DEVELOPMENT OF NEW NEUROPROTECTIVE THERAPIES FOR GLAUCOMA

Authors

  • Lucas Alves de Almeida Instituto de Olhos Ciências Médicas (IOCM)
  • Abel Mendonça Alves Instituto de Olhos Ciências Médicas (IOCM)
  • Daniel Fulgêncio de Moura Instituto de Olhos Ciências Médicas (IOCM)

DOI:

https://doi.org/10.51891/rease.v11i9.20701

Keywords:

Glaucoma. Neuroprotective Therapies. Retinal Ganglion Cells. Oxidative Stress.

Abstract

Glaucoma, the leading cause of irreversible blindness worldwide, affecting approximately 76 million individuals, is a progressive optic neuropathy characterized by the death of retinal ganglion cells (RGCs) and degeneration of the optic nerve. Although elevated intraocular pressure (IOP) is the main modifiable risk factor, conventional therapies focused exclusively on reducing it prove insufficient to prevent disease progression in a significant proportion of patients. In this context, this study aims to critically analyze, through a literature review, the development of new therapeutic strategies with neuroprotective potential. The pathophysiological mechanisms underlying RGC apoptosis, such as oxidative stress, glutamate excitotoxicity, and dysregulation of neurotrophic factors, were reviewed. The analysis highlights that emerging approaches, including the use of antioxidants (e.g., N-acetylcysteine), NMDA receptor antagonists (e.g., memantine), and gene therapy for overexpression of growth factors (e.g., BDNF), represent promising alternatives. It is concluded that neuroprotective therapies, acting as a complement to IOP control, have the potential to modify the natural course of the disease, preserve visual function, and improve patients' quality of life, despite challenges such as bioavailability and the need for robust clinical validation.

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Published

2025-09-05

How to Cite

Almeida, L. A. de, Alves, A. M., & Moura, D. F. de. (2025). DEVELOPMENT OF NEW NEUROPROTECTIVE THERAPIES FOR GLAUCOMA. Revista Ibero-Americana De Humanidades, Ciências E Educação, 11(9), 915–922. https://doi.org/10.51891/rease.v11i9.20701