Objective. The aim of this study was to assess age-related visual functions (visual acuity and contrast sensitivity) and compare the results by different age groups. Material and Methods. A total of 231 patients were examined. The patients were divided into 5 age groups: 10 patients in group 1, 30–39 years; 40 patients in the group 2, 40–49 years; 77 patients in the group 3, 50–59 years; 71 patients in the group 4, 60–70 years; and 33 patients in the group 5, 71–85 years. A typical Snellen’s chart (the direction of the gap in Landolt C) was used for noncorrected and best-corrected visual acuity testing. Contrast sensitivity was evaluated by employing a Ginsburg Box, VSCR-CST-6500. Results. Noncorrected visual acuity was significantly better in the group 2 than the group 3 (0.86 [0.28] vs. 0.69 [0.33], P=0.018). Moreover, noncorrected and best-corrected visual acuity was significantly better in the group 4 than the group 5 (0.52 [0.35] vs. 0.35 [0.28], P<0.001; and 0.9 [0.21] vs. 0.69 [0.27], P<0.005, respectively). Contrast sensitivity at the nighttime without glare was significantly worse in the group 2 than the group 1 at the spatial frequencies of 3, 12, and 18 cycles per degree (P=0.001, P=0.05, and P=0.01, respectively). The patients in the group 2 had significantly worse contrast sensitivity at the nighttime and daytime with glare at the spatial frequencies of 1.5, 12, and 18 cycles per degree (P=0.054, P=0.04, and P=0.01 and P=0.011, P=0.031, and P=0.011, respectively). The greatest differences in contrast sensitivity were observed between the groups 4 and 5, and it was 2 to 4 times better in the group 4. Comparing these groups, all the differences at the nighttime and daytime with and without glare were significant. Conclusions. Contrast sensitivity was worst among the oldest persons (71–85 years), and it began to worsen already in the persons aged 40–49 years. Contrast sensitivity was very similar in the age groups of 40–49 and 50–59 years.

Background: Age-related macular degeneration (AMD) affects the central part of the retina and causes blindness. In developed countries, AMD occurs in people over 50 years old. Important factors for AMD pathogenesis are an immune response, inflammation, and genetic factors. This study aimed to determine the impact of IL1RL1 rs1041973 and IL1RAP rs4624606 single nucleotide polymorphisms (SNPs) on the occurrence of AMD and the outcome of treatment with aflibercept and bevacizumab. Patients and Methods: 563 patients with AMD and 281 healthy candidates were evaluated. Patients with exudative AMD were treated with intravitreal bevacizumab and aflibercept and, after 6 months based on the changes in bestcorrected visual acuity and central macular thickness, were classified as 'responders' or 'poor-responders'. Genotyping of IL1RL1 rs1041973 and IL1RAP rs4624606 was accomplished using real-time PCR. Age was compared using the Mann-Whitney U-test. Categorical data (gender, genotype, and allele distributions) compared between groups using the χ 2 test or the Fisher's exact test. Associations of gene polymorphisms were calculated using logistic regression analysis with adjustment for age in exudative and atrophic AMD analysis. An adjusted significance threshold for multiple comparisons α=0.025 was applied. Results: Statistically significant differences in the distribution of IL1RAP rs4624606 genotypes (TT, TA and AA) were found between males with atrophic AMD and controls: 50%, 42.9% and 7.1% vs. 69.7%, 30.3% and 0%, respectively, p=0.015. Moreover, we found that 'responders' had a significantly better best-corrected visual acuity than 'poor-responders' before treatment (p=0.032). The central macular thickness was significantly lower in exudative AMD patients with IL1RL1 rs1041973 AA genotype than in wild type and heterozygous (CC+CA) genotype carriers before treatment (p=0.017). Conclusion: IL1RAP rs4624606 may be associated with atrophic AMD in males while IL1RL1 rs1041973 may play a protective role against macular thickening in exudative AMD patients. Age-related macular degeneration (AMD), the leading cause of blindness in developed countries, is a complex disease caused entirely by environmental, demographic, and genetic factors (1, 2). AMD is classified into early or intermediate stages with the formation of drusen, an amorphous extracellular deposit in the retina, and characteristic pigmentary changes, and late stages, which may either be atrophic (geographic atrophy) or wet (neovascular type) (3). Early stages of the disease are often clinically asymptomatic. It progresses slowly and evolves into late AMD only in 10-20% of patients, of which two-thirds have neovascular and one-third atrophic AMD type (4). Late forms are characterized by the irreversible loss of central vision. Treatment in clinical practice is currently available only for the neovascular type: intraocular injections with VEGF inhibitors; there are no clinically approved treatment options for atrophic AMD and/or the possibility to stop early AMD forms...

Considering the immunological impairment in age-related macular degeneration (AMD), we aimed to determine the associations of IL-9 rs1859430, rs2069870, rs11741137, rs2069885, and rs2069884 and IL-10 rs1800871, rs1800872, and rs1800896 polymorphisms and their haplotypes, as well as the serum levels of IL-9 and IL-10 with AMD. 1209 participants were enrolled in our study. SNPs were genotyped using TaqMan SNP genotyping assays by real-time PCR method. IL-9 and IL-10 serum levels were evaluated using ELISA kits. Our study results have shown that haplotypes A-G-C-G-G and G-A-T-A-T of IL-9 SNPs are associated with the decreased odds of early AMD occurrence ( p = 0.035 and p = 0.015 , respectively). A set of rare haplotypes was associated with the decreased odds of exudative AMD occurrence ( p = 0.033 ). Also, IL-10 serum levels were lower in exudative AMD than in controls ( p = 0.049 ), patients with early AMD ( p = 0.017 ), and atrophic AMD ( p = 0.008 ). Furthermore, exudative AMD patients with IL-10 rs1800896 CT and TT genotypes had lower IL-10 serum concentrations than those with wild-type (CC) genotype ( p = 0.048 ). In conclusion, our study suggests that IL-10 serum levels can be associated with a minor allele at IL-10 rs1800896 and exudative AMD. The haplotypes of IL-9 SNPs were also associated with the decreased odds of early and exudative AMD.

The results of the color contrast sensitivity test decreased by half in patients with AMD compared with ophthalmologically healthy patients when they performed the F-M 100 test and by one and half when they performed a MCCS test in the blue color range.

Our study aimed to reveal the associations between VEGFA SNPs (rs1570360, rs699947, rs3025033, and rs2146323), their haplotypes, VEGF-A and VEGF-R2 serum concentrations, and early and exudative AMD. A total of 339 subjects with early AMD and 419 with exudative AMD groups, and 374 healthy subjects, were genotyped for four VEGFA SNPs (rs1570360, rs699947, rs3025033, and rs2146323). VEGF-A and VEGFR-2 serum concentrations were measured in exudative AMD and controls. The results revealed that rs3025033 G allele was significantly associated with lower odds of exudative AMD under the dominant model (OR = 0.67; 95% CI: 0.49–0.80; p = 0.0088) and additive (OR = 0.7; 95% CI: 0.54–0.90; p = 0.0058) models after Bonferroni correction. In the female group, rs3025033 AG genotype was associated with exudative AMD under the codominant model (OR = 0.57; 95% CI: 0.37–0.87; p = 0.009) and G allele under the dominant (OR = 0.55; 95% CI: 0.37–0.82; p = 0.0032) and additive models (OR = 0.60; 95% CI: 0.42–0.84; p = 0.0028). Haplotype analysis revealed that individuals carrying rs1570360, rs699947, rs3025033, and rs2146323 haplotype A-A-G-A had decreased risk of exudative AMD (OR = 0.46, 95% CI: 0.23–0.90; p = 0.023). The VEGF-A and VEGF-R2 serum concentrations did not differ between study groups; we found that patients with exudative AMD carrying at least one C allele at rs699947 have statistically significantly higher VEGF-A serum concentrations compared to AA genotype carriers (485.95 (945.93) vs. 194.97 (-), respectively, p = 0.046). In conclusion, we found that VEGFA rs3025033 and haplotype rs1570360A-rs699947A-rs3025033G- rs2146323A play a protective role for exudative AMD in the Caucasian population. Furthermore, rs699947 is associated with elevated VEGF-A serum concentrations in exudative AMD.