scholarly journals Subthreshold Nano-Second Laser Treatment and Age-Related Macular Degeneration

2021 ◽  
Vol 10 (3) ◽  
pp. 484
Author(s):  
Amy C. Cohn ◽  
Zhichao Wu ◽  
Andrew I. Jobling ◽  
Erica L. Fletcher ◽  
Robyn H. Guymer
Keyword(s):  
Macular Degeneration ◽  
Laser Treatment ◽  
Short Pulse ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Nanosecond Laser ◽  
Age Related ◽  
Short Pulse Lasers

The presence of drusen is an important hallmark of age-related macular degeneration (AMD). Laser-induced regression of drusen, first observed over four decades ago, has led to much interest in the potential role of lasers in slowing the progression of the disease. In this article, we summarise the key insights from pre-clinical studies into the possible mechanisms of action of various laser interventions that result in beneficial changes in the retinal pigment epithelium/Bruch’s membrane/choriocapillaris interface. Key learnings from clinical trials of laser treatment in AMD are also summarised, concentrating on the evolution of laser technology towards short pulse, non-thermal delivery such as the nanosecond laser. The evolution in our understanding of AMD, through advances in multimodal imaging and functional testing, as well as ongoing investigation of key pathological mechanisms, have all helped to set the scene for further well-conducted randomised trials to further explore potential utility of the nanosecond and other subthreshold short pulse lasers in AMD.

scholarly journals Classical, Micropulse and NanoSecond Laser Therapy in Dry-Form (Non-Neovascular) Age-Related Macular Degeneration

2017 ◽  
pp. 155-159
Keyword(s):  
Macular Degeneration ◽  
Vision Loss ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Treatment Modalities ◽  
Nanosecond Laser ◽  
Laser Applications ◽  
Age Related ◽  
Neuroprotective Treatment

Age-related macular degeneration (AMD), which is a multifactorial, degenerative disease of the retina, is the most common reason for legal blindness over 50 years of age. Dry-form (non-neovascular) AMD is the common type, and frequently non-progressive to total vision loss. Epidemiological, histopathological, and biochemical data demonstrate that AMD is associated with oxidative damage, lipofuscin accumulation, chronic inflammation, and mutations in the complement system. Drusen, hyperpigmentation/hypopigmentation in retinal pigment epithelium, and geographical atrophy can also be observed in dry-form AMD. Various treatment modalities can be used according to the stages of the disease. Antioxidants, visual cycle inhibitors, anti-inflammatory agents, neuroprotective treatment, conventional, micropulse, and nano-second laser applications are intended to regulate the various mechanisms involved in the pathogenesis of the disease.

scholarly journals Mechanism of Inflammation in Age-Related Macular Degeneration: An Up-to-Date on Genetic Landmarks

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Francesco Parmeggiani ◽  
Francesco S. Sorrentino ◽  
Mario R. Romano ◽  
Ciro Costagliola ◽  
Francesco Semeraro ◽  
...  
Keyword(s):  
Macular Degeneration ◽  
Complex Disease ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Basic Research ◽  
Cholesterol Homeostasis ◽  
Age Related Macular Degeneration ◽  
Age Related ◽  
Immune Mediated

Age-related macular degeneration (AMD) is the most common cause of irreversible visual impairment among people over 50 years of age, accounting for up to 50% of all cases of legal blindness in Western countries. Although the aging represents the main determinant of AMD, it must be considered a multifaceted disease caused by interactions among environmental risk factors and genetic backgrounds. Mounting evidence and/or arguments document the crucial role of inflammation and immune-mediated processes in the pathogenesis of AMD. Proinflammatory effects secondary to chronic inflammation (e.g., alternative complement activation) and heterogeneous types of oxidative stress (e.g., impaired cholesterol homeostasis) can result in degenerative damages at the level of crucial macular structures, that is photoreceptors, retinal pigment epithelium, and Bruch’s membrane. In the most recent years, the association of AMD with genes, directly or indirectly, involved in immunoinflammatory pathways is increasingly becoming an essential core for AMD knowledge. Starting from the key basic-research notions detectable at the root of AMD pathogenesis, the present up-to-date paper reviews the best-known and/or the most attractive genetic findings linked to the mechanisms of inflammation of this complex disease.

scholarly journals Classical, Micropulse and NanoSecond Laser Therapy in Dry-Form (Non-Neovascular) Age-Related Macular Degeneration

2017 ◽  
pp. 155-159
Keyword(s):  
Macular Degeneration ◽  
Vision Loss ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Treatment Modalities ◽  
Nanosecond Laser ◽  
Laser Applications ◽  
Age Related ◽  
Neuroprotective Treatment

Age-related macular degeneration (AMD), which is a multifactorial, degenerative disease of the retina, is the most common reason for legal blindness over 50 years of age. Dry-form (non-neovascular) AMD is the common type, and frequently non-progressive to total vision loss. Epidemiological, histopathological, and biochemical data demonstrate that AMD is associated with oxidative damage, lipofuscin accumulation, chronic inflammation, and mutations in the complement system. Drusen, hyperpigmentation/hypopigmentation in retinal pigment epithelium, and geographical atrophy can also be observed in dry-form AMD. Various treatment modalities can be used according to the stages of the disease. Antioxidants, visual cycle inhibitors, anti-inflammatory agents, neuroprotective treatment, conventional, micropulse, and nano-second laser applications are intended to regulate the various mechanisms involved in the pathogenesis of the disease.

Classical, Micropulse and NanoSecond Laser Therapy in Dry-Form (Non-Neovascular) Age-Related Macular Degeneration

2017 ◽  
pp. 155-159
Keyword(s):  
Macular Degeneration ◽  
Vision Loss ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Treatment Modalities ◽  
Nanosecond Laser ◽  
Laser Applications ◽  
Age Related ◽  
Neuroprotective Treatment

Age-related macular degeneration (AMD), which is a multifactorial, degenerative disease of the retina, is the most common reason for legal blindness over 50 years of age. Dry-form (non-neovascular) AMD is the common type, and frequently non-progressive to total vision loss. Epidemiological, histopathological, and biochemical data demonstrate that AMD is associated with oxidative damage, lipofuscin accumulation, chronic inflammation, and mutations in the complement system. Drusen, hyperpigmentation/hypopigmentation in retinal pigment epithelium, and geographical atrophy can also be observed in dry-form AMD. Various treatment modalities can be used according to the stages of the disease. Antioxidants, visual cycle inhibitors, anti-inflammatory agents, neuroprotective treatment, conventional, micropulse, and nano-second laser applications are intended to regulate the various mechanisms involved in the pathogenesis of the disease.

scholarly journals Melatonin in Retinal Physiology and Pathology: The Case of Age-Related Macular Degeneration

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Janusz Blasiak ◽  
Russel J. Reiter ◽  
Kai Kaarniranta
Keyword(s):  
Oxidative Stress ◽  
Macular Degeneration ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Protective Role ◽  
Premature Aging ◽  
Age Related Macular Degeneration ◽  
Age Related ◽  
Established Role

Melatonin, an indoleamine, is synthesized mainly in the pineal gland in a circadian fashion, but it is produced in many other organs, including the retina, which seems to be especially important as the eye is a primary recipient of circadian signals. Melatonin displays strong antioxidative properties, which predispose it to play a protective role in many human pathologies associated with oxidative stress, including premature aging and degenerative disease. Therefore, melatonin may play a role in age-related macular degeneration (AMD), a disease affecting photoreceptors, and retinal pigment epithelium (RPE) with an established role of oxidative stress in its pathogenesis. Several studies have shown that melatonin could exert the protective effect against damage to RPE cells evoked by reactive oxygen species (ROS), but it has also been reported to increase ROS-induced damage to photoreceptors and RPE. Melatonin behaves like synthetic mitochondria-targeted antioxidants, which concentrate in mitochondria at relatively high levels; thus, melatonin may prevent mitochondrial damage in AMD. The retina contains telomerase, an enzyme implicated in maintaining the length of telomeres, and oxidative stress inhibits telomere synthesis, while melatonin overcomes this effect. These features support considering melatonin as a preventive and therapeutic agent in the treatment of AMD.

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 Complement C5 is not critical for the formation of sub-RPE deposits in Efemp1 mutant mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Donita L. Garland ◽  
Eric A. Pierce ◽  
Rosario Fernandez-Godino
Keyword(s):  
Macular Degeneration ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Deposit Formation ◽  
Genetic Ablation ◽  
Age Related ◽  
Complement Dysregulation

AbstractThe complement system plays a role in the formation of sub-retinal pigment epithelial (RPE) deposits in early stages of age-related macular degeneration (AMD). But the specific mechanisms that connect complement activation and deposit formation in AMD patients are unknown, which limits the development of efficient therapies to reduce or stop disease progression. We have previously demonstrated that C3 blockage prevents the formation of sub-RPE deposits in a mouse model of EFEMP1-associated macular degeneration. In this study, we have used double mutant Efemp1R345W/R345W:C5-/- mice to investigate the role of C5 in the formation of sub-RPE deposits in vivo and in vitro. The data revealed that the genetic ablation of C5 does not eliminate the formation of sub-RPE deposits. Contrarily, the absence of C5 in RPE cultures promotes complement dysregulation that results in increased activation of C3, which likely contributes to deposit formation even in the absence of EFEMP1-R345W mutant protein. The results also suggest that genetic ablation of C5 alters the extracellular matrix turnover through an effect on matrix metalloproteinases in RPE cell cultures. These results confirm that C3 rather than C5 could be an effective therapeutic target to treat early AMD.

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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