Common risk factors for many ocular pathologies involve non-pathologic, age-related damage to the optic nerve. Understanding the mechanisms of age-related changes can facilitate targeted treatments for ocular pathologies that arise at any point in life. In this review, we examine these age-related, neurodegenerative changes in the optic nerve, contextualize these changes from the anatomic to the molecular level, and appreciate their relationship with ocular pathophysiology. From simple structural and mechanical changes at the optic nerve head (ONH), to epigenetic and biochemical alterations of tissue and the environment, multiple age-dependent mechanisms drive extracellular matrix (ECM) remodeling, retinal ganglion cell (RGC) loss, and lowered regenerative ability of respective axons. In conjunction, aging decreases the ability of myelin to preserve maximal conductivity, even with “successfully” regenerated axons. Glial cells, however, regeneratively overcompensate and result in a microenvironment that promotes RGC axonal death. Better elucidating optic nerve neurodegeneration remains of interest, specifically investigating human ECM, RGCs, axons, oligodendrocytes, and astrocytes; clarifying the exact processes of aged ocular connective tissue alterations and their ultrastructural impacts; and developing novel technologies and pharmacotherapies that target known genetic, biochemical, matrisome, and neuroinflammatory markers. Management models should account for age-related changes when addressing glaucoma, diabetic retinopathy, and other blinding diseases.

/pdf/aging-effects-on-optic-nerve-neurodegeneration-1lbnd0pm.pdf

Aging Effects on Optic Nerve Neurodegeneration

http://www.cell.com/article/S2405844023008411/pdf

The impact of horizontal eye movements versus intraocular pressure on optic nerve head biomechanics: A tridimensional finite element analysis study

Reactive gliosis of Müller cells plays an important role in the pathogenesis of diabetic retinopathy (DR). Liraglutide, a glucagon-like peptide-1 receptor (GLP-1R) agonist, has been shown to improve DR by inhibiting reactive gliosis. However, the mechanism of inhibition has yet to be elucidated. The investigated the effects of liraglutide on Müller glia reactivity in the early stages of DR and the underlying mechanisms. Proteomics combined with bioinformatics analysis, HE staining, and immunofluorescence staining revealed ganglion cell loss, reactive gliosis of Müller cells, and extracellular matrix (ECM) imbalance in rats with early stages of DR. Exposure to high glucose (HG) induced the decrease in ITGB1 expression in Müller cells and decreased FN1 levels in the extracellular fluid, but not the intracellular level. High glucose levels up-regulated the expression of GFAP and TNF-α in rMC1 cells and down-regulated the content of FN1 in extracellular fluid, thereby improving the reactive gliosis. GLP-1R knockdown and HG + DAPT inhibition experiments indicated that liraglutide ameliorates DR in diabetic rats by balancing the ECM and ameliorates high-glucose-induced Müller glia reactivity by inhibiting the activation of the Notch1/Hes1 pathway. Thus, the study provides new targets and ideas for improvement of DR in early stages.

Liraglutide intervention improves high-glucose-induced reactive gliosis of Müller cells and ECM dysregulation

The chapter reflects updates in the section on congenital and familial disorders including relevant syndromes. The section on ischemic optic neuropathies has been revised, as has been the section on optic nerve tumors. 

Optic Nerve

Additional file 1: Figure S1. Processing of RNASeq data. Figure S2. Comparing expression of known meningeal markers between young and aged animals. Figure S3. Cluster analysis of IPA. Figure S4. Overview expression of collagens and laminins. Table S1. Sample overview. 

Additional file 1 of Impact of aging on meningeal gene expression

The extracellular matrix composition of the optic nerve subarachnoid space

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The extracellular matrix composition of the optic nerve subarachnoid space