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Microglial activation has been linked to many neurodegenerative diseases including glaucoma. However, the functional significance of microglial alterations during glaucomatous neurodegeneration is unclear. In this important study, Bosco et al. (98) examined microglial alterations by numbers, distribution, and activation in glaucomatous neurodegeneration onset and progression using a chronic mouse model of glaucoma, the DBA/2J (D2) mouse that induces spontaneous intraocular pressure (IOP) elevation and progressive retinal ganglion cell (RGC) degeneration by age-dependent manner. The authors demonstrate that microglial activations are present in the inner central retina and unmylelinated optic nerve regions in D2 mice by three months of age, as well as in the optic disc and peripheral retina at five to eight months of age.
Early disease diagnosis by detection of microglial activation may be a valuable approach in glaucoma
They suggest that microglial activation may contribute to both glaucomatous neurodegeneration onset and progression. In the study, because the molecular mechanism of microglia-mediated alterations in both onset and progression is lacking, it would be interesting to determine the microglial activation-mediated biochemical cascades that will provide the functional significance of microglial alterations including activation in both glaucomatous neurodegeneration onset and progression. Emerging evidence by these authors and others indicates that there is early RGC pathology (three months) that is not linked with IOP elevation in glaucomatous D2 mice and human glaucoma. It would be very important to understand the early pathophysiological events that may predict early RGC dysfunction in glaucoma. The authors propose that early disease diagnosis by detection of microglial activation may be a valuable approach in glaucoma. Therefore, the significance of the early activation of microglial cells during glaucomatous neurodegeneration should be further clarified.