*2.3.1 Complement factor H knockout (Cfh−/−) mice*

CFH is a regulatory protein that prevents C3b from binding to complement factor B and ultimately prevents the formation of C3 convertase. Loss of regulation of this pathway causes deposition of C3 in the kidneys and ultimately membranoproliferative glomerulonephritis (MPGN) Type II. These patients also develop drusen similar to those in AMD [17]. *Cfh*−/− mice also developed MPGN and retinal changes such as increased retinal autofluorescence, complement deposition, and disorganization of photoreceptor outer segments (POS). However, these mice also showed thinning of BrM, which is atypical of AMD, possibly from increased phagocytic activity mediated by complement [17].
