scholarly journals Fructosamine-3-Kinase as a Potential Treatment Option for Age-Related Macular Degeneration

2020 ◽  
Vol 9 (9) ◽  
pp. 2869
Author(s):  
Sander De Bruyne ◽  
Caroline Van den Broecke ◽  
Henk Vrielinck ◽  
Samira Khelifi ◽  
Olivier De Wever ◽  
...  

Age-related macular degeneration is the leading cause of blindness in the developed world. Since advanced glycation end products (AGEs) are implicated in the pathogenesis of AMD through various lines of evidence, we investigated the potential of fructosamine-3-kinase (FN3K) in the disruption of retinal AGEs, drusenoid material and drusenoid lesions in patients with AMD. AGE-type autofluorescence was measured to evaluate the effects of FN3K on glycolaldehyde-induced AGE-modified neural porcine retinas and unmodified human neural retinas. Eye pairs from cigarette-smoke- and air-exposed mice were treated and evaluated histologically. Automated optical image analysis of human tissue sections was performed to compare control- and FN3K-treated drusen and near-infrared (NIR) microspectroscopy was performed to examine biochemical differences. Optical coherence tomography (OCT) was used to evaluate the effect of FN3K on drusenoid deposits after treatment of post-mortem human eyes. FN3K treatment provoked a significant decrease (41%) of AGE-related autofluorescence in the AGE-modified porcine retinas. Furthermore, treatment of human neural retinas resulted in significant decreases of autofluorescence (−24%). FN3K-treated murine eyes showed less drusenoid material. Pairwise comparison of drusen on tissue sections revealed significant changes in color intensity after FN3K treatment. NIR microspectroscopy uncovered clear spectral differences in drusenoid material (Bruch’s membrane) and drusen after FN3K treatment. Ex vivo treatment strongly reduced size of subretinal drusenoid lesions on OCT imaging (up to 83%). In conclusion, our study demonstrated for the first time a potential role of FN3K in the disruption of AGE-related retinal autofluorescence, drusenoid material and drusenoid lesions in patients with AMD.

Vision ◽  
2018 ◽  
Vol 2 (4) ◽  
pp. 38
Author(s):  
Taariq Mohammed ◽  
Yuehong Tong ◽  
Julia Agee ◽  
Nayanika Challa ◽  
Rainer Heintzmann ◽  
...  

To characterize fluorophore signals from drusen and retinal pigment epithelium (RPE) and their changes in age related macular degeneration (AMD), the authors describe advances in ex vivo hyperspectral autofluorescence (AF) imaging of human eye tissue. Ten RPE flatmounts from eyes with AMD and 10 from eyes without AMD underwent 40× hyperspectral AF microscopic imaging. The number of excitation wavelengths tested was initially two (436 nm and 480 nm), then increased to three (436 nm, 480 nm, and 505 nm). Emission spectra were collected at 10 nm intervals from 420 nm to 720 nm. Non-negative matrix factorization (NMF) algorithms decomposed the hyperspectral images into individual emission spectra and their spatial abundances. These include three distinguishable spectra for RPE fluorophores (S1, S2, and S3) in both AMD and non-AMD eyes, a spectrum for drusen (SDr) only in AMD eyes, and a Bruch’s membrane spectrum that was detectable in normal eyes. Simultaneous analysis of datacubes excited atthree excitation wavelengths revealed more detailed spatial localization of the RPE spectra and SDr within drusen than exciting only at two wavelengths. Within AMD and non-AMD groups, two different NMF initialization methods were tested on each group and converged to qualitatively similar spectra. In AMD, the peaks of the SDr at ~510 nm (436 nm excitation) were particularly consistent. Between AMD and non-AMD groups, corresponding spectra in common, S1, S2, and S3, also had similar peak locations and shapes, but with some differences and further characterization warranted.


2007 ◽  
Vol 84 (2) ◽  
pp. 378-380 ◽  
Author(s):  
Robert F. Mullins ◽  
Marissa A. Olvera ◽  
Abbot F. Clark ◽  
Edwin M. Stone

2020 ◽  
Author(s):  
M Rizzi ◽  
K Powell ◽  
MR Robinson ◽  
T Matsuki ◽  
J Hoke ◽  
...  

AbstractMacular degeneration is the leading cause of blindness in the developed world. Whilst most patients lose sight owing to atrophic changes, no treatments currently exist that improve the vision deficit due to atrophy. Here, we identify loss of lateral inhibition as a specific mechanism by which photoreceptor degeneration reduces visual function beyond the atrophic area. We find that this inhibition is adaptive, and that if modulated can improve visual function, making inhibitory circuits an unexpected therapeutic target for age related macular degeneration and related disorders.


2021 ◽  
Vol 5 (1) ◽  
pp. 168-176
Author(s):  
Abdul Karim Ansyori

Photodynamic therapy (PDT) is a therapy that uses drugs, called photosensitizers or photosensitizing agents, and a specific type of light. When photosensitizers are exposed to certain wavelengths of light, they produce oxygen that kills nearby cells. PDT is achieved by a photodynamic reaction induced by the excitation of a photosensitizer exposed to light. In the field of ophthalmology, PDT was approved for the first time about ten years ago for cases of age-related macular degeneration (AMD). Neovascular age-related macular degeneration (AMD) is a vision-threatening disease characterized by pathological macular neovascularization. After that, PDT was approved for use in choroidal neovascularization (CNV) cases in pathological myopia.3 This literature review aims to describe the history of PDT use and the basic principles of photodynamic therapy in ophthalmology.


2019 ◽  
Vol 186 ◽  
pp. 107718 ◽  
Author(s):  
Seeneevasan Aberami ◽  
Sampath Nikhalashree ◽  
Muthuvel Bharathselvi ◽  
Jyotirmay Biswas ◽  
Konerirajapuram Natarajan Sulochana ◽  
...  

Age-related macular degeneration (AMD) is the major cause of blindness for the elderly population in the developed world. Although vision loss is mainly due to the neovascular form, dry AMD remains a challenge for ophthalmologists because of the lack of effective therapies. The Age-Related Eye Disease Study (AREDS) demonstrated the protective effect of dietary supplementation of antioxidants to slow down the progression of dry AMD. On the other hand, there has been no proven drug treatment for dry AMD to date. This review is aimed to discuss recent non-nutritional treatments for dry AMD and geographic atrophy.


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