scholarly journals Current Treatment Limitations in Age-Related Macular Degeneration and Future Approaches Based on Cell Therapy and Tissue Engineering

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
P. Fernández-Robredo ◽  
A. Sancho ◽  
S. Johnen ◽  
S. Recalde ◽  
N. Gama ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Cell Therapy ◽  
Macular Degeneration ◽  
Pigment Epithelium ◽  
Treatment Options ◽  
Age Related Macular Degeneration ◽  
Western World ◽  
Ageing Population ◽  
The European Union ◽  
Age Related

Age-related macular degeneration (AMD) is the leading cause of blindness in the Western world. With an ageing population, it is anticipated that the number of AMD cases will increase dramatically, making a solution to this debilitating disease an urgent requirement for the socioeconomic future of the European Union and worldwide. The present paper reviews the limitations of the current therapies as well as the socioeconomic impact of the AMD. There is currently no cure available for AMD, and even palliative treatments are rare. Treatment options show several side effects, are of high cost, and only treat the consequence, not the cause of the pathology. For that reason, many options involving cell therapy mainly based on retinal and iris pigment epithelium cells as well as stem cells are being tested. Moreover, tissue engineering strategies to design and manufacture scaffolds to mimic Bruch’s membrane are very diverse and under investigation. Both alternative therapies are aimed to prevent and/or cure AMD and are reviewed herein.

Tissue Engineering approaches towards the regeneration of Biomimetic Scaffolds for Age-Related Macular Degeneration

2021 ◽  
Author(s):  
Shambhavi Bagewadi ◽  
Sowmya Parameswaran ◽  
Krishnakumar Subramanian ◽  
Swaminathan Sethuraman ◽  
Anuradha Subramanian
Keyword(s):  
Tissue Engineering ◽  
Retinal Pigment Epithelium ◽  
Macular Degeneration ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Irreversible Loss ◽  
The Third ◽  
Age Related ◽  
Biomimetic Scaffolds

Age-related macular degeneration (AMD) is the third major cause of blindness in people aged above 60 years. It causes dysfunction of retinal pigment epithelium (RPE) and leads to irreversible loss...

scholarly journals A Potential New Role for Zinc in Age-Related Macular Degeneration through Regulation of Endothelial Fenestration

2021 ◽  
Vol 22 (21) ◽  
pp. 11974
Author(s):  
Fiona Cunningham ◽  
Sabrina Cahyadi ◽  
Imre Lengyel
Keyword(s):  
Macular Degeneration ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Western World ◽  
Uniform Size ◽  
Age Related ◽  
Typical Morphology ◽  
Fenestrated Endothelium ◽  
Zinc Concentrations

Age-related macular degeneration (AMD) is a common blinding disease in the western world that is linked to the loss of fenestration in the choriocapillaris that sustains the retinal pigment epithelium and photoreceptors in the back of the eye. Changes in ocular and systemic zinc concentrations have been associated with AMD; therefore, we hypothesized that these changes might be directly involved in fenestrae formation. To test this hypothesis, an endothelial cell (bEND.5) model for fenestrae formation was treated with different concentrations of zinc sulfate (ZnSO4) solution for up to 20 h. Fenestrae were visualized by staining for Plasmalemmal Vesicle Associated Protein-1 (PV-1), the protein that forms the diaphragms of the fenestrated endothelium. Size and distribution were monitored by transmission electron microscopy (TEM). We found that zinc induced the redistribution of PV-1 into areas called sieve plates containing ~70-nm uniform size and typical morphology fenestrae. As AMD is associated with reduced zinc concentrations in the serum and in ocular tissues, and dietary zinc supplementation is recommended to slow disease progression, we propose here that the elevation of zinc concentration may restore choriocapillaris fenestration resulting in improved nutrient flow and clearance of waste material in the retina.

Tissue Translocation Device for Surgical Correction of Age-Related Macular Degeneration

2013 ◽  
Vol 7 (4) ◽  
Author(s):  
George Mathai ◽  
David Rosen ◽  
Shreyes Melkote ◽  
Timothy Olsen
Keyword(s):  
Shape Memory ◽  
Macular Degeneration ◽  
Ex Vivo ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Potential Method ◽  
Age Related Macular Degeneration ◽  
Western World ◽  
Age Related

Age-related macular degeneration (AMD) is the leading cause of blindness in the western world in those over age 60. While this disorder is complex, the origin of injury appears to be at the level of the retinal pigment epithelium (RPE), Bruchs membrane, and inner choroid. A potential method to replace damaged tissue in AMD is to harvest healthy donor tissue (RPE-Bruchs-Choroid) from an eye and translocate it to the injured subretinal region. Such an autograft avoids immune mediated rejection and can theoretically restore function to the neurosensory retina (light sensitive part of the retina) by restoring the damaged tissue. Such a procedure requires the design of a device that mechanically supports the integrity of the graft while inside the eye, without injuring or disrupting the tissue. This paper presents the systematic design and manufacture of a thin shape memory foil-based tissue translocation device. The selected embodiment of the design uses thermal adhesion of the tissue to the foil surfaces for tissue support. The shape memory effect enables insertion of the device into the eye via a small incision. The device is manufactured using micromachining techniques and has been tested both ex vivo and in vivo with acceptable anatomic results.

Age-related macular degeneration treatment: current view (literature review)

2014 ◽  
Vol 21 (1) ◽  
pp. 43-50
Author(s):  
Monika Kalesinskaitė ◽  
Diana Uljanionok ◽  
Rasa Liutkevičienė
Keyword(s):  
Macular Degeneration ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Treatment Options ◽  
Geographic Atrophy ◽  
Age Related Macular Degeneration ◽  
Current View ◽  
Neovascular Amd ◽  
Age Related ◽  
Dry Amd

Age-related macular degeneration (AMD) – is a damage of the macula, accompanied by a significant and irreversible loss of central vision. It is a major cause of blindness and visual impairment in older adults (>60 years). Damage of the retina always includes both eyes, though the intensity can vary. Early AMD is defined as the presence of drusen and retinal pigmentary abnormalities (RPE); late AMD includes dry AMD (geographic atrophy of the RPE in the absence of neovascular AMD) or neovascular AMD  (detachment of the retinal pigment epithelium, hemorrhages, and/or scars). Unfortunately, the etiology and pathogenesis of AMD aren’t fully understood up to now, so treatment options are limited and not always effective. This article briefly reviews the options of initial and late forms of AMD treatment

scholarly journals Peroxisome Proliferator-Activated Receptor and Age-Related Macular Degeneration

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-11 ◽  
Author(s):  
Alexandra A. Herzlich ◽  
Jingsheng Tuo ◽  
Chi-Chao Chan
Keyword(s):  
Macular Degeneration ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Disease Process ◽  
Ppar Gamma ◽  
Age Related Macular Degeneration ◽  
Western World ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Age Related

Age-related macular degeneration (AMD) is the leading cause of new blindness in the western world and is becoming more of a socio-medical problem as the proportion of the aged population increases. There are multiple efforts underway to better understand this disease process. AMD involves the abnormal retinal pigment epithelium (RPE), drusen formation, photoreceptor atrophy, and choroidal neovascularization. Peroxisome proliferator-activated receptors (PPARs) play an important role in lipid degeneration, immune regulation, regulation of reactive oxygen species (ROSs), as well as regulation of vascular endothelial growth factor (VEGF), matrix metalloproteinase-9 (MMP-9), and docosahexaenoic acid (DHA). These molecules have all been implicated in the pathogenesis of AMD. In addition, PPAR gamma is expressed in RPE, an essential cell in photoreceptor regeneration and vision maintenance. This review summarizes the interactions between PPAR, AMD-related molecules, and AMD-related disease processes.

scholarly journals Role of amyloid β-peptide in the pathogenesis of age-related macular degeneration

2021 ◽  
Vol 6 (1) ◽  
pp. e000774
Author(s):  
Minwei Wang ◽  
Shiqi Su ◽  
Shaoyun Jiang ◽  
Xinghuai Sun ◽  
Jiantao Wang
Keyword(s):  
Mitochondrial Dysfunction ◽  
Macular Degeneration ◽  
Vision Loss ◽  
Cell Structure ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Amyloid Β ◽  
Age Related Macular Degeneration ◽  
Amyloid Β Peptide ◽  
Age Related

Age-related macular degeneration (AMD) is the most common eye disease in elderly patients, which could lead to irreversible vision loss and blindness. Increasing evidence indicates that amyloid β-peptide (Aβ) might be associated with the pathogenesis of AMD. In this review, we would like to summarise the current findings in this field. The literature search was done from 1995 to Feb, 2021 with following keywords, ‘Amyloid β-peptide and age-related macular degeneration’, ‘Inflammation and age-related macular degeneration’, ‘Angiogenesis and age-related macular degeneration’, ‘Actin cytoskeleton and amyloid β-peptide’, ‘Mitochondrial dysfunction and amyloid β-peptide’, ‘Ribosomal dysregulation and amyloid β-peptide’ using search engines Pubmed, Google Scholar and Web of Science. Aβ congregates in subretinal drusen of patients with AMD and participates in the pathogenesis of AMD through enhancing inflammatory activity, inducing mitochondrial dysfunction, altering ribosomal function, regulating the lysosomal pathway, affecting RNA splicing, modulating angiogenesis and modifying cell structure in AMD. The methods targeting Aβ are shown to inhibit inflammatory signalling pathway and restore the function of retinal pigment epithelium cells and photoreceptor cells in the subretinal region. Targeting Aβ may provide a novel therapeutic strategy for AMD.

scholarly journals A Review of Completed and Ongoing Complement Inhibitor Trials for Geographic Atrophy Secondary to Age-Related Macular Degeneration

2021 ◽  
Vol 10 (12) ◽  
pp. 2580
Author(s):  
Omar A. Halawa ◽  
Jonathan B. Lin ◽  
Joan W. Miller ◽  
Demetrios G. Vavvas
Keyword(s):  
Macular Degeneration ◽  
Geographic Atrophy ◽  
Age Related Macular Degeneration ◽  
Western World ◽  
Complement Factor ◽  
Complement Protein ◽  
Pivotal Phase ◽  
Complement Inhibition ◽  
Exudative Amd ◽  
Age Related

Age-related macular degeneration (AMD) is a leading cause of irreversible blindness among older adults in the Western world. While therapies exist for patients with exudative AMD, there are currently no approved therapies for non-exudative AMD and its advanced form of geographic atrophy (GA). The discovery of genetic variants in complement protein loci with increased susceptibility to AMD has led to the investigation of the role of complement inhibition in AMD with a focus on GA. Here, we review completed and ongoing clinical trials evaluating the safety and efficacy of these studies. Overall, complement inhibition in GA has yielded mixed results. The inhibition of complement factor D has failed pivotal phase 3 trials. Studies of C3 and C5 inhibition meeting their primary endpoint are limited by high rates of discontinuation and withdrawal in the treatment arm and higher risks of conversion to exudative AMD. Studies evaluating other complement members (CFB, CFH, CFI and inhibitors of membrane attack complex—CD59) are ongoing and could offer other viable strategies.

scholarly journals Retinal Pigment Epithelium Expressed Toll-like Receptors and Their Potential Role in Age-Related Macular Degeneration

2021 ◽  
Vol 22 (16) ◽  
pp. 8387
Author(s):  
Alexa Klettner ◽  
Johann Roider
Keyword(s):  
Retinal Pigment Epithelium ◽  
Inflammatory Response ◽  
Macular Degeneration ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Current Status ◽  
Toll Like Receptors ◽  
Cell Degeneration ◽  
Age Related

(1) Background: Inflammation is a major pathomechanism in the development and progression of age-related macular degeneration (AMD). The retinal pigment epithelium (RPE) may contribute to retinal inflammation via activation of its Toll-like receptors (TLR). TLR are pattern recognition receptors that detect the pathogen- or danger-associated molecular pattern. The involvement of TLR activation in AMD is so far not understood. (2) Methods: We performed a systematic literature research, consulting the National Library of Medicine (PubMed). (3) Results: We identified 106 studies, of which 54 were included in this review. Based on these studies, the current status of TLR in AMD, the effects of TLR in RPE activation and of the interaction of TLR activated RPE with monocytic cells are given, and the potential of TLR activation in RPE as part of the AMD development is discussed. (4) Conclusion: The activation of TLR2, -3, and -4 induces a profound pro-inflammatory response in the RPE that may contribute to (long-term) inflammation by induction of pro-inflammatory cytokines, reducing RPE function and causing RPE cell degeneration, thereby potentially constantly providing new TLR ligands, which could perpetuate and, in the long run, exacerbate the inflammatory response, which may contribute to AMD development. Furthermore, the combined activation of RPE and microglia may exacerbate neurotoxic effects.

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