Glaucoma and neuroinflammation: An overview.
Quaranta Luciano, Bruttini Carlo, Micheletti Eleonora, Konstas Anastasios G P, Michelessi Manuele, Oddone Francesco, Katsanos Andreas, Sbardella Diego, De Angelis Giovanni, Riva Ivano
AI Summary
This overview highlights neuroinflammation's potential role in glaucoma's development and progression, linking it to retinal ganglion cell degeneration and offering new therapeutic targets.
Abstract
Glaucoma is an optic neuropathy characterized by well-defined optic disc morphological changes (i.e., cup enlargement, neuroretinal border thinning, and notching, papillary vessel modifications) consequent to retinal ganglion cell loss, axonal degeneration, and lamina cribrosa remodeling. These modifications tend to be progressive and are the main cause of functional damage in glaucoma. Despite the latest findings about the pathophysiology of the disease, the exact trigger mechanisms and the mechanism of degeneration of retinal ganglion cells and their axons have not been completely elucidated. Neuroinflammation may play a role in both the development and the progression of the disease as a result of its effects on retinal environment and retinal ganglion cells. We summarize the latest findings about neuroinflammation in glaucoma and examine the connection between risk factors, neuroinflammation, and retinal ganglion cell degeneration.
MeSH Terms
Shields Classification
Key Concepts4
Neuroinflammation may play a role in both the development and the progression of glaucoma as a result of its effects on retinal environment and retinal ganglion cells.
Glaucoma is an optic neuropathy characterized by well-defined optic disc morphological changes (i.e., cup enlargement, neuroretinal border thinning, and notching, papillary vessel modifications) consequent to retinal ganglion cell loss, axonal degeneration, and lamina cribrosa remodeling.
These modifications (optic disc morphological changes, retinal ganglion cell loss, axonal degeneration, and lamina cribrosa remodeling) tend to be progressive and are the main cause of functional damage in glaucoma.
Despite the latest findings about the pathophysiology of glaucoma, the exact trigger mechanisms and the mechanism of degeneration of retinal ganglion cells and their axons have not been completely elucidated.
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