chemoattractants, complement
    • components, and enzymes involved in free-radical and lipofuscin metabolism. 
  3. Will the Cfh polymorphism lead to a mouse model of AMD with spontaneous CNV?
    • Cross our transgenic mice with human c-reactive protein (hCrp) transgenic mice
    • Look for histopathologic changes, clinically-visible drusen, pigmentary changes and CNV
    • Triggers of inflammation/oxidative stress: light exposure
    • Cross mice to Superoxide Dismutase 1 deficient mice to increase oxidative stress
  4. Is the immune system involved in the pathogenesis of drusen or CNV?  Are there subsets of inflammatory cells that are essential?
    • Analyze the deposition of complement, CRP and inflammatory molecules in the subretinal/sub-
    • RPE space in our transgenic mice.
    • Analyze the timing and type of cellular infiltration
    • Deplete subsets of immune cells using antibodies
  5. Can our animal model help us identify novel molecules to inhibit the development of drusen or CNV?