Glaucoma Progressing Stage Estimated from Visual Field Test Data with Glaucoma Patient; and Zinc(Ⅱ) Induced Regenerative Ativity from Optic Nerve Damage

Tsuneo Ishida

doi:10.52916/jmrs214057

Abstract

Glaucoma progressing stages (Stages 1～5) estimated from Visual Field Index (VFI); Mean Deviation (MD); and Pattern Standard Deviation (PSD) data has been elucidated; in which the glaucomatous pathology is in the proceeding stage 2-3 with T. Ishida's glaucoma patient compared with referring with VFI; MD; and PSD values to the literatures. Zinc(Ⅱ) induced VFI improvement should be taken into account when interpreting rates of VFI change over time that zinc promotes Retinal Ganglion Cells (RGCs) survival; in which zinc intake in RGCs survival may be zinc acetate 25-50 mg/day. Zinc(Ⅱ) induced recovery activity from optic nerve damage of the eye consists of four processes as follows. (1) Intraocular inflammatory stimulation process; Zinc concentrations 123-292 μg/g inhibit intraocular inflammation with atypical growth factor oncomodulin (Ocm) binding to its cognate receptor on RGCs. (2) RGC survival process; Zn2+ chelators enhance RGC survival and promote axon regeneration through the optic nerve. (3) Neural axon regeneration process; Zn2+ chelation promotes axon regeneration. Norepinephrine Transporters (Net) inhibitor promotes RGCs survival and axonal regeneration. (4) Eye to brain pathway process; Zn2+ chelator TPEN promotes both enduring RGC survival and considerable axon regeneration. Zinc induced recovery for NO production in RGCs that the NO conveys from the eye to the brain through the axons of RGCs; in which zinc concentration 100 μM may be suited for the optic nerve recovery. Accordingly; Zinc(Ⅱ) could enhance optic nerve damage recovery that Zn2+ may be bound with optic nerve damage proteins; in which Zn2+ ions may bind with intraocular protein; RGC survival protein; axonal protein; and optic nerve disorder proteins during recovery process by Zn2+ ions-centered tetrahedrally binding proteins molecular coordination pattern.

Highlights

COVID-19 virus pandemic continues to disrupt the delivery of ophthalmic care that more uncertainty of glaucoma care, the change in glaucoma patient experience and attitudes, visual acuity deterioration as well as true glaucomatous progression caused by the COVID pandemic could elucidate the psychological and physiological impacts [1]
Glaucoma has been treated as a disease of early cellular senescence that the existing evidence to support this view of glaucoma is examined in the light of glaucoma pathophysiology as a premature aging process, in which examined on longevity, retinal ganglion cell death, stem cells present opportunities and prevent repair optic nerve damage, and approaches to saving sight in glaucoma [5]
Zinc(II) induced Visual Field Index (VFI) improvement may be involved that zinc promotes Retinal Ganglion Cells (RGCs) survival, VFI improvement, considering that VFI substantially underestimates the amount of neural loss early in the disease and disease severity should be taken into account when interpreting rates of VFI change over time, in which zinc intake in RGCs survival may be zinc acetate 25-50 mg/day [18]

Summary

Introduction

COVID-19 virus pandemic continues to disrupt the delivery of ophthalmic care that more uncertainty of glaucoma care, the change in glaucoma patient experience and attitudes, visual acuity deterioration as well as true glaucomatous progression caused by the COVID pandemic could elucidate the psychological and physiological impacts [1]. Zinc(II) induced recovery activity from optic nerve damage of the eye consists of four processes as follows. (2) RGC survival process; Zn2+ chelators enhance RGC survival and promote axon regeneration through the optic nerve.

Results

Conclusion