AMD is associated with an inflammatory response to modified “self-elements” at the interface of the eye and the rest of the body. The aim of this project is to analyze the contribution of the local barrier cells, the retinal pigment epithelium (RPE), to the dysregulation of soluble immune molecules, called the complement system(Figure Below). Furthermore, we would like to dampen the over-activation of this system in the eye using an antibody against properdin, its only known positive regulator.
Models that closely mimic the respective disease progression in patients could support the development of an appropriate therapeutic approach. Thereby, pharmacological interventions using chemical substances in order to specifically induce degeneration in different retinal cell types are also used in ophthalmic research. Such in vivo models have several advantages including the induction of the damage in adult animals of various species and/or strains and the possibility to modulate the onset and severity of retinal damage.according to the scientific question. We are employing the following pharmacological models: Sodium iodate (NaIO3) inducing necrosis in the RPE followed by apoptosis in the photoreceptors and methylnitrosourea (MNU) specifically toxic to the photoreceptors.