NDLI: Retinal Neurodegeneration in the Course of Diabetes-Pathogenesis and Clinical Perspective.

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Retinal Neurodegeneration in the Course of Diabetes-Pathogenesis and Clinical Perspective.

Content Provider	Europe PMC
Author	Araszkiewicz, Aleksandra Zozulinska-Ziolkiewicz, Dorota
Copyright Year	2016
Abstract	Diabetic retinopathy is generally considered as a microvascular disease which develops as a result of chronic hyperglycaemia. However, the neuronal apoptosis and reactive gliosis are recently postulated as early changes in diabetic retinopathy. This phenomenon is described as a neurodegeneration and suggests that diabetic retinopathy should be recognized as a neurovascular complication. In this review, we discuss the mechanisms leading to the neurodegeneration of the retina in diabetic patients including: low-grade inflammatory process, oxidative stress, activation of polymorphonuclear neutrophils, glutamate excitotoxicity and imbalance in the neuroprotective factors. Secondly, we point out the clinical significance of measuring the retinal neurodegeneration.
ISSN	1570159X
Journal	Current Neuropharmacology
Volume Number	14
PubMed Central reference number	PMC5333590
Issue Number	8
PubMed reference number	26915422
e-ISSN	18756190
DOI	10.2174/1570159X14666160225154536
Language	English
Publisher	Bentham Science Publishers
Publisher Date	2016-01-01
Access Restriction	Open
Rights License	This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited. © 2016 Bentham Science Publishers
Subject Keyword	Diabetes mellitus diabetic retinopathy inflammatory process neurodegeneration oxidative stress retina
Content Type	Text
Resource Type	Article
Subject	Neurology Neurology (clinical) Pharmacology Pharmacology (medical) Psychiatry and Mental Health

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