Neurodegeneration and Neuroprotection in Diabetic Retinopathy

Diabetic retinopathy is widely considered to be a neurovascular disease. This is in contrast to its previous identity as solely a vascular disease. Early in the disease progression of diabetes, the major cells in the neuronal component of the retina consist of retinal ganglion cells and glial cells,...

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Main Authors:	Ola, Mohammad Shamsul, Nawaz, Mohd Imtiaz, Khan, Haseeb A., Alhomida, Abdullah S.
Format:	Online
Language:	English
Published:	MDPI 2013
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3588002/

id	pubmed-3588002
recordtype	oai_dc
spelling	pubmed-35880022013-03-13 Neurodegeneration and Neuroprotection in Diabetic Retinopathy Ola, Mohammad Shamsul Nawaz, Mohd Imtiaz Khan, Haseeb A. Alhomida, Abdullah S. Review Diabetic retinopathy is widely considered to be a neurovascular disease. This is in contrast to its previous identity as solely a vascular disease. Early in the disease progression of diabetes, the major cells in the neuronal component of the retina consist of retinal ganglion cells and glial cells, both of which have been found to be compromised. A number of retinal function tests also indicated a functional deficit in diabetic retina, which further supports dysfunction of neuronal cells. As an endocrinological disorder, diabetes alters metabolism both systemically and locally in several body organs, including the retina. A growing body of evidences indicates increased levels of excitotoxic metabolites, including glutamate, branched chain amino acids and homocysteine in cases of diabetic retinopathy. Also present, early in the disease, are decreased levels of folic acid and vitamin-B12, which are potential metabolites capable of damaging neurons. These altered levels of metabolites are found to activate several metabolic pathways, leading to increases in oxidative stress and decreases in the level of neurotrophic factors. As a consequence, they may damage retinal neurons in diabetic patients. In this review, we have discussed those potential excitotoxic metabolites and their implications in neuronal damage. Possible therapeutic targets to protect neurons are also discussed. However, further research is needed to understand the exact molecular mechanism of neurodegeneration so that effective neuroprotection strategies can be developed. By protecting retinal neurons early in diabetic retinopathy cases, damage of retinal vessels can be protected, thereby helping to ameliorate the progression of diabetic retinopathy, a leading cause of blindness worldwide. MDPI 2013-01-28 /pmc/articles/PMC3588002/ /pubmed/23358247 http://dx.doi.org/10.3390/ijms14022559 Text en © 2013 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0 This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Ola, Mohammad Shamsul Nawaz, Mohd Imtiaz Khan, Haseeb A. Alhomida, Abdullah S.
spellingShingle	Ola, Mohammad Shamsul Nawaz, Mohd Imtiaz Khan, Haseeb A. Alhomida, Abdullah S. Neurodegeneration and Neuroprotection in Diabetic Retinopathy
author_facet	Ola, Mohammad Shamsul Nawaz, Mohd Imtiaz Khan, Haseeb A. Alhomida, Abdullah S.
author_sort	Ola, Mohammad Shamsul
title	Neurodegeneration and Neuroprotection in Diabetic Retinopathy
title_short	Neurodegeneration and Neuroprotection in Diabetic Retinopathy
title_full	Neurodegeneration and Neuroprotection in Diabetic Retinopathy
title_fullStr	Neurodegeneration and Neuroprotection in Diabetic Retinopathy
title_full_unstemmed	Neurodegeneration and Neuroprotection in Diabetic Retinopathy
title_sort	neurodegeneration and neuroprotection in diabetic retinopathy
description	Diabetic retinopathy is widely considered to be a neurovascular disease. This is in contrast to its previous identity as solely a vascular disease. Early in the disease progression of diabetes, the major cells in the neuronal component of the retina consist of retinal ganglion cells and glial cells, both of which have been found to be compromised. A number of retinal function tests also indicated a functional deficit in diabetic retina, which further supports dysfunction of neuronal cells. As an endocrinological disorder, diabetes alters metabolism both systemically and locally in several body organs, including the retina. A growing body of evidences indicates increased levels of excitotoxic metabolites, including glutamate, branched chain amino acids and homocysteine in cases of diabetic retinopathy. Also present, early in the disease, are decreased levels of folic acid and vitamin-B12, which are potential metabolites capable of damaging neurons. These altered levels of metabolites are found to activate several metabolic pathways, leading to increases in oxidative stress and decreases in the level of neurotrophic factors. As a consequence, they may damage retinal neurons in diabetic patients. In this review, we have discussed those potential excitotoxic metabolites and their implications in neuronal damage. Possible therapeutic targets to protect neurons are also discussed. However, further research is needed to understand the exact molecular mechanism of neurodegeneration so that effective neuroprotection strategies can be developed. By protecting retinal neurons early in diabetic retinopathy cases, damage of retinal vessels can be protected, thereby helping to ameliorate the progression of diabetic retinopathy, a leading cause of blindness worldwide.
publisher	MDPI
publishDate	2013
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3588002/
_version_	1611959331604922368

Neurodegeneration and Neuroprotection in Diabetic Retinopathy

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