Abstract:BACKGROUND: The aim of this study was to evaluate the long-term treatment success and safety of ab externo canaloplasty in glaucoma patients. Abstract:METHODS AND MATERIAL: This study included 44 eyes undergoing canaloplasty. Patients were followed up at 2, 6, 12 months, 3 years and 5 years. Abstract:RESULTS: The preoperative intraocular pressure (IOP) was 23.6 ± 6.4 mmHg and was reduced to 15.8 ± 4.5 mmHg at 12 months, 15.6 ± 3.8 mmHg at 3 years and 14.9 ± 3.9 mmHg at 5 years after canaloplasty (p < 0.0001). The relative IOP reduction was 33.6 ± 17.6% after 12 months, 30.4 ± 22.7% after 3 years and 35.1 ± 17.7% after 5 years. Topical glaucoma medications were reduced from 3.0 ± 1.3 to 1.2 ± 1.3 at 12 months, 1.3 ± 1.4 at 3 years and 1.2 ± 1.3 at 5 years (p < 0.0001). The complete surgical success rate (without topical glaucoma medications) was 32.3%, 26.9%, and 20.0% after 5 years for IOP < 21 mmHg, < 18 mmHg, and < 16 mmHg, respectively. The qualified surgical success (with topical glaucoma medications) was 72.0%, 65.8%, and 43.1%, respectively. Six patients underwent 360° trabeculotomy and five patients received laser Descemet puncture during the first 6 months after surgery. Abstract:CONCLUSION: Canaloplasty is a safe and effective procedure to achieve a significant reduction in IOP and glaucoma medications up to 5 years after surgery. Greater SC widths were associated with lower IOP values.

Das Glaukom ist eine der häufigsten Erblindungsursachen weltweit, so auch in Deutschland. Dennoch ist unklar, ob alle Betroffenen ausreichend über ihre Erkrankung sowie mögliche Therapien und deren Nebenwirkungen informiert sind. Umfrage unter GlaukompatientInnen, um den Stand der Aufklärung über die Erkrankung und mögliche Therapien zu erfassen. Der Fragenbogen bestand aus 11 Fragen zur Aufklärung und Therapiezufriedenheit bezüglich des Glaukoms. Er wurde vom Bundesverband Glaukom-Selbsthilfe e. V. in Zusammenarbeit mit der Sektion Glaukom der Deutschen Ophthalmologischen Gesellschaft (DOG) entwickelt. Der Fragebogen wurde den Mitgliedern des Bundesverbandes sowie über die Homepage und Patientenforen zugänglich gemacht und in Wartezimmern ausgelegt. Es nahmen 334 GlaukompatientInnen von Juli 2024 bis Juni 2025 an der Umfrage teil; 15,5

Glaucoma, a leading cause of irreversible blindness, is primarily managed by lowering intraocular pressure, yet treatment remains limited by poor adherence, ocular surface toxicity, and systemic adverse effects. This review focuses specifically on treatment simplification strategies in topical glaucoma therapy, exploring the paradigm shift towards a "Less is better" approach in glaucoma care, with particular emphasis on the use of preservative -free formulations, lower active ingredient concentrations, and fixed combinations. These approaches aim to improve treatment tolerability, adherence, and clinical outcomes while minimizing toxicity, complexity, and environmental burden. Although barriers such as higher costs and limited long-term data remain, this new approach represents a patient-centred, sustainable, and clinically effective model for the future of glaucoma management.

BACKGROUND:Glaucoma is one of the most frequent causes of blindness worldwide, including in Germany; however, it is unclear whether all those affected are sufficiently informed about their condition, possible treatment and their side effects. OBJECTIVE:Survey of glaucoma patients to assess the level of awareness about the disease and its treatment. METHODS:The questionnaire consisted of 11 specific questions that asked about education and satisfaction with treatment for glaucoma. It was developed by the Federal Association Glaucoma Self-help (Bundesverband Glaukom-Selbsthilfe e. V). in collaboration with the Glaucoma Section of the German Society of Ophthalmology (DOG) and made available to members of the association as well via the website and patient forums and in waiting rooms. RESULTS:A total of 334 glaucoma patients participated in the survey between July 2024 and June 2025. Of the respondents 15.5% stated that they were very well informed, while 40.1% reported they had been inadequately informed. There was a lack of information on treatment options and side effects as well as on the prescribed eye drops. Patients therefore sought alternative sources of information (e.g., the internet). Results were also mixed when it came to information about treatment use and side effects and 89.5% said they knew how to use their treatment. Approximately 50% were able to discuss changes to their treatment or information about alternative treatments with their doctor. CONCLUSION:The findings from this survey should be used to develop more targeted patient education strategies in the future. Patient-centered understandable and continuous education should be a central component of treatment. This would contribute to improved adherence and thus also to the quality of life of those affected.

Abstract:BACKGROUND: Neurodegenerative diseases are an increasing challenge for healthcare systems in the context of demographic change. They affect the central nervous system, including the brain-manifesting, for example, as dementia-as well as the retina, as seen in glaucoma or age-related macular degeneration. Malnutrition-defined as quantitative or qualitative under- or overnutrition-affects key mechanisms that contribute to neuronal and retinal neurodegeneration. Abstract:OBJECTIVE: The aim of this study is to systematically present the pathophysiological mechanisms of malnutrition-related neurodegeneration, to evaluate the current evidence on dietary patterns and cognitive health, and to derive practical clinical strategies for nutritional optimization. Abstract:METHODS: Narrative literature review based on peer-reviewed publications from the fields of nutritional medicine, geriatrics, neurology, ophthalmology, and public health. Abstract:RESULTS: Malnutrition promotes oxidative stress, mitochondrial dysfunction, chronic neuroinflammation, and vascular dysregulation, and it influences neurotransmitter synthesis. These mechanisms are relevant to both cerebral and ocular neurodegenerative processes. The Mediterranean diet and the MIND diet are associated with a significantly reduced risk of cognitive impairment; for ocular diseases, interventional studies in age-related macular degeneration in particular demonstrate protective effects of antioxidant supplementation, whereas evidence for glaucoma is currently based predominantly on observational data. Screening approaches and micronutrient diagnostics enable early identification of at-risk individuals. Building on this, individualised dietary interventions and targeted supplementation of selected nutrients could be potentially preventive and stabilising therapeutic strategies. Abstract:CONCLUSION: Malnutrition is a key modifiable risk factor for neurodegenerative diseases of the brain and retina. More intense integration of nutritional diagnostics and therapy into neurological, geriatric, and ophthalmological care structures appears warranted.

The lymphatic vascular system maintains fluid homeostasis, allows uptake of dietary lipids, and serves as a conduit for immune cell trafficking. Functional aspects of the lymphatic vasculature are governed by specific features of lymphatic endothelial cells that line these vessels. Dysfunction of lymphatic endothelial cells can result in various consequences at the organ and at the systemic level including lymphedema formation. In this review, we explore the underlying molecular mechanisms and signaling cascades that drive lymphatic development and vessel formation. We discuss human genetic disorders that lead to primary lymphedema and corresponding in vivo disease models that have helped to expand our molecular understanding pertaining to the signaling cascades governing lymphatic vessel development and maturation, in particular the VEGFC/VEGFR3 and ANG/TIE signaling axes. Furthermore, we highlight recent advancements regarding the anatomy and function of meningeal lymphatics and the Schlemm's canal in the context of development and disease.

BackgroundRecent research suggests that retinal changes occur at early stages of Alzheimer's disease (AD). However, gaps remain in understanding the detailed pathophysiological processes and their molecular underpinnings.ObjectiveThis study investigates alterations in the retinal neurovascular unit (NVU) and associated proteomic changes in the TgF344-AD rat model to determine how these changes relate to brain and known AD pathology.MethodsTransgenic rats and age-matched wild-type rats were studied. Proteomic analysis was conducted to identify changes in critical signaling pathways across the retina, the visual sensory thalamus (the lateral geniculate body, LGN) and hippocampus. Immunofluorescence staining was used to detect amyloid-β, glial, neuronal and vascular markers in the retina, and p-phenylenediamine staining examined axons of retinal ganglion cells.ResultsSignificant axonal degeneration in the optic nerve and optic tract of AD rats was detected, while axonal integrity in the optic chiasm, retinal ganglion cell numbers and retinal layer thickness remained unaffected. Proteomics showed a general downregulation of pathways essential for neural survival, glial function and vascular stability, with striking similarities between the retina and LGN. A significant reduction in amacrine cell numbers, increased microglial reactivity, decreased Müller cell immunoreactivity and reduced retinal pericyte density were also observed.ConclusionsThese findings suggest that retrograde and anterograde axonal degeneration, coupled with NVU dysfunction, are key features of retinal pathology in AD. The TgF344-AD rat model provides valuable insights into these changes, highlighting the retina as a potential site for early AD detection, monitoring and intervention.

Globally, glaucoma stands as a primary cause of irreversible blindness, marked by intricate pathophysiological processes in which neuroinflammation plays a pivotal role. As the principal immune cells within the central nervous system, microglia play a dual function in the progression of glaucoma. Under standard physiological states, microglia safeguard the retina by offering neurotrophic support and removing cellular debris. In the pathological progression of glaucoma, microglia become activated and release significant levels of inflammatory factors, resulting in retinal ganglion cell injury, cell death, and impaired neuroregeneration. This review focuses on examining the dual functions of microglia in glaucoma, evaluating their influence on retinal neurodegeneration and repair, and suggesting that modulating microglial activity could serve as a promising therapeutic strategy. Understanding the mechanisms of microglial action in glaucoma is crucial for unveiling the complex pathophysiological processes of the disease and developing new therapeutic strategies.

PURPOSE:This study aims to analyse the efficacy of GBE administration in patients with glaucoma and healthy volunteers. METHODS:This systematic review was performed according to the PRISMA 2020 guidelines. All clinical studies investigating the efficacy of GBE administration on the intraocular pressure (IOP), the corrected pattern standard deviation (CPSD) and the mean deviation of visual field testing, and heart rate were considered. The weighted mean difference (MD) effect measure, 95% confidence interval (CI), and t-test were used for continuous variables. RESULTS:Data from 8 studies, including 428 patients, were retrieved. The mean age of all patients was 51.1 ± 15.5 years. The median follow-up was 3.7 (IQR 9.4) months. The administration of GBE was not associated with an improvement in IOP (MD -1.5; 95%CI -7.1 to 9.6; P = 0.5), mean deviation (MD 0.7; 95%CI -9.4 to 8.2; P = 0.8), CPSD (MD -1.6; 95%CI -3.8 to 6.9; P = 0.5), or heart rate (MD -2.5; 95%CI -11.5 to 16.5; P = 0.4) from baseline to the last follow-up. There was no difference between GBE versus the control group in IOP (MD 1.1; 95%CI -5.7 to 3.5; P = 0.4), mean deviation (MD -0.4; 95%CI -9.1 to 9.9; P = 0.9), CPSD (MD 0.3; 95%CI -6.8 to 6.2; P = 0.9), and heart rate (MD -1.3; 95%CI -15.1 to 17.7; P = 0.8) at the last follow-up. CONCLUSION:Currently, the evidence is not sufficient to conclude that GBE affects IOP, mean deviation, CPSD, or heart rate in glaucoma patients and healthy volunteers. These conclusions must be interpreted with caution given the limitations of the reviewed studies, particularly the follow-up time of the included studies.

OBJECTIVES:To compare the outcomes of Paul (PGI) and Ahmed glaucoma implants (AGI) in patients with complex glaucoma. METHODS:64 patients undergoing PGI and 40 patients undergoing AGI were included in this study. Intraocular pressure (IOP), the number of IOP-lowering eye drops, and complications were evaluated during an 18-month follow-up. RESULTS:At 18 months, follow-up was completed by 26 patients (65.0%) in the AGI group and 45 patients (70.3%) in the PGI group. IOP was significantly reduced 18 months following PGI (12.3 ± 4.0 vs. 28.0 ± 9.3 mmHg, p < 0.001) and AGI (15.6 ± 5.2 vs. 30.7 ± 8.9 mmHg, p < 0.001) compared to preoperatively. The PGI achieved significantly lower IOP compared to the AGI group (p = 0.042). Similarly, the use of IOP-lowering eye drops decreased significantly at 18 months in the PGI (0.5 ± 0.8, p < 0.001) and AGI (1.3 ± 1.0, p < 0.001) groups, from baseline values of 3.3 ± 1.3 in PGI and 3.5 ± 1.3 in AGI. The number of IOP-lowering eye drops was significantly lower in the PGI than in the AGI group at both 12 (p = 0.031) and 18 months (p = 0.018). At the 18-month follow-up, qualified success rates for target pressures ≤18 mmHg were higher after PGI than AGI (IOP ≤ 18 mmHg: 66.6% vs. 84.2%, p = 0.017, ≤ 15 mmHg: 46.3% vs. 64.8%, p = 0.049, ≤ 12 mmHg: 24.9% vs. 43.0%, p = 0.047). There was no significant difference in the complication rates between PGI and AGI. CONCLUSION:Both PGI and AGI effectively reduced IOP and the number of IOP-lowering eye drops over an 18-month follow-up period. The PGI demonstrated significantly greater reductions in IOP and IOP-lowering eye drops than AGI at 18 months. The safety profiles of PGI and AGI were comparable.

Glaucoma drainage devices (GDD) are an important treatment option for advanced and complex glaucoma patients. To prevent tube erosion, different materials may be used to patch the tube. The aim of this study was to compare tube erosion rates of allogenous fascia lata versus corneal stromal patches relating to Ahmed glaucoma implant (AGI) and Paul glaucoma implant (PGI) surgeries. In this retrospective study, 84 patients were included. The tube was covered with allogenous fascia lata (n = 43) or a corneal stromal patch (n = 41). 32 eyes of 31 patients underwent AGI and 52 eyes of 52 patients underwent PGI surgeries. The number of tube erosions was evaluated during 18 months of follow-up. Tube erosions occurred in 4 patients with fascia lata patches (9.3%) and 1 patient (2.4%) with a corneal stromal patch (p = 0.184). In the superior quadrants (n = 78; 92.9% of all GDD), tube erosions were significantly more frequent with fascia lata (n = 4) compared to corneal stromal (n = 0) patches (p = 0.045). There was no difference in the number of tube erosions between the AGI (n = 2) and PGI (n = 3) group (p = 0.928). Tube erosions after GDD are rare. Fascia lata patches were more frequently associated with tube erosions than corneal stromal patches.

Neuronal injury in glaucoma persists despite effective intraocular pressure (IOP) control, necessitating neuroprotective strategies for retinal ganglion cells (RGCs). In this study, we investigated the neuroprotective role of the γ-hydroxybutyrate analog HOCPCA in a glaucoma model, focusing on its effects on CaMKII signaling, oxidative stress, and neuroinflammatory responses. Retinal tissue from high IOP animal models was analyzed via proteomics. In vitro mouse retinal explants were subjected to elevated pressure and oxidative stress, followed by HOCPCA treatment. HOCPCA significantly mitigated the RGC loss induced by oxidative stress and elevated pressure, preserving neuronal function. It restored CaMKIIα and β levels, preserving RGC integrity, while also modulating oxidative stress and neuroinflammatory responses. These findings suggest that HOCPCA, through its interaction with CaMKII, holds promise as a neuroprotective therapy for glaucoma.

Introduction Glaucoma is one of the most common causes of blindness and affects more than 70 million people worldwide. The disease is characterised by the loss of retinal ganglion cells associated with a progressive optic neuropathy, resulting in an impairment of visual functions, for example, visual field loss. Nowadays, the only modifiable risk factor is the increase in intraocular pressure, and its treatment is to lower this pressure by medication, laser treatment or surgery to avoid disease progression. New methods for preventing and reversing vision loss are thus urgently needed. Several small and two multicentre studies have presented evidence that repetitive transorbital alternating current stimulation (rtACS) can lead to long-lasting visual field improvement. This could open a new and inexpensive therapeutic option for optic atrophy. However, the level of evidence for this method is still fairly rather poor, and further trials are needed. Therefore, this clinical trial aims to prove the effectiveness of rtACS compared with sham stimulation in patients with primary open-angle glaucoma (POAG).Methods and analysis VIRON (Vision Restoration in Optic Neuropathy) is a national, multicentre, prospective, randomised, placebo-controlled, double-blind trial with three arms. The primary objective is to assess the effectiveness of rtACS in patients with POAG compared with sham stimulation. The primary outcome is the change in mean defect (MD) in the visual field immediately after 10 sessions of rtACS (days 9, 16 and 23) compared with the values of initial perimetry (days −21 to –14 and 0) after applying electrical stimulation with a classical montage, compared with sham and electrical stimulation using individualised montage. Secondary outcome measures comprise a long-term effect with changes in MD at 24 weeks after stimulation, and data from the National Eye Institute Visual Function-25 and quality of life (Short Form 36) questionnaires. The target population are patients with glaucomatous optic atrophy and significant glaucomatous visual field defects (MD of 5–22 dB) due to POAG.After randomisation, patients received either classical rtACS (group 1), individual rtACS (group 2) or sham stimulation (group 3) in daily 25 min stimulation sessions in two series of five consecutive days separated by a weekend interval. In group 1, active stimulation will be via the routinely applied montage using two electrodes affixed on the right and left side of the head, next to the eyes, with straightforward fixation. In group 2, the current flow will be individually modelled (MRI-based) to target areas of partial visual field defects by optimising electrode positions in conjunction with an optimised visual fixation direction. Group 3 with sham stimulation will serve as control.The calculated sample size required to achieve a statistical power of 80% for a relevant effect size and allow for dropouts was 300 (100 per group). The trial has already begun with the first patient in July 2023. The planned recruitment period is 24 months with an estimated end of the study in November 2025 (last patient out). An adjusted extension of the study period is planned.Ethics and dissemination VIRON was approved by the Central Ethics Committee of the University Medical Center Göttingen (19 October 2022) and those of the individual participating centres (Bonn: 446/23-EP, Hamburg: 2023-200889-BO-bet, Cologne: 23-1487 and Mainz: 2023-17399-§23b). The study protocol complies with the Declaration of Helsinki, the national medicine device regulation (MDR) laws and the international standards of good clinical practice (GCP).The study protocol (V.5, 24 November 2023) was designed following the Standard Protocol Items: Recommendations for Interventional Trials guidelines and is registered on https://drks.de/search/de/trial/DRKS00029129.As study initiatior the University Medical Center Göttingen (UMG) is responsible for data ownership and data management of the VIRON study. The study data will be published within 6 months of the study being completed. After the publication of the primary results, all data are anonymised and published in an open-access journal to ensure access to the data for third parties.Trial registration number https://drks.de/search/de/trial/DRKS00029129.

Glaucoma, a leading cause of irreversible blindness worldwide, is characterized by the progressive degeneration of retinal ganglion cells (RGCs). While elevated intraocular pressure (IOP) significantly contributes to disease progression, managing IOP alone does not completely halt it. The mechanisms underlying RGCs loss in glaucoma remain unclear, but ferroptosis-an iron-dependent form of oxidative cell death-has been implicated, particularly in IOP-induced RGCs loss. There is an urgent need for neuroprotective treatments. Our previous research showed that hydrogen sulfide (H2S) protects RGCs against glaucomatous injury. This study aims to investigate the interplay between elevated pressure, mitochondrial dysfunction, iron homeostasis, and ferroptosis in RGCs death, focusing on how H2S may mitigate pressure-induced ferroptosis and protect RGCs. We demonstrate alterations in iron metabolism and mitochondrial function in a subacute IOP elevation model in vivo. In vitro, we confirm that elevated pressure, iron overload, and mitochondrial dysfunction lead to RGCs loss, increased retinal ferrous iron and total iron content, and heightened reactive oxygen species (ROS). Notably, pressure increases NADPH oxidase 2 (NOX2) and decreases glutathione peroxidase 4 (GPX4), a key regulator of ferroptosis. NOX2 deletion or inhibition by H2S prevents pressure-induced RGCs loss and ferroptosis. Our findings reveal that H2S chelates iron, regulates iron metabolism, reduces oxidative stress, and mitigates ferroptosis, positioning slow- releasing H2S donors are positioning as a promising multi-target therapy for glaucoma, with NOX2 emerging as a key regulator of ferroptosis.