Immune Mediated Degeneration and Possible Protection in Glaucoma.

摘要: The underlying pathomechanisms for glaucoma, one of the most common causes blindness worldwide, are still not identified. In addition to increased intraocular pressure (IOP), oxidative stress, excitotoxicity, and immunological processes seem play a role. Several pharmacological or molecular/genetic methods currently investigated as treatment options this disease. Altered autoantibody levels were detected in serum, aqueous humor, tissue sections glaucoma patients. To further analyze role immune system, an IOP-independent, experimental autoimmune (EAG) animal model was developed. model, immunization with ocular antigens leads antibody depositions, misdirected T-cells, retinal ganglion cell death degeneration optic nerve, similar glaucomatous Moreover, activation complement system microglia alterations identified EAG well hypertension models. inhibition these factors can alleviate models without high IOP. Currently, several neuroprotective approaches tested distinct It is necessary have systems that cover pathomechanisms, but also allow screening new drugs. vitro commonly used, including single lines, mixed-cultures, even organoids. ex vivo organ cultures, therapeutics be whole retina. Furthermore, reveal insights situation. With all models, possible drugs therapy strategies last years. For example, hypothermia treatment, neurotrophic blockage excitotoxity. However, studies required independent behind glaucoma. There open issue whether mechanisms directly indirectly trigger pathways. Hence, it might imbalance between protective destructive mechanisms. evaluated more detail, since deeper could lead better