Henein, C; Khaw, P; (2019) The interplay between inflammation, immunity and commensal microflora in glaucomatous neurodegeneration. [Editorial comment]. Annals of Eye Science (AES) , 4 (10) 10.21037/aes.2019.02.04.

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Abstract

This investigation sheds some light on intersecting mechanistic pathways in glaucomatous neurodegeneration. Progressive degeneration of retinal ganglion cells (RGCs) resulting in optic nerve head cupping and visual loss are characteristic features of glaucoma. The pathophysiological causes of this degeneration are not clearly defined but most certainly involves multifactorial and polygenic mechanisms. Large genome-wide association studies suggest a role of angiopoietin-receptor tyrosine kinase signalling, lipid metabolism, mitochondrial function, and developmental processes as underlying risks for elevated intraocular pressure (IOP) and primary open angle glaucoma (POAG)(8). Although age and raised IOP remain the most prominent risk factors for glaucoma, disease phenotypes of normal tension glaucoma suggest mechanisms beyond pressure-mediated neurodegeneration.

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