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Neuroinflammation as a target for glaucoma therapy.

Annagrazia Adornetto1, Rossella Russo1, Vincenzo Parisi2

  • 1Department of Pharmacy, Health and Nutritional Sciences, Section of Preclinical and Translational Pharmacology, University of Calabria, Rende, Italy.

Neural Regeneration Research
|December 13, 2018
PubMed
Summary

Glaucoma pathogenesis involves neuroinflammation and immune responses, impacting retinal ganglion cells. Modulating these responses offers a promising therapeutic strategy for optic nerve protection.

Keywords:
glaucomaimmune responseinflammasomemicroglianeurodegenerationneuroinflammationoxidative stressretinal ganglion cells

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Area of Science:

  • Ophthalmology
  • Neuroscience
  • Immunology

Background:

  • Glaucoma pathogenesis remains unclear, but neuroinflammation and immune responses are increasingly implicated.
  • Inflammation, glial cell activation, and cytokine release are common in clinical and experimental glaucoma.
  • Both damaging and healing aspects characterize retinal inflammation, influencing disease outcomes.

Purpose of the Study:

  • To explore the role of neuroinflammation and immune responses in glaucoma pathogenesis.
  • To highlight the potential of immunomodulatory therapies for glaucoma treatment.

Main Methods:

  • Review of existing clinical and experimental data on glaucoma and inflammation.
  • Analysis of the involvement of glial cells (astrocytes, Muller cells, microglia) in the glaucomatous process.
  • Examination of the role of inflammatory mediators like cytokines and reactive oxygen species.

Main Results:

  • Evidence suggests a significant role for neuroinflammation and immune responses in glaucoma.
  • Glial cell activation and the release of inflammatory mediators are consistent findings.
  • The balance of pathogenic and reparative inflammatory processes influences disease progression.

Conclusions:

  • Neuroinflammation and immune responses are key components of glaucoma pathogenesis.
  • Targeting immune and inflammatory pathways presents a promising therapeutic avenue.
  • Modulating these responses may help preserve optic nerve structure and prevent retinal ganglion cell loss.