scholarly journals Natural Products: Evidence for Neuroprotection to Be Exploited in Glaucoma

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3158
Author(s):  
Annagrazia Adornetto ◽  
Laura Rombolà ◽  
Luigi Antonio Morrone ◽  
Carlo Nucci ◽  
Maria Tiziana Corasaniti ◽  
...  
Keyword(s):  
Natural Products ◽  
Risk Factor ◽  
Intraocular Pressure ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Main Risk Factor ◽  
Number Of Patients ◽  
Elevated Intraocular Pressure ◽  
Underlying Mechanisms

Glaucoma, a leading cause of irreversible blindness worldwide, is an optic neuropathy characterized by the progressive death of retinal ganglion cells (RGCs). Elevated intraocular pressure (IOP) is recognized as the main risk factor. Despite effective IOP-lowering therapies, the disease progresses in a significant number of patients. Therefore, alternative IOP-independent strategies aiming at halting or delaying RGC degeneration is the current therapeutic challenge for glaucoma management. Here, we review the literature on the neuroprotective activities, and the underlying mechanisms, of natural compounds and dietary supplements in experimental and clinical glaucoma.

Next-Generation Techniques for Analysis of Lamina Cribrosa Microstructure

2012 ◽  
Author(s):  
C. Ross Ethier ◽  
Richie Abel ◽  
E. A. Sander ◽  
John G. Flanagan ◽  
Michael Girard
Keyword(s):  
Risk Factor ◽  
Intraocular Pressure ◽  
Retinal Ganglion Cells ◽  
Visual Information ◽  
Ganglion Cells ◽  
Lamina Cribrosa ◽  
Retinal Ganglion ◽  
Irreversible Damage ◽  
Ocular Disorders ◽  
The Brain

Glaucoma describes a group of potentially blinding ocular disorders, afflicting c. 60 million people worldwide. Of these, c. 8 million are bilaterally blind, estimated to increase to 11 million by 2020. The central event in glaucoma is slow and irreversible damage of retinal ganglion cells, responsible for carrying visual information from the retina to the brain (Figure 1). Intraocular pressure (IOP) is a risk factor for glaucoma1–4, and significant, sustained IOP reduction is unequivocally beneficial in the clinical management of glaucoma patients2, 3, 5. Unfortunately, we do not understand how elevated IOP leads to the loss of retinal ganglion cells.

scholarly journals An Overview of Glaucoma: Bidirectional Translation between Humans and Pre-Clinical Animal Models

2021 ◽  
Author(s):  
Sophie Pilkinton ◽  
T.J. Hollingsworth ◽  
Brian Jerkins ◽  
Monica M. Jablonski
Keyword(s):  
Risk Factor ◽  
Intraocular Pressure ◽  
Optic Nerve ◽  
Animal Models ◽  
Retinal Ganglion Cells ◽  
Optic Nerve Head ◽  
Ganglion Cells ◽  
Treatment Modalities ◽  
Retinal Ganglion ◽  
Glaucomatous Damage

Glaucoma is a multifactorial, polygenetic disease with a shared outcome of loss of retinal ganglion cells and their axons, which ultimately results in blindness. The most common risk factor of this disease is elevated intraocular pressure (IOP), although many glaucoma patients have IOPs within the normal physiological range. Throughout disease progression, glial cells in the optic nerve head respond to glaucomatous changes, resulting in glial scar formation as a reaction to injury. This chapter overviews glaucoma as it affects humans and the quest to generate animal models of glaucoma so that we can better understand the pathophysiology of this disease and develop targeted therapies to slow or reverse glaucomatous damage. This chapter then reviews treatment modalities of glaucoma. Revealed herein is the lack of non-IOP-related modalities in the treatment of glaucoma. This finding supports the use of animal models in understanding the development of glaucoma pathophysiology and treatments.

Design of Experiments for Exposure of Astrocytes to Elevated Hydrostatic Pressure and Hypoxia

2008 ◽  
Author(s):  
Shadi Rajabi ◽  
Craig A. Simmons ◽  
C. Ross Ethier
Keyword(s):  
Intraocular Pressure ◽  
Visual Field ◽  
Retinal Ganglion Cells ◽  
Vision Loss ◽  
Ganglion Cells ◽  
Visual Field Loss ◽  
Retinal Ganglion ◽  
Common Cause ◽  
Elevated Intraocular Pressure

Glaucoma, a chronic optic neuropathy, is the second most common cause of blindness, affecting 67 million people worldwide. The damage in glaucoma occurs at the optic nerve head (ONH), where the axons of the retinal ganglion cells leave the eye posteriorly. Glaucoma is frequently associated with elevated intraocular pressure (IOP), and visual field loss can be prevented by significant lowering of IOP. Hence, the role of pressure in glaucoma is important. Unfortunately, the mechanism by which pressure leads to vision loss in glaucoma is very poorly understood.

scholarly journals Oral administration of a dual ETA/ETB receptor antagonist promotes neuroprotection in a rodent model of glaucoma

2020 ◽  
Author(s):  
Nolan R. McGrady ◽  
Dorota L. Stankowska ◽  
Hayden B. Jefferies ◽  
Raghu R. Krishnamoorthy
Keyword(s):  
Intraocular Pressure ◽  
Oral Administration ◽  
Receptor Antagonist ◽  
Ocular Hypertension ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Brown Norway ◽  
Retinal Ganglion ◽  
Elevated Intraocular Pressure ◽  
Iop Elevation

AbstractPurposeGlaucoma is a neurodegenerative disease associated with elevated intraocular pressure and characterized by optic nerve axonal degeneration, cupping of the optic disc and loss of retinal ganglion cells (RGCs). The endothelin (ET) system of vasoactive peptides (ET-1, ET-2, ET-3) and their G-protein coupled receptors (ETA and ETB receptors) have been shown to be contributors to the pathophysiology of glaucoma. The purpose of this study was to determine if administration of the endothelin receptor antagonist, macitentan, after the onset of IOP elevation, was neuroprotective to retinal ganglion cells in ocular hypertensive rats.MethodsBrown Norway rats were subjected to the Morrison model of ocular hypertension by injection of hypertonic saline through episcleral veins. Macitentan (5 and 10 mg/kg body wt/day) was administered orally following the elevation of IOP and rats with IOP elevation were maintained for 4 weeks. RGC function was determined by pattern electroretinography at 2 and 4 weeks post IOP elevation. Rats were euthanized by approved humane methods and retinal flat-mounts generated were immunostained with RGC-selective markers RBPMS and Brn3a. RGC counts were conducted in a masked manner.ResultsA significant protection of retinal ganglion cells against cell loss was found following oral administration of macitentan (5 and 10 mg/kg body wt/day) in rats with elevated intraocular pressure. In addition, treatment with macitentan was able to preserve RGC function as measured by pattern ERG analysis.ConclusionsMacitentan was able to promote neuroprotection independent of IOP-lowering suggesting that this could complement existing treatments to prevent neurodegeneration during ocular hypertension. The findings presented have implications for the use of macitentan as an oral formulation to promote neuroprotection in glaucoma patients.

scholarly journals Neuroprotective effect of Erigeron Breviscapus (vant) Hand-mazz extract on retinal ganglion cells in rabbits with chronic elevated intraocular pressure

2011 ◽  
Vol 5 (2) ◽  
pp. 195-203 ◽  
Author(s):  
Yi-sheng Zhong ◽  
Min-hong Xiang ◽  
Wen Ye ◽  
Ping Huang ◽  
Yu Cheng ◽  
...  
Keyword(s):  
Intraocular Pressure ◽  
Optic Nerve ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Neuroprotective Effect ◽  
Treated Group ◽  
Ultrastructural Changes ◽  
Retinal Ganglion ◽  
Elevated Intraocular Pressure ◽  
Erigeron Breviscapus

Abstract Background: Retinal ganglion cells (RGCs) are protected in rats with acute elevated intraocular pressure (IOP) by Erigeron breviscapus (vant.) hand-mazz (EBHM). However, it is unclear whether EBHM has neuroprotective effect on RGCs in animal with chronic elevated IOP. Objective: Investigate the protective effect of EBHM extract on RGCs in rabbits with chronic elevated IOP. Methods: Unilateral chronic elevated IOP was produced in rabbits by repeated injection of 2% methylcellulose into the anterior chamber. Secondary degeneration was measured with and without EBHM extract treatment for 60 days. At 60 days, the cells density of the RGCs layer, the thickness of retinal nerve fiber layer (RNFL), and the optic nerve axons were observed and analyzed using an image analysis system. The ultrastructural changes of RGCs and optic nerve axons were observed using transmission electron microscopy. Results: Compared with their contralateral control eyes with normal IOP, in the retinas of 3-4 mm from the optic disc, the cells density of the RGCs layer in the eyes with chronic elevated IOP was 23.2±6.5 cells (n = 6) and 36.0±8.9 cells (n = 10) per three 400x fields at 60 days in untreated and EBHM-treated group, respectively. The RNFL thickness in eyes with chronic elevated IOP was 3.4±0.4 μm (n = 6) and 5.0±1.0 μm (n = 10) at 60 days in untreated and EBHM-treated group, respectively. The axons number per 15057.8 μm2 in eyes with chronic elevated IOP was 370.4±41.0 (n = 6) and 439.0±50.8 (n = 10) at 60 days in untreated and EBHM-treated group, respectively. The number of the organelles in RGCs plasm appeared decreased and mitochondrion vacuolated in the elevated IOP eyes of EBHM-treated group, while some dispersive mitochondrion and rough surfaced endoplasmic reticulum and ribosome still existed in the RGCs plasm. The myelin sheath plates condensed and degenerated, and the microfilaments and microtubules decreased or disappeared in the elevated IOP eyes, but the axons degeneration in the chronic elevated IOP with EBHM treatment was less than that in the chronic elevated IOP without treatment. Conclusion: EBHM extract provided a neuroprotective effect on retinal ganglion cells in rabbits with chronic elevated IOP.

scholarly journals Effects of elevated intraocular pressure on mouse retinal ganglion cells

2005 ◽  
Vol 45 (2) ◽  
pp. 169-179 ◽  
Author(s):  
Jianzhong Ji ◽  
Peter Chang ◽  
Mark E. Pennesi ◽  
Zhuo Yang ◽  
Jian Zhang ◽  
...  
Keyword(s):  
Intraocular Pressure ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Elevated Intraocular Pressure

scholarly journals Expression of a Barhl1a reporter in subsets of retinal ganglion cells and commissural neurons of the developing zebrafish brain

2020 ◽  
Author(s):  
Shahad Albadri ◽  
Olivier Armant ◽  
Tairi Aljand-Geschwill ◽  
Filippo Del Bene ◽  
Matthias Carl ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Amacrine Cells ◽  
Optic Chiasm ◽  
Retinal Ganglion ◽  
Commissural Neurons ◽  
Axonal Projections ◽  
Underlying Mechanisms ◽  
And Function

AbstractPromoting the regeneration or survival of retinal ganglion cells (RGCs) is one focus of regenerative medicine. Homeobox Barhl transcription factors might be instrumental in these processes. In mammals, only barhl2 is expressed in the retina and is required for both subtype identity acquisition of amacrine cells and for the survival of RGCs downstream of Atoh7, a transcription factor necessary for RGC genesis. The underlying mechanisms of this dual role of Barhl2 in mammals have remained elusive. Whole genome duplication in the teleost lineage generated the barhl1a and barhl2 paralogues. In the Zebrafish retina, Barhl2 functions as determinant of subsets of amacrine cells lineally related to RGCs independently of Atoh7. In contrast, barhl1a expression depends on Atoh7 but its expression dynamics and function have not been studied. Here we describe for the first time a Barhl1a:GFP reporter line in vivo showing that Barhl1a turns on exclusively in subsets of RGCs and their post-mitotic precursors. We also show transient expression of Barhl1a:GFP in diencephalic neurons extending their axonal projections as part of the post-optic commissure, at the time of optic chiasm formation. This work sets the ground for future studies on RGC subtype identity, axonal projections and genetic specification of Barhl1a-positive RGCs and commissural neurons.

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