Glaucoma is a complex and progressive optic neuropathy characterized by retinal ganglion cell (RGC) degeneration and optic nerve damage, ultimately leading to irreversible vision loss. While elevated intraocular pressure (IOP) is the primary modifiable risk factor, disease progression often occurs even with effective IOP control, highlighting the need for alternative therapeutic strategies.

This thesis explores current theories of glaucoma pathogenesis, with a focus on immunological dysregulation, neuroinflammation, and vascular abnormalities. Particular attention is given to monoclonal antibodies (mAbs) as emerging tools in targeted pharmacological therapy, with the potential to offer neuroprotection and disease modification.

In addition, the work reviews innovative treatment strategies and advanced drug delivery systems that aim to go beyond symptom management and address the underlying causes of glaucoma. By integrating immunological, pharmacological, and biotechnological perspectives, the thesis supports the potential of mechanism-driven therapies to reshape glaucoma treatment and improve long-term visual outcomes.