Abstract

Neurodegenerative disorders are characterized by typical neuronal degeneration and axonal loss in the central nervous system (CNS). Demyelination occurs when myelin or oligodendrocytes experience damage. Pathological changes in demyelination contribute to neurodegenerative diseases and worsen clinical symptoms during disease progression. Glaucoma is a neurodegenerative disease characterized by progressive degeneration of retinal ganglion cells (RGCs) and the optic nerve. Since it is not yet well understood, we hypothesized that demyelination could play a significant role in glaucoma. Therefore, this study started with the morphological and functional manifestations of demyelination in the CNS. Then, we discussed the main mechanisms of demyelination in terms of oxidative stress, mitochondrial damage, and immuno-inflammatory responses. Finally, we summarized the existing research on the relationship between optic nerve demyelination and glaucoma, aiming to inspire effective treatment plans for glaucoma in the future.

Highlights

  • Neurodegenerative diseases are a group of heterogeneous diseases with progressive and selective loss of neurons (Lin and Beal, 2006)

  • In patients with primary open-angle glaucoma, researchers have observed the delay of visual evoked potentials (VEPs) latency and an increase of λ⊥ in the optic radiation in diffusion tensor imaging (DTI) (You et al, 2019)

  • Morphological Changes of Demyelination in Glaucoma The morphology of myelin sheath is mainly observed by immunohistochemistry (LFB staining), immunofluorescence (MBP staining) and electron microscopy (EM)

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Summary

Introduction

Neurodegenerative diseases are a group of heterogeneous diseases with progressive and selective loss of neurons (Lin and Beal, 2006). Morphological and functional changes in oligodendrocytes, myelin, and axons can be observed when demyelination occurs. The contents of myelin proteins, such as MBP and myelin oligodendrocyte glycoprotein (MOG), are dramatically decreased in the myelin sheaths (Renner et al, 2017).

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Conclusion

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