scholarly journals Early retinal neurodegeneration in preclinical diabetic retinopathy: a multifactorial investigation

Eye ◽  
2019 ◽  
Vol 34 (6) ◽  
pp. 1100-1107 ◽  
Author(s):  
Ibrahim Toprak ◽  
Semin Melahat Fenkci ◽  
Guzin Fidan Yaylali ◽  
Cigdem Martin ◽  
Volkan Yaylali
Keyword(s):  
Diabetic Retinopathy ◽  
Retinal Neurodegeneration

Retinal microglia polarization in diabetic retinopathy

2021 ◽  
Vol 38 ◽  
Author(s):  
Xin Li ◽  
Zi-Wei Yu ◽  
Hui-Yao Li ◽  
Yue Yuan ◽  
Xin-Yuan Gao ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Diabetic Retinopathy ◽  
Cytokine Production ◽  
Immune Cell ◽  
Microvascular Disease ◽  
Retinal Diseases ◽  
Microglia Polarization ◽  
Retinal Microglia ◽  
The Central Nervous System ◽  
Retinal Neurodegeneration

Abstract Microglia, the main immune cell of the central nervous system (CNS), categorized into M1-like phenotype and M2-like phenotype, play important roles in phagocytosis, cell migration, antigen presentation, and cytokine production. As a part of CNS, retinal microglial cells (RMC) play an important role in retinal diseases. Diabetic retinopathy (DR) is one of the most common complications of diabetes. Recent studies have demonstrated that DR is not only a microvascular disease but also retinal neurodegeneration. RMC was regarded as a central role in neurodegeneration and neuroinflammation. Therefore, in this review, we will discuss RMC polarization and its possible regulatory factors in early DR, which will provide new targets and insights for early intervention of DR.

scholarly journals Retinal Neurodegeneration in Diabetic Patients Without Diabetic Retinopathy

2016 ◽  
Vol 57 (14) ◽  
pp. 6455 ◽  
Author(s):  
Joana Tavares Ferreira ◽  
Marta Alves ◽  
Arnaldo Dias-Santos ◽  
Lívio Costa ◽  
Bruno Oliveira Santos ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Diabetic Patients ◽  
Retinal Neurodegeneration

scholarly journals Detecting retinal neurodegeneration in people with diabetes: Findings from the UK Biobank

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0257836
Author(s):  
Roomasa Channa ◽  
Kyungmoo Lee ◽  
Kristen A. Staggers ◽  
Nitish Mehta ◽  
Sidra Zafar ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Glycated Hemoglobin ◽  
Retinal Thickness ◽  
Self Report ◽  
Inner Plexiform Layer ◽  
Uk Biobank ◽  
Fiber Layer ◽  
Cross Sectional ◽  
Retinal Neurodegeneration ◽  
The Uk

Importance Efforts are underway to incorporate retinal neurodegeneration in the diabetic retinopathy severity scale. However, there is no established measure to quantify diabetic retinal neurodegeneration (DRN). Objective We compared total retinal, macular retinal nerve fiber layer (mRNFL) and ganglion cell-inner plexiform layer (GC-IPL) thickness among participants with and without diabetes (DM) in a population-based cohort. Design/setting/participants Cross-sectional analysis, using the UK Biobank data resource. Separate general linear mixed models (GLMM) were created using DM and glycated hemoglobin as predictor variables for retinal thickness. Sub-analyses included comparing thickness measurements for patients with no/mild diabetic retinopathy (DR) and evaluating factors associated with retinal thickness in participants with and without diabetes. Factors found to be significantly associated with DM or thickness were included in a multiple GLMM. Exposure Diagnosis of DM was determined via self-report of diagnosis, medication use, DM-related complications or glycated hemoglobin level of ≥ 6.5%. Main outcomes and measures Total retinal, mRNFL and GC-IPL thickness. Results 74,422 participants (69,985 with no DM; 4,437 with DM) were included. Median age was 59 years, 46% were men and 92% were white. Participants with DM had lower total retinal thickness (-4.57 μm, 95% CI: -5.00, -4.14; p<0.001), GC-IPL thickness (-1.73 μm, 95% CI: -1.86, -1.59; p<0.001) and mRNFL thickness (-0.68 μm, 95% CI: -0.81, -0.54; p<0.001) compared to those without DM. After adjusting for co-variates, in the GLMM, total retinal thickness was 1.99 um lower (95% CI: -2.47, -1.50; p<0.001) and GC-IPL was 1.02 μm lower (95% CI: -1.18, -0.87; p<0.001) among those with DM compared to without. mRNFL was no longer significantly different (p = 0.369). GC-IPL remained significantly lower, after adjusting for co-variates, among those with DM compared to those without DM when including only participants with no/mild DR (-0.80 μm, 95% CI: -0.98, -0.62; p<0.001). Total retinal thickness decreased 0.40 μm (95% CI: -0.61, -0.20; p<0.001), mRNFL thickness increased 0.20 μm (95% CI: 0.14, 0.27; p<0.001) and GC-IPL decreased 0.26 μm (95% CI: -0.33, -0.20; p<0.001) per unit increase in A1c after adjusting for co-variates. Among participants with diabetes, age, DR grade, ethnicity, body mass index, glaucoma, spherical equivalent, and visual acuity were significantly associated with GC-IPL thickness. Conclusion GC-IPL was thinner among participants with DM, compared to without DM. This difference persisted after adjusting for confounding variables and when considering only those with no/mild DR. This confirms that GC-IPL thinning occurs early in DM and can serve as a useful marker of DRN.

scholarly journals Lower Somatostatin Expression Is an Early Event in Diabetic Retinopathy and Is Associated With Retinal Neurodegeneration

Diabetes Care ◽  
2007 ◽  
Vol 30 (11) ◽  
pp. 2902-2908 ◽  
Author(s):  
E. Carrasco ◽  
C. Hernandez ◽  
A. Miralles ◽  
P. Huguet ◽  
J. Farres ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Early Event ◽  
Retinal Neurodegeneration ◽  
Somatostatin Expression

scholarly journals Iron Overload in Diabetic Retinopathy: A Cause or a Consequence of Impaired Mechanisms?

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Andreea Ciudin ◽  
Cristina Hernández ◽  
Rafael Simó
Keyword(s):  
Diabetic Retinopathy ◽  
Iron Overload ◽  
Iron Homeostasis ◽  
Cell Function ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Renin Angiotensin System ◽  
Retinal Neurodegeneration ◽  
Novel Therapeutic Strategies

Iron is an essential ion for life, playing a central role in many metabolic processes. The most important property of free iron is its capacity to be reversibly oxidized and reduced, but at same time this make it highly pro-oxidant molecule. In this regard, iron is able to generate powerful reactive oxygen species (ROS). For this reason, careful control on iron availability is central to the maintenance of normal cell function in the retina. In the diabetic eye there is an impairment of iron homeostasis, thus leading to iron overload. The mechanisms involved in this process include: (1) Destruction of heme molecules induced by hyperglycemia (2) Intraretinal and vitreal hemorrhages (3) Overexpression of the renin-angiotensin system. The main consequences of iron overload are the following: (1) Retinal neurodegeneration due to the increase of oxidative stress (2) Increase of AGE-RAGE binding (3) Defective phagocytosis of retinal pigment epithelium, which generates the accumulation of autoantigens and the synthesis of proinflammatory cytokines. Further studies addressed to explore not only the role of iron in the pathogenesis of diabetic retinopathy, but also to design novel therapeutic strategies based on the regulation of iron homeostasis are needed.

scholarly journals Associations of diabetic retinopathy with retinal neurodegeneration on the background of diabetes mellitus. Overview of recent medical studies with an assessment of the impact on healthcare systems

Open Medicine ◽  
2018 ◽  
Vol 13 (1) ◽  
pp. 130-136 ◽  
Author(s):  
Rafał Muc ◽  
Agnieszka Saracen ◽  
Iwona Grabska-Liberek
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Retinopathy ◽  
Treatment Strategies ◽  
The Body ◽  
Medical Studies ◽  
Body Tissues ◽  
Retinal Neurodegeneration ◽  
Mutual Relations ◽  
Microvascular And Macrovascular Complications ◽  
The Impact

AbstractDiabetes Mellitus (DM) is one of the biggest healthcare and financial problems worldwide. The disease is strongly associated with microvascular and macrovascular complications, causing co-existing diseases like Diabetic Retinopathy, Diabetic Neuropathy and Diabetic Nephropathy. Annual healthcare expenditures for diabetes treatment and complications prevention cost 727 billion USD in year 2017.Diabetes Mellitus, Diabetic Retinopathy and Diabetic Retinal Neuropathy are closely related diseases - originating from incorrectly controlled glycemia, blood pressure and lipid levels in the course of increasing resistance of the body tissues to insulin.Irrespectively of thorough programs for Diabetes Mellitus prevention and treatment, Diabetic Retinopathy management requires targeted treatment strategies for both microvasculopathy and retinal neurodegeneration, to delay disease severity course and risk of blindness.The study and conclusions in this article are based on web-available data and officially published articles related to the diabetes mellitus and associated diseases – Diabetic Retinopathy and Diabetic Retinal Neuropathy. The articles have been reviewed and analyzed to assess mutual relations between the discussed diseases.

scholarly journals Retinal neurodegeneration may precede microvascular changes characteristic of diabetic retinopathy in diabetes mellitus

2016 ◽  
Vol 113 (19) ◽  
pp. E2655-E2664 ◽  
Author(s):  
Elliott H. Sohn ◽  
Hille W. van Dijk ◽  
Chunhua Jiao ◽  
Pauline H. B. Kok ◽  
Woojin Jeong ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Retinopathy ◽  
Plexiform Layer ◽  
Capillary Density ◽  
Diabetic Mouse ◽  
Inner Plexiform Layer ◽  
Fiber Layer ◽  
Microvascular Changes ◽  
Retinal Neurodegeneration

Diabetic retinopathy (DR) has long been recognized as a microvasculopathy, but retinal diabetic neuropathy (RDN), characterized by inner retinal neurodegeneration, also occurs in people with diabetes mellitus (DM). We report that in 45 people with DM and no to minimal DR there was significant, progressive loss of the nerve fiber layer (NFL) (0.25 μm/y) and the ganglion cell (GC)/inner plexiform layer (0.29 μm/y) on optical coherence tomography analysis (OCT) over a 4-y period, independent of glycated hemoglobin, age, and sex. The NFL was significantly thinner (17.3 μm) in the eyes of six donors with DM than in the eyes of six similarly aged control donors (30.4 μm), although retinal capillary density did not differ in the two groups. We confirmed significant, progressive inner retinal thinning in streptozotocin-induced “type 1” and B6.BKS(D)-Leprdb/J “type 2” diabetic mouse models on OCT; immunohistochemistry in type 1 mice showed GC loss but no difference in pericyte density or acellular capillaries. The results suggest that RDN may precede the established clinical and morphometric vascular changes caused by DM and represent a paradigm shift in our understanding of ocular diabetic complications.

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