Studies suggest an immunological component in the pathology of glaucoma. An increased occurrence of paraproteins and autoantibodies against nuclear antigens like Sjo¨gren’s syndrom A, was demonstrated in glaucoma patients. Furthermore, studies show not only up-regulated, but also down-regulated antibodies in glaucoma patients. In the serum and aqueous humor of glaucoma patients general complex autoantibody patterns against retinal and optic nerve antigens were found but also more specific autoantibody changes such as an up- regulation of abs against e.g. alpha foldrin and Hsp 70, and a downregulation of abs against aB Crystallin and Vimentin leading to the conclusion that there is a role for the autoantibodies in the pathogenesis of glaucoma. Previous studies incubating neuroretinal cells with the serum and the abs of glaucoma patients found changed protein expression patterns in cells incubated with glaucoma serum in comparison to serum from healthy people. Furthermore the cells reacted differently towards the serum after removal of IgG abs. These results underline the hypothesis that changes in the autoantibodies could play a role in the pathogenesis of the disease. One autoantibody down-regulated in glaucoma patients is high throughput screening targeted against c-synuclein. This study aimed to investigate, which effect the down-regulated ab against c-synuclein has on stressed neuroretinal cells. A dose response effect as well as a negative effect of high c-synuclein ab concentrations couldn’t be observed. Studies show that ab-uptake into cells can be saturable. Our immunohistochemical staining results showing small amounts of abs in the cells at one defined time point support the assumption that ab uptake of the used cells is restricted. Furthermore, high ab concentrations not necessarily have a negative effect, as other studies could show that even high concentrations of ab, also internalized by cells, do not have a negative influence on the viability of cells. This could be due to the fact that the binding partners of the abs are saturated and further abs cannot be bound and therefore have no additional effect. When using unspecific abs such as anti-myoglobin abs no protective or negative effect was detected. Studies demonstrate an impact of c-synuclein on apoptotic pathways in RGC. Knocking down c-synuclein in RGC-5 leads to decreased viability through the regulation of kinases and phosphatases. In general, the effect of changes in c-synuclein expression either in vivo or in vitro shows opposing results. In vivo studies show that an up-regulation of c-synuclein can lead to neurodegeneration, which stands in contrast to other reports demonstrating that an overexpression of c-synuclein has no negative effect whereas other studies show that there is no effect on neuronal cells when inactivating csynuclein. Additionally studies show that c-synuclein can participate in signal transduction pathways. In Y79 cells overexpression of synoretin, the bovine orthologous of c-synuclein, induces increased MAPK activity as well as its downstream effector Elk-1.