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Glaucoma is considered a chronic disease that requires lifelong management. Chronic diseases are known to be highly associated with psychological disturbances such as depression and anxiety. There have also been many studies on association between anxiety or depression and glaucoma. The majority of these studies explained that the glaucoma diagnosis causes anxiety or depression. However, It is also necessary to evaluate whether the psychological disturbance itself affect glaucoma. Therefore, we investigated the association of anxiety and depression with glaucoma progression, and elucidate mechanisms underlying that. We included 251 eyes with open angle glaucoma who were followed up for at least 2 years in this retrospective case–control study. The Beck Anxiety Inventory (BAI) and Beck Depressive Inventory-II (BDI-II) were used to assess anxiety and depression in glaucoma patients. Patients were classified into groups (high-anxiety group; HA-G, low-anxiety group; LA-G, high-depression group; HD-G, low-depression group; LD-G) according to their score on the BAI or BDI-II (separately). In logistic regression analysis, disc hemorrhage, peak intraocular pressure (IOP) and RNFL thickness loss rate were significantly associated with high anxiety ( p  = 0.017, p  = 0.046, p  = 0.026). RNFL thinning rate and disc hemorrhage were significant factors associated with anxiety in multivariate models ( p  = 0.015, p  = 0.019). Multivariate linear regression analysis showed a significant positive correlation between the rate of RNFL thickness loss and BAI score (B = 0.058; 95% confidential interval = 0.020–0.097; p  = 0.003), and RNFL loss and IOP fluctuation (B = 0.092; 95% confidential interval = 0.030–0.154; p  = 0.004). For the depression scale, visual field mean deviation and heart rate variability were significantly associated with high depression in multivariate logistic regression analysis ( p  = 0.003, p  = 0.006). We suggest that anxiety increase the risk of glaucoma progression and they are also associated with IOP profile and disc hemorrhage.

Diabetes mellitus and glaucoma are the two major causes of selective retinal ganglion cell (RGC) death. To determine the relationship between autophagy and RGC death, we compared autophagy and the related molecular pathways in diabetic and glaucomatous retinas and examined their effect on RGC survival. Biochemical analysis of microtubule-associated protein light chain 3 (LC3)-II and beclin-1 were observed. To determine the pathways involved in autophagy induction, adenosine monophosphate-activated protein kinase (AMPK) and the mechanistic target of rapamycin (mTOR) were also explored. Beclin-1 and the LC3B-II to LC3B-I ratio significantly elevated at 4 and 8 weeks after glaucoma induction; however, only a slight increase was apparent in the diabetic retina. Significant upregulation of phosphorylated AMPK and downregulation of phosphorylated mTOR was evident in the diabetic retina. After autophagy was inhibited with 3-methyladenine (3-MA), apoptosis of RGCs was significantly increased in the diabetic retinas. However, 3-MA inhibition of autophagy decreased the apoptosis of RGCs in glaucomatous retinas. Therefore, our results suggest that RGC death is differentially regulated by autophagy and that the pathways involved differ depending on the triggering injury.

Pathologic myopia causes vision impairment and blindness, and therefore, necessitates a prompt diagnosis. However, there is no standardized definition of pathologic myopia, and its interpretation by 3D optical coherence tomography images is subjective, requiring considerable time and money. Therefore, there is a need for a diagnostic tool that can automatically and quickly diagnose pathologic myopia in patients. This study aimed to develop an algorithm that uses 3D optical coherence tomography volumetric images (C-scan) to automatically diagnose patients with pathologic myopia. The study was conducted using 367 eyes of patients who underwent optical coherence tomography tests at the Ophthalmology Department of Incheon St. Mary’s Hospital and Seoul St. Mary’s Hospital from January 2012 to May 2020. To automatically diagnose pathologic myopia, a deep learning model was developed using 3D optical coherence tomography images. The model was developed using transfer learning based on four pre-trained convolutional neural networks (ResNet18, ResNext50, EfficientNetB0, EfficientNetB4). Grad-CAM was used to visualize features affecting the detection of pathologic myopia. The performance of each model was evaluated and compared based on accuracy, sensitivity, specificity, and area under the receiver operating characteristic curve (AUROC). The model based on EfficientNetB4 showed the best performance (95% accuracy, 93% sensitivity, 96% specificity, and 98% AUROC) in identifying pathologic myopia.

This retrospective study investigated the risk of primary open-angle glaucoma (POAG) among individuals identified as glaucoma suspects and examined associated cardiovascular risk factors. We conducted a longitudinal, nationwide cohort study using data from the Korean National Health Insurance Service (KNHIS) and included 362,285 participants aged ≥ 40 years from the Korean National Health Screening Program (NHSP) without pre-existing POAG in 2009 and 2010. Of these, glaucoma suspects ( n  = 32,220) were defined as individuals with at least two recorded instances of the KCD code H400 for glaucoma suspect and no prior antiglaucoma medication prescriptions before health screening. The primary outcome was the diagnosis of POAG and the prescription of antiglaucoma medications. Over a 6-year follow-up, 4.92% of glaucoma suspects developed POAG. Through multivariate Cox regression analysis, glaucoma suspects with diabetes, hypertension, dyslipidemia, or coronary heart disease exhibited a greater risk of conversion to POAG than those without these comorbidities ([HR, 1.354; 95%CI, 1.201 to 1.527] for diabetes, [HR, 1.139; 95%CI, 1.019 to 1.273] for systemic hypertension, [HR, 1.128; 95%CI, 1.013 to 1.26] for dyslipidemia, [HR, 1.124, 95%CI, 1.007 to 1.254] for coronary heart disease).This nationwide study observed that among glaucoma suspects, having cardiovascular risk factors/disease was associated with higher risk of developing POAG.

In patients with glaucomatous parafoveal scotoma, evidence of compromised vascular circulation was commonly seen. The purpose of this study is to evaluate the relationship between macular vascular density (VD) and central visual function and structure in glaucoma patients. We enrolled 46 eyes of normal tension glaucoma (NTG) patients with parafoveal scotoma. All subjects underwent measurement of segmented macular thickness in each layer and optical coherence tomography angiography (OCTA) to assess VD of macula. Correlation coefficients of VD with structural parameters were identified and multivariate regression analyses were performed to verify factors affecting the MD of SITA 10-2. Superficial VD in NFL, GCL and IPL showed significant correlation with thickness of those layers, but deep VD in INL did not show meaningful correlation with any structural parameters. However, deep VD showed significant correlations with central visual field parameters such as MD of SITA 10-2. By multivariate regression analysis, the significant factors affecting central visual function were deep VD. Different multivariate regression models including segmented macular thicknesses were compared and R 2 value was best for the model with deep VD, not containing superficial VD (R 2  = 0.326, p  = 0.001). Assigning subjects as worse or better visual functional group using regression line, deep VD of worse functional group was significantly lower than that of better group. In couclusion, decreased deep VD was an independent risk factor for central scotoma in addition to structural thinning. Taking both macular thickness and vascular circulation into acount, the deterioration of central visual function could be predicted more precisely.

Temporal visual field damage (VFD) is the common type of non-glaucomatous VF defects found in eyes with myopia. However, little is known about the factors associated with its progression. We investigated the characteristic of myopic eyes with progressive temporal VF defects. This retrospective, observational study included a total of 116 eyes: 39 eyes with temporal VFDs and an axial length greater than 24.5 mm, 77 eyes with typical glaucomatous VFDs who were followed up more than 5 years. VF progression was evaluated with Trend-based global progression analysis. In the temporal VFD group, the greater tilt ratios, the higher prevalence of β-zone peripapillary atrophy (β-PPA), the substantial increase in β-PPA were found, compared to the typical glaucomatous VFD groups (all P -values ≤ 0.001). The temporal VFD group had the slower progression than the typical glaucomatous VFD group on trend-based GPA ( P  = 0.047). In the multivariate linear regression analysis, the change of β-PPA area over years was related to temporal VFD progression (B, − 0.000088, P  = 0.003). In conclusion, myopic eyes with the temporal VFD, which come with growing β-PPA area, should be monitored with extra caution.

We investigated the characteristics of localized vessel density defects (VD) either in the deep or superficial vascular layer of normal-tension glaucoma patients using optical coherence tomography angiography (OCTA). In this retrospective, cross-sectional study, 74 eyes with localized retinal nerve fiber layer (RNFL) defect were included. The relationships between the widths of the VD in the superficial and deep layer and ocular factors were evaluated. Eyes with greater deep VD were significantly older ( P  = 0.023). The IOP measured at OCTA exam was significantly related to the width of the deep VD ( P  = 0.009). By contrast, average ganglion cell inner plexiform layer thickness (GCIPLT) was substantially related to the width of the superficial VD ( P  = 0.004). In logistic regression analysis, aging was noticeably associated with wider deep VD, whereas worse mean deviation (MD) had a significant association with wider superficial VD ( P  = 0.001, P  = 0.003, respectively). In sum, while changes of the superficial layer seemed an overall ramification of glaucomatous damages, the deep layer was more likely to be affected by factors related to ocular microcirculation, such as IOPs and older age. Thus, looking into the deep vascular layer using OCTA could identify risk factors related to the disturbance in ocular microcirculation.

Using either 24-2 or 10-2 visual field (VF) testing only is not enough to cover all the various types of glaucomatous VF defects. We investigated the performance of the combined 24-2 and 10-2 perimetry when conducted together and separately using the structure–function relationship. A total of 30 glaucoma patients with isolated peripheral nasal step, 37 patients with isolated paracentral scotoma, and 38 patients with both paracentral and nasal scotoma were included. To create the combined Humphrey VF test, a custom test pattern was established using the built-in custom point options, an example of the X, Y coordinate system. In glaucoma patients with peripheral nasal step, the superotemporal topographic structure–function relationship with peripapillary retinal nerve fiber layer (RNFL) thickness was superior in relation to the combined or 24-2 perimetry relative to the 10-2 perimetry (both P < 0.05). The combined VF test showed more favorable inferotemporal or inferonasal structure–function correlation with the corresponding ganglion cell–inner plexiform layer (GCIPL) thickness when compared with results gleaned using the 24-2 VF test (P < 0.05). Simultaneously performed 24-2 and 10-2 VF tests demonstrated a superior topographic structure–function relationship when compared with them separately performed in some sectors.

Human minibrain is an effective model for studying drug effects on neurodegenerative diseases like AD. AR1001, a phosphodiesterase-5 (PDE5) inhibitor, is being tested in a global Phase 3 clinical trial for early AD at a dosage of 30 mg QD (NCT05531526). This study aims to evaluate effects of AR1001 in the minibrain model. Three models of human minibrain were used: single-cultured astrocytes, single-cultured microglia, and a triculture (neurons, astrocytes and microglia). In the single-culture models, cells were seeded on day 1 and treated with oAβ (1μM) and IFN-γ, with or without AR1001 (0.1, 1, and 10μM), from day 0 to day 2. Analyses using immunohistochemistry, ELISA, and immunofluorescence microscopy were conducted on day 2. In the tri-culture model, neural precursor cells in the central compartment were differentiated for 3 weeks, followed by AR1001 treatment every 2 days for 6 weeks. Microglia were added to the annular compartment, and experiments concluded 4 days later. In single-cultured astrocytes, AR1001 significantly enhanced oAβ clearance at 1 and 10μM reducing oAβ-induced inflammatory markers, such as C3 (10μM), NO (0.1, 1, and 10μM), and H O (1 and 10μM). In single-cultured microglia, AR1001 notably increased microglia recruitment (10μM) and oAβ clearance (0.1, 1, and 10μM), while decreasing inflammatory markers like CD86 (0.1, 1, and 10μM) and NO (10μM), and elevating the anti-inflammatory marker CD206 (0.1, 1, and 10μM). In the tri-culture model, AR1001 inhibited microglial recruitment into the central compartment (0.1, 1, and 10μM) and reduced Aβ1-42 in the medium (1 and 10μM). It also reduced CD86 (1 and 10μM) and C3 (0.1, 1, and 10μM), while showing trends of increasing CCL2, CCL5, CXCL1, CXCL10, serpin E1 and C-GSF, and decreasing IL-8. Additionally, AR1001 markedly restored synapsin 1 and NeuN levels (1 and 10μM) and inhibited increases in p -tau181 and p -tau217 (0.1, 1, and 10μM) induced by oAβ. We found that AR1001 effectively clears oAβ and exhibits anti-inflammatory effects in astrocytes and microglia. It also provides significant protective effects in neurons, reducing p -tau levels. These findings highlight the multiple beneficial effects of AR1001 on key brain components: astrocytes, microglia, and neurons.

This study investigated the region-specific roles of transforming growth factor-β2 (TGF-β2) and angiotensin II (AngII) in extracellular matrix (ECM) remodeling and inflammatory responses within scleral tissues surrounding the optic nerve head (ONH), using primary human fibroblasts from posterior sclera, peripapillary sclera (ppScl), and fibroblast-like cells from lamina cribrosa (LC). In vivo validation was performed in a chronic ocular hypertension rat model. Fibrotic and inflammatory markers were analyzed by Western blotting, quantitative PCR, and immunocytochemistry following TGF-β2 or AngII stimulation, and in vivo effects were assessed after subtenon injection of pathway-specific inhibitors. TGF-β2 induced robust upregulation of α-smooth muscle actin, collagen type I, and fibronectin across all scleral regions, whereas AngII elicited regionally confined pro-inflammatory responses, particularly in the LC and ppScl, characterized by increased cyclooxygenase-2 expression. Inhibition of either pathway reduced ECM deposition in vivo, but only AngII blockade significantly attenuated glial activation and preserved retinal ganglion cells. These findings demonstrate that TGF-β2 predominantly drives fibrosis, while AngII promotes region-specific neuroinflammation, and that inflammation, rather than fibrosis alone, plays a critical role in glaucomatous neurodegeneration. Targeting both fibrotic and inflammatory mechanisms in a region-specific manner may offer improved neuroprotection in glaucoma.