Age-related Macular Degeneration (AMD) is a multifactorial disease that occurs only in senior population. According to Harman’s theory (1956), senescence happens due to excessive accumulation and reduced elimination of free radicals in tissues. At the young age, intensive metabolic processes in the outer layers of the retina and pigment epithelium do not lead to the disease because the pigment epithelium itself and the antioxidant protection function well. If they do not work, the immune system becomes involved. Macrophages, microglia, complement system all contribute to the removal of toxic products. R. Medzhidov in 2008 proposed to call this phenomenon ’para-inflammation’. With aging, this protection may fail, especially if there is a genetic predisposition or aggravating environmental factors. Although AMD cannot be truly called an inflammatory disease, the factors of chronic inflammation are present in it. This is especially true for the alternative complement pathway. People carrying polymorphism of the H gene that normally blocks excessive complement activity are reliably known to have AMD more often. The normal functioning of the complement system contributes to para-inflammation, while its hyperactivation leads to more tissue damage inducing the disease. The impairment of the hemo-ophthalmic barrier caused by the defeat of RPE makes antigens of the outer layers of the retina accessible. Depending on the genetic characteristics of the patient, these antigens are represented differently to his immune system, and since they do not have immune tolerance, varying degrees of autoimmune reaction should be expected. The treatment should be aimed at reduction of the oxidative stress, and injection of inhibitors of vascular endothelial growth factors, glucocorticoids, etc. The study of para-inflammation and inflammation in AMD will help create a new generation of effective drugs that affect the key links in these processes.