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Open AccessJournal ArticleDOI

A Dietary Combination of Forskolin with Homotaurine, Spearmint and B Vitamins Protects Injured Retinal Ganglion Cells in a Rodent Model of Hypertensive Glaucoma.

TLDR
The hypothesis is that the diet supplement may be used to counteract the inflammatory processes triggered by glial cell activation, thus leading to spared RGC loss and the preservation of visual dysfunction, and the present compound may be viewed as a potential remedy to be added to the currently approved drug therapies for improving RGC protection.
Abstract
There is indication that nutritional supplements protect retinal cells from degeneration. In a previous study, we demonstrated that dietary supplementation with an association of forskolin, homotaurine, spearmint extract and B vitamins efficiently counteracts retinal dysfunction associated with retinal ganglion cell (RGC) death caused by optic nerve crush. We extended our investigation on the efficacy of dietary supplementation with the use of a mouse model in which RGC degeneration depends as closely as possible on intraocular pressure (IOP) elevation. In this model, injecting the anterior chamber of the eye with methylcellulose (MCE) causes IOP elevation leading to RGC dysfunction. The MCE model was characterized in terms of IOP elevation, retinal dysfunction as determined by electrophysiological recordings, RGC loss as determined by brain-specific homeobox/POU domain protein 3A immunoreactivity and dysregulated levels of inflammatory and apoptotic markers. Except for IOP elevation, dysfunctional retinal parameters were all recovered by dietary supplementation indicating the involvement of non-IOP-related neuroprotective mechanisms of action. Our hypothesis is that the diet supplement may be used to counteract the inflammatory processes triggered by glial cell activation, thus leading to spared RGC loss and the preservation of visual dysfunction. In this respect, the present compound may be viewed as a potential remedy to be added to the currently approved drug therapies for improving RGC protection.

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Citations
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Journal ArticleDOI

Glaucoma: A Degenerative Optic Neuropathy Related to Neuroinflammation?

TL;DR: The experimental and clinical data obtained to date are summarized and the need to develop neuroprotective and immunomodulatory therapies to prevent blindness in glaucoma patients are highlighted.
Journal ArticleDOI

Nicotinamide-Rich Diet in DBA/2J Mice Preserves Retinal Ganglion Cell Metabolic Function as Assessed by PERG Adaptation to Flicker.

TL;DR: F-PERG adaptation may provide a non-invasive tool to assess RGC autoregulation in response to increased metabolic demand and test the effect of dietary/pharmacological treatments on optic nerve disorders.
Journal ArticleDOI

Melatonin and the control of intraocular pressure.

TL;DR: The current work highlights the important role of melatonin and its analogues in the healthy and in the glaucomatous eyes, with special attention to the control of intraocular pressure.
Journal ArticleDOI

Natural Products: Evidence for Neuroprotection to Be Exploited in Glaucoma.

TL;DR: The literature on the neuroprotective activities, and the underlying mechanisms, of natural compounds and dietary supplements in experimental and clinical glaucoma are reviewed.
Journal ArticleDOI

Protection of retinal ganglion cells in glaucoma: Current status and future.

TL;DR: A review of the recent neuroprotective strategies for glaucoma can be found in this paper, both in clinical trials and in laboratory research, with a focus on the role of retinal ganglion cells (RGCs).
References
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Journal ArticleDOI

Dose translation from animal to human studies revisited

TL;DR: BSA correlates well across several mammalian species with several parameters of biology, including oxygen utilization, caloric expenditure, basal metabolism, blood volume, circulating plasma proteins, and renal function, and is advocated as a factor when converting a dose for translation from animals to humans.
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Vitamin B3 modulates mitochondrial vulnerability and prevents glaucoma in aged mice

TL;DR: Studying glaucoma-prone mice, it is shown that mitochondrial abnormalities are an early driver of neuronal dysfunction, occurring before detectable degeneration, and this supports therapeutic use of vitamin B3 in glau coma and potentially other age-related neurodegenerations.
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Progressive ganglion cell loss and optic nerve degeneration in DBA/2J mice is variable and asymmetric.

TL;DR: A comparison of the data collected from the two cohorts of mice used for this study suggests that the initial site of damage in this disease is to the axons in the optic nerve, followed by the subsequent death of the ganglion cell soma.
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A randomized trial of brimonidine versus timolol in preserving visual function: results from the Low-Pressure Glaucoma Treatment Study.

TL;DR: Low-pressure glaucoma patients treated with brimonidine 0.2% who do not develop ocular allergy are less likely to have field progression than patients treating with timolol 0.5%, and similar differences in progression were observed when analyzed by GCPM and the 3-omitting method.
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Reactive oxygen species, nutrition, hypoxia and diseases: Problems solved?

TL;DR: In this review, aspects and problems on the role of intracellular ROS formation and nutrition with the link to diseases and their problematic therapeutical issues are discussed.
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