Western Eye Hospital

Dimethyl sulfoxide (DMSO) is an important aprotic solvent that can solubilize a wide variety of otherwise poorly soluble polar and nonpolar molecules. This, coupled with its apparent low toxicity at concentrations <10%, has led to its ubiquitous use and widespread application. Here, we demonstrate that DMSO induces retinal apoptosis in vivo at low concentrations (5 μl intravitreally dosed DMSO in rat from a stock concentration of 1, 2, 4, and 8% v/v). Toxicity was confirmed in vitro in a retinal neuronal cell line, at DMSO concentrations >1% (v/v), using annexin V, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), and AlamarBlue cell viability assays. DMSO concentrations >10% (v/v) have recently been reported to cause cellular toxicity through plasma membrane pore formation. Here, we show the mechanism by which low concentrations (2-4% DMSO) induce caspase-3 independent neuronal death that involves apoptosis-inducing factor (AIF) translocation from mitochondria to the nucleus and poly-(ADP-ribose)-polymerase (PARP) activation. These results highlight safety concerns of using low concentrations of DMSO as a solvent for in vivo administration and in biological assays. We recommend that methods other than DMSO are employed for solubilizing drugs but, where no alternative exists, researchers compute absolute DMSO final concentrations and include an untreated control group in addition to DMSO vehicle control to check for solvent toxicity.

Clinicians used to observing individual patients, and epidemiologists trained to observe the course of disease, may be forgiven for misunderstanding the term observational method as used in qualitative research. In contrast to the clinician or epidemiologist, the qualitative researcher systematically watches people and events to find out about behaviours and interactions in natural settings. Observation, in this sense, epitomises the idea of the researcher as the research instrument. It involves "going into the field"--describing and analysing what has been seen. In health care settings this method has been insightful and illuminating, but it is not without pitfalls for the unprepared researcher.

Antimicrobial resistance (AMR) is a serious threat to global public health, with approximately 5 million deaths associated with bacterial AMR in 2019. Tackling AMR requires a multifaceted and cohesive approach that ranges from increased understanding of mechanisms and drivers at the individual and population levels, AMR surveillance, antimicrobial stewardship, improved infection prevention and control measures, and strengthened global policies and funding to development of novel antimicrobial therapeutic strategies. In this rapidly advancing field, this Review provides a concise update on AMR, encompassing epidemiology, evolution, underlying mechanisms (primarily those related to last-line or newer generation of antibiotics), infection prevention and control measures, access to antibiotics, antimicrobial stewardship, AMR surveillance, and emerging non-antibiotic therapeutic approaches. The Review also discusses the potential roles of artificial intelligence in addressing AMR, including antimicrobial susceptibility testing, AMR surveillance, antimicrobial stewardship, diagnosis, and antimicrobial drug discovery and development. This Review highlights the urgent need for addressing the global effects of AMR and for rapid advancement of relevant technology in this dynamic field.

Microglia play an important role in the pathology of CNS disorders, however, there remains significant uncertainty about the neuroprotective/degenerative role of these cells due to a lack of techniques to adequately assess their complex behaviour in response to injury. Advancing microscopy techniques, transgenic lines and well-characterized molecular markers, have made histological assessment of microglia populations more accessible. However, there is a distinct lack of tools to adequately extract information from these images to fully characterise microglia behaviour. This, combined with growing economic pressures and the ethical need to minimise the use of laboratory animals, led us to develop tools to maximise the amount of information obtained. This study describes a novel approach, combining image analysis with spatial statistical techniques. In addition to monitoring morphological parameters and global changes in microglia density, nearest neighbour distance, and regularity index, we used cluster analyses based on changes in soma size and roundness to yield novel insights into the behaviour of different microglia phenotypes in a murine optic nerve injury model. These methods should be considered a generic tool to quantitatively assess microglia activation, to profile phenotypic changes into microglia subpopulations, and to map spatial distributions in virtually every CNS region and disease state.

The development of the devastating neurodegenerative condition, Alzheimer's disease, is strongly associated with amyloid-beta (Abeta) deposition, neuronal apoptosis, and cell loss. Here, we provide evidence that implicates these same mechanisms in the retinal disease glaucoma, a major cause of irreversible blindness worldwide, previously associated simply with the effects of intraocular pressure. We show that Abeta colocalizes with apoptotic retinal ganglion cells (RGC) in experimental glaucoma and induces significant RGC apoptosis in vivo in a dose- and time-dependent manner. We demonstrate that targeting different components of the Abeta formation and aggregation pathway can effectively reduce glaucomatous RGC apoptosis in vivo, and finally, that combining treatments (triple therapy) is more effective than monotherapy. Our work suggests that targeting the Abeta pathway provides a therapeutic avenue in glaucoma management. Furthermore, our work demonstrates that the combination of agents affecting multiple stages in the Abeta pathway may be the most effective strategy in Abeta-related diseases.

Over 60 million people worldwide are diagnosed with glaucomatous optic neuropathy, which is estimated to be responsible for 8.4 million cases of irreversible blindness globally. Glaucoma is associated with characteristic damage to the optic nerve and patterns of visual field loss which principally involves the loss of retinal ganglion cells (RGCs). At present, intraocular pressure (IOP) presents the only modifiable risk factor for glaucoma, although RGC and vision loss can continue in patients despite well-controlled IOP. This, coupled with the present inability to diagnose glaucoma until relatively late in the disease process, has led to intense investigations towards the development of novel techniques for the early diagnosis of disease. This review outlines our current understanding of the potential mechanisms underlying RGC and axonal loss in glaucoma. Similarities between glaucoma and other neurodegenerative diseases of the central nervous system are drawn before an overview of recent developments in techniques for monitoring RGC health is provided, including recent progress towards the development of RGC specific contrast agents. The review concludes by discussing techniques to assess glaucomatous changes in the brain using MRI and the clinical relevance of glaucomatous-associated changes in the visual centres of the brain.

AIM: To determine the incidence, methods of diagnosis, treatment strategies and outcomes for acute retinal necrosis (ARN) in the UK. METHODS: A 12-month active case ascertainment study was carried out between March 2001 and March 2002 to record cases of ARN presenting to ophthalmologists via the British Ophthalmological Surveillance Unit (BOSU) reporting system. Questionnaires were sent to the reporting consultants, requesting data on patient characteristics, presentation, clinical findings, investigations and treatment. Diagnosis was made using the American Uveitis Society diagnostic criteria. Further questionnaires were sent at 2 weeks and 6 months to assess outcome and therapies. RESULTS: 74 cases of ARN were reported by 58 consultants between March 2001 and March 2002. Questionnaires were returned for 49 cases (66.2%), of which 18 (36.7%) were excluded. Of the 31 cases included, 22 (71.0%) were male and 9 (29.0%) were female. The age range was 13 to 85 years (mean 54.3 years). 28 cases (90.3%) were unilateral, with 3 patients (9.7%) presenting with bilateral ARN. An aqueous or vitreous biopsy was performed in only 18 patients, with one patient having both. Herpes viral DNA analysis was performed on all 19 biopsies, with identification of the viral DNA in 16; results from 3 biopsies were not documented. Varicella zoster virus (VZV) was the commonest cause identified in 10 patients (56%). Of the 31 subjects, 27 (87.1%) were treated for ARN with systemic antiviral treatment: with intravenous antiviral in 23 cases (85.2%) and oral antiviral in 4 cases (14.8%). 21 of these patients went on to receive oral antiviral maintenance therapy. In addition to antiviral treatment, systemic steroids were given to 16 subjects (51.6%). Surgical intervention for retinal detachment was performed on 5 patients. CONCLUSIONS: During the 12-month study period, 31 cases of ARN met the diagnostic criteria set by the American Uveitis Society. The incidence in the UK based on this study is approximately 1 case per 1.6 to 2.0 million population per year. We have ascertained that the management of ARN throughout the UK is variable, suggesting that national guidelines would be of benefit.

In the last 20 years, research focused on developing retinal imaging as a source of potential biomarkers for Alzheimer's disease and other neurodegenerative diseases, has increased significantly. The Alzheimer's Association and the Alzheimer's & Dementia: Diagnosis, Assessment, Disease Monitoring editorial team (companion journal to Alzheimer's & Dementia) convened an interdisciplinary discussion in 2019 to identify a path to expedite the development of retinal biomarkers capable of identifying biological changes associated with AD, and for tracking progression of disease severity over time. As different retinal imaging modalities provide different types of structural and/or functional information, the discussion reflected on these modalities and their respective strengths and weaknesses. Discussion further focused on the importance of defining the context of use to help guide the development of retinal biomarkers. Moving from research to context of use, and ultimately to clinical evaluation, this article outlines ongoing retinal imaging research today in Alzheimer's and other brain diseases, including a discussion of future directions for this area of study.

PURPOSE: To determine, with novel software, the feasibility of measuring the tortuosity and width of retinal veins and arteries from digital retinal images of infants at risk of retinopathy of prematurity (ROP). METHODS: The Computer-Aided Image Analysis of the Retina (CAIAR) program was developed to enable semiautomatic detection of retinal vasculature and measurement of vessel tortuosity and width from digital images. CAIAR was tested for accuracy and reproducibility of tortuosity and width measurements by using computer-generated vessel-like lines of known frequency, amplitude, and width. CAIAR was then tested by using clinical digital retinal images for correlation of vessel tortuosity and width readings compared with expert ophthalmologist grading. RESULTS: When applied to 16 computer-generated sinusoidal vessels, the tortuosity measured by CAIAR correlated very well with the known values. Width measures also increased as expected. When the CAIAR readings were compared with five expert ophthalmologists' grading of 75 vessels on 10 retinal images, moderate correlation was found in 10 of the 14 tortuosity output calculations (Spearman rho = 0.618-0.673). Width was less well correlated (rho = 0.415). CONCLUSIONS: The measures of tortuosity and width in CAIAR were validated using sequential model vessel analysis. On comparison of CAIAR output with assessments made by expert ophthalmologists, CAIAR correlates moderately with tortuosity grades, but less well with width grades. CAIAR offers the opportunity to develop an automated image analysis system for detecting the vascular changes at the posterior pole, which are becoming increasingly important in diagnosing treatable ROP.

BACKGROUND: By enabling individuals to self-regulate their brainwave activity in the field of optimal performance in healthy individuals, neurofeedback has been found to improve cognitive and artistic performance. Here we assessed whether two distinct EEG neurofeedback protocols could develop surgical skill, given the important role this skill plays in medicine. RESULTS: National Health Service trainee ophthalmic microsurgeons (N = 20) were randomly assigned to either Sensory Motor Rhythm-Theta (SMR) or Alpha-Theta (AT) groups, a randomized subset of which were also part of a wait-list 'no-treatment' control group (N = 8). Neurofeedback groups received eight 30-minute sessions of EEG training. Pre-post assessment included a skills lab surgical procedure with timed measures and expert ratings from video-recordings by consultant surgeons, together with state/trait anxiety self-reports. SMR training demonstrated advantages absent in the control group, with improvements in surgical skill according to 1) the expert ratings: overall technique (d = 0.6, p < 0.03) and suture task (d = 0.9, p < 0.02) (judges' intraclass correlation coefficient = 0.85); and 2) with overall time on task (d = 0.5, p = 0.02), while everyday anxiety (trait) decreased (d = 0.5, p < 0.02). Importantly the decrease in surgical task time was strongly associated with SMR EEG training changes (p < 0.01), especially with continued reduction of theta (4-7 Hz) power. AT training produced marginal improvements in technique and overall performance time, which were accompanied by a standard error indicative of large individual differences. Notwithstanding, successful within session elevation of the theta-alpha ratio correlated positively with improvements in overall technique (r = 0.64, p = 0.047). CONCLUSION: SMR-Theta neurofeedback training provided significant improvement in surgical technique whilst considerably reducing time on task by 26%. There was also evidence that AT training marginally reduced total surgery time, despite suboptimal training efficacies. Overall, the data set provides encouraging evidence of optimised learning of a complex medical specialty via neurofeedback training.

Alzheimer's disease (AD) is the most common form of dementia affecting the growing aging population today, with prevalence expected to rise over the next 35 years. Clinically, patients exhibit a progressive decline in cognition, memory, and social functioning due to deposition of amyloid β (Aβ) protein and intracellular hyperphosphorylated tau protein. These pathological hallmarks of AD are measured either through neuroimaging, cerebrospinal fluid analysis, or diagnosed post-mortem. Importantly, neuropathological progression occurs in the eye as well as the brain, and multiple visual changes have been noted in both human and animal models of AD. The eye offers itself as a transparent medium to cerebral pathology and has thus potentiated the development of ocular biomarkers for AD. The use of non-invasive screening, such as retinal imaging and visual testing, may enable earlier diagnosis in the clinical setting, minimizing invasive and expensive investigations. It also potentially improves disease management and quality of life for AD patients, as an earlier diagnosis allows initiation of medication and treatment. In this review, we explore the evidence surrounding ocular changes in AD and consider the biomarkers currently in development for early diagnosis.

It was recently shown that the E2F-pRB complex is a negative transcriptional regulator. However, it was not determined whether the whole complex or pRB alone is required for repression. Here we show that pRB and the related protein p107 are capable of direct transcriptional repression independent of E2F. When fused to the DNA binding domain of GAL4, pRB or p107 represses transcription of promoters with GAL4 binding sites. Thus, E2F acts as a tether for pRB or p107 but is not actively involved in repression of other enhancers. This function of pRB maps to the pocket and is abrogated by mutation of this domain. This result suggests an intriguing model in which the pocket has a dual function, first to bind E2F and second to repress transcription directly, possibly through interaction with other proteins. We also show that direct transcriptional repression by pRB is regulated by phosphorylation. Mutations which render pRB constitutively hypophosphorylated potentiate repression, while phosphorylation induced by cyclin A or E reduces repression ninefold.

The last decade has seen a substantial increase in research focused on the identification, development, and validation of diagnostic and prognostic retinal biomarkers for Alzheimer's disease (AD). Sensitive retinal biomarkers may be advantageous because they are cost and time efficient, non-invasive, and present a minimal degree of patient risk and a high degree of accessibility. Much of the work in this area thus far has focused on distinguishing between symptomatic AD and/or mild cognitive impairment (MCI) and cognitively normal older adults. Minimal work has been done on the detection of preclinical AD, the earliest stage of AD pathogenesis characterized by the accumulation of cerebral amyloid absent clinical symptoms of MCI or dementia. The following review examines retinal structural changes, proteinopathies, and vascular alterations that have been proposed as potential AD biomarkers, with a focus on studies examining the earliest stages of disease pathogenesis. In addition, we present recommendations for future research to move beyond the discovery phase and toward validation of AD risk biomarkers that could potentially be used as a first step in a multistep screening process for AD risk detection.

AIMS: To compare the success rates of vitrectomy and gas with vitrectomy, gas, and buckle in the treatment of inferior break retinal detachments. METHODS: A retrospective case note review of 86 patients who presented with inferior break retinal detachments was carried out. An inferior break was defined as a horseshoe tear present between 4 and 8 o'clock. Patients were analysed in two groups; group A consisted of 41 patients who underwent a vitrectomy and gas, group B consisted of 45 patients who underwent a vitrectomy, gas, and scleral buckle. The features of the retinal detachment, peroperative and postoperative complications, and outcomes of treatment were recorded for each patient. RESULTS: The primary anatomical success rate at 3 months was 89% in group A versus 73% in group B (p = 0.11). There was no statistical difference in the complication rate between the two groups (p = 0.819). The most common cause of treatment failure was proliferative vitreoretinopathy, 20% (n = 9) in group B compared with 5% (n = 2) in group A and this reached statistical significance (p = 0.0159). There was a higher rate of epiretinal membrane development in group B (p = 0.0004). The final attachment rate was not statistically different between the two groups, 95% (39) in group A and 93% (42) in group B (p = 1.0). CONCLUSION: Vitrectomy and gas without the application of a scleral buckle may be used to safely treat inferior break retinal detachments. It may be used as an alternative to vitrectomy, gas, and buckle which has an increased risk of choroidal haemorrhage, requires a longer operating time, and has all the associated complications of a scleral buckle.

PURPOSE: Clinical outcomes for phacoemulsification surgery are still compared with the almost 10-year-old benchmark of the 1997-98 National Cataract Surgery Survey (NCSS) published in this journal. Extraneous to the peer-reviewed research literature, more recent databases suggest much better results may be being obtained. This offered the rare opportunity to perform an audit as research investigating if this was indeed the case and a new benchmark is needed, with the additional standard of rigorous study peer review by independent senior ophthalmologists. At this pilot centre for Patient Choice provision, all cataract surgery was performed on Consultant-supervised training lists, a novel extension in-sourcing care using public resources rather than to an independent sector that may not be supervised by NHS Consultants. Patient satisfaction was also surveyed. We asked whether the NCSS is out-of-date, and whether good outcomes on Choice schemes are compatible with Consultant-led training within the National Health Service? METHODS: An audit of 1000 consecutive patients undergoing cataract surgery on Patient Choice at the Western Eye Hospital between October 2002 and September 2004. All subjects were scheduled for phacoemulsification. A novel policy was extending "choice" onto training list slots for this period. A validated questionnaire assessed patient satisfaction. RESULTS: A best corrected visual acuity of 6/12 or better was obtained in 93% of cases. Over 80% of cases were +/-1 D of target refraction (65.7% within 0.5 D). The total incidence of complications was 8.7%. Overall incidence of major complications was 2.4%. Incidence of vitreous loss was 1.1% and that of endophthalmitis 0.1%. Complications rates were lowest for consultants (less than 1%). User satisfaction with having cataract surgery on "patient choice" was high. CONCLUSIONS: Cataract surgery under patient choice on supervised training lists is associated with a visual outcome and an incidence of complications at least as good as the published national average. User satisfaction is high. Cataract surgery under patient choice is compatible with training activity in receiving hospitals. The improvement in outcomes since the 1997-98 NCSS suggest that the accepted standards for complication rates should be updated to reflect the fact that phacoemulsification has become an established procedure.

We studied 40 patients with a total of 44 retinal arterial macroaneurysms. All patients were followed up for at least six months. Macroaneurysms (MAs) have variable clinical presentations and are still frequently misdiagnosed before fluorescein angiography. Haemorrhagic MAs were most frequently misdiagnosed (75%), and had a sudden onset with a relatively poor visual outcome. Patients with these MAs had higher systolic blood pressures and significantly fewer associated retinal vein occlusions (p less than 0.05) than other types of MA. Exudative MAs caused a gradual onset of symptoms, were frequently associated with retinal vein occlusions, and were the most frequent indication for laser treatment. Only one of 10 quiescent MAs subsequently developed significant exudation or haemorrhage. We confirm the association of MAs with retinal and systemic vascular disease. In addition we found that MA patients had a significantly higher blood packed cell volume (haematocrit) than controls (p less than 0.05). Laser treatment significantly shortened the duration of MA patency (p = 0.006).

AIM: To evaluate current clinical practice in the UK in the management of the anophthalmic socket; choice of enucleation, evisceration, type of orbital implant, wrap, motility pegging and complications. METHODS: All consultant ophthalmologists in the UK were surveyed by postal questionnaire. Questions included their practice subspecialty and number of enucleations and eviscerations performed in 2003. Specific questions addressed choice of implant, wrap, motility pegging and complications. RESULTS: 456/896 (51%) consultants responded, of which 162 (35%) had a specific interest in oculoplastics, lacrimal, orbits or oncology. Only 243/456 (53%) did enucleations or eviscerations. 92% inserted an orbital implant after primary enucleation, 69% after non-endophthalmitis evisceration, whereas only 43% did so after evisceration for endophthalmitis (50% as a delayed procedure). 55% used porous orbital implants (porous polyethylene, hydroxyapatite or alumina) as their first choice and 42% used acrylic. Most implants inserted were spherical, sized 18-20 mm in diameter. 57% wrapped the implant after enucleation, using salvaged autogenous sclera (20%), donor sclera (28%) and synthetic Vicryl or Mersilene mesh (42%). A minority (7%) placed motility pegs in selected cases, usually as a secondary procedure. 14% of respondents reported implant exposure for each type of procedure and extrusion was reported by 4% after enucleation and 3% after evisceration. CONCLUSIONS: This survey highlights contemporary anophthalmic socket practice in the UK. Most surgeons use porous orbital implants with a synthetic wrap after enucleation and only few perform motility pegging.

Retinal cell apoptosis occurs in many ocular neurodegenerative conditions including glaucoma—the major cause of irreversible blindness worldwide. Using a new imaging technique that we have called DARC (detection of apoptosing retinal cells), which until now has only been demonstrated in animal models, we assessed if annexin 5 labelled with fluorescent dye DY-776 (ANX776) could be used safely in humans to identify retinal cell apoptosis. Eight patients with glaucomatous neurodegeneration and evidence of progressive disease, and eight healthy subjects were randomly assigned to intravenous ANX776 doses of 0.1, 0.2, 0.4 and 0.5 mg in an open-label, phase 1 clinical trial. In addition to assessing the safety, tolerability and pharmacokinetics of ANX776, the study aimed to explore whether DARC could successfully visualize individual retinal cell apoptosis in vivo in humans, with the DARC count defined as the total number of unique ANX776-labelled spots. DARC enabled retinal cell apoptosis to be identified in the human retina using ANX776. Single ANX776-labelled cells were visualized in a dose-dependent pattern (P5 0.001) up to 6 h after injection. The DARC count was significantly higher (2.37-fold, 95% confidence interval: 1.4–4.03, P = 0.003) in glaucoma patients compared to healthy controls, and was significantly (P = 0.045) greater in patients who later showed increasing rates of disease progression, based on either optic disc, retinal nerve fibre layer or visual field parameters. Additionally, the DARC count significantly correlated with decreased central corneal thickness (Spearman’s R = 0.68, P = 0.006) and increased cup-disc ratios (Spearman’s R = 0.47, P = 0.038) in glaucoma patients and with increased age (Spearman’s R = 0.77, P = 0.001) in healthy controls. Finally, ANX776 was found to be safe and well-tolerated with no serious adverse events, and a short half-life (10–36 min). This proof-of-concept study demonstrates that retinal cell apoptosis can be identified in the human retina with increased levels of activity in glaucomatous neurodegenerative disease. To our knowledge, this is the first time individual neuronal apoptosis has been visualized in vivo in humans and is the first demonstration of detection of individual apoptotic cells in a neurodegenerative disease. Furthermore, our results suggest the level of apoptosis (‘DARC count’) is predictive of disease activity, indicating the potential of DARC as a surrogate marker. Although further trials are clearly needed, this study validates experimental findings supporting the use of DARC as a method of detection and monitoring of patients with glaucomatous neurodegeneration, where retinal ganglion cell apoptosis is an established process and where there is a real need for tools to non-invasively assess treatment efficacy.

In recent years the focus of glaucoma research has shifted toward neuroprotection, as the traditional strategies of lowering intraocular pressure have been shown to be unable to prevent progressive vision loss in some glaucoma patients. As a result various neuroprotective drug-based approaches have been shown capable of reducing the death of retinal ganglion cells, which is the hallmark of glaucomatous optic neuropathy. There has been increasing evidence that glaucomatous neurodegeneration is analogous to other neurodegenerative diseases in the central nervous system, with recent work from our group elucidating a strong link between basic cellular processes in glaucoma and Alzheimer's disease. Additionally, there is a growing trend for using existing neuroprotective strategies in central nervous system diseases for the treatment of glaucoma. In fact, a trial treating patients with primary open-angle glaucoma with memantine, a drug approved for the treatment of Alzheimer's disease, has recently been completed. Results of this trial are not yet available. In this review, we will examine currently advocated neuroprotective drug-based strategies in the potential management of glaucoma.

Abstract Glaucoma is a multifactorial neurodegenerative disease associated with retinal ganglion cells (RGC) loss. Increasing reports of similarities in glaucoma and other neurodegenerative conditions have led to speculation that therapies for brain neurodegenerative disorders may also have potential as glaucoma therapies. Memantine is an N ‐methyl‐ d ‐aspartate (NMDA) antagonist approved for Alzheimer's disease treatment. Glutamate‐induced excitotoxicity is implicated in glaucoma and NMDA receptor antagonism is advocated as a potential strategy for RGC preservation. This study describes the development of a topical formulation of memantine‐loaded PLGA‐PEG nanoparticles (MEM‐NP) and investigates the efficacy of this formulation using a well‐established glaucoma model. MEM‐NPs &lt;200 nm in diameter and incorporating 4 mg mL −1 of memantine were prepared with 0.35 mg mL −1 localized to the aqueous interior. In vitro assessment indicated sustained release from MEM‐NPs and ex vivo ocular permeation studies demonstrated enhanced delivery. MEM‐NPs were additionally found to be well tolerated in vitro (human retinoblastoma cells) and in vivo (Draize test). Finally, when applied topically in a rodent model of ocular hypertension for three weeks, MEM‐NP eye drops were found to significantly (p &lt; 0.0001) reduce RGC loss. These results suggest that topical MEM‐NP is safe, well tolerated, and, most promisingly, neuroprotective in an experimental glaucoma model.