Peripheral Ganglion Cell Complex Thickness and Retinal Microvasculature in Myopia Using Wide-Field Swept-Source OCT.

Purpose: This study aims to investigate the impact of axial elongation on ganglion cell complex thickness (GCCT) and retinal capillary density (CD) using wide-field swept-source optical coherence tomography angiography. Methods: A retrospective cross-sectional analysis was conducted involving 506 eyes. Fovea-centered scans were obtained to assess the subregional GCCT and capillary density across the whole retina, the superficial capillary plexus (SCP), and deep capillary plexus (DCP) among three groups: normal control, high myopia (HM) eyes with axial length < 28 mm, and HM eyes with axial length > 28 mm. Regional variations (central vs. peripheral, quadrants difference [superior, inferior, nasal, and temporal]) were analyzed. Results: In HM eyes with axial length > 28 mm, GCCT and retinal CD exhibit a general decline in most regions (P < 0.05). In HM eyes with axial length < 28 mm, significant reductions were observed specifically in peripheral regions, as in the GCCT beyond the 3 × 3 mm2 area and CD in the 9-12 mm whole retina, 9-12 mm superior SCP, and 6-12 mm DCP (P < 0.05). Maximum GCCT and retinal CD reduction with axial elongation was observed in subregions beyond 6 × 6  mm2. Conclusions: GCCT beyond the 3 × 3 mm2 area and peripheral retinal CD beyond the 6 × 6  mm2 area were more susceptible to axial elongation and are thereby deserving of particular attention. Translational Relevance: It is necessary to evaluate different regions during the clinical assessment of the effect of myopia on the fundus and pay close attention to the peripheral retina.

Correlation of Visual System Biomarkers With Motor Deficits in Experimental Autoimmune Encephalomyelitis-Optic Neuritis.

Purpose: Experimental autoimmune encephalomyelitis (EAE) scoring, the most commonly used primary outcome metric for an in vivo model of multiple sclerosis (MS), is highly variable and subjective. Here we explored the use of visual biomarkers in EAE as more objective and clinically relevant primary outcomes. Methods: Motor impairment in myelin oligodendrocyte glycoprotein-immunized C57BL/6J mice was quantified using a five-point EAE grading scale. Pattern electroretinography (pERG) and retinal ganglion cell/inner plexiform layer (RGC/IPL) complex thickness were measured 60 days after induction. Optic nerve histopathology was analyzed at endpoint. Results: EAE mice displayed motor impairments ranging from mild to severe. Significant correlations were seen between pERG amplitude and last EAE score, mean EAE score, and cumulative EAE score. Optical coherence tomography (OCT) analysis demonstrated a significant correlation between thinning of the RGC/IPL complex and both EAE score and pERG amplitude. Optic nerve histopathology showed significant correlations between demyelination and cumulative EAE score, pERG amplitude, and RGC/IPL complex thickness, as well as between immune cell infiltration and cumulative EAE score, pERG amplitude, and RGC/IPL complex thickness in EAE mice. Conclusions: Unlike EAE scoring, pERG and OCT show direct measurement of retinal structure and function. Therefore we conclude that visual outcomes are well suited as a direct assessment of optic nerve involvement in this EAE model of MS while also being indicative of motor impairment. Translational Relevance: Standardizing directly translatable measurements as primary outcome parameters in the murine EAE model could lead to more rapid and relevant testing of new therapeutic approaches for mitigating MS.

Evaluation of thickness of individual macular retinal layers in diabetic eyes from optical coherence tomography.

The effect of diabetes mellitus (DM) on individual retinal layers remains incompletely understood. We evaluated the intra-retinal layer thickness alterations in 71 DM eyes with no diabetic retinopathy (DR), 90 with mild DR, and 63 with moderate DR without macular edema, using spectral-domain optical coherence tomography (SD-OCT) and the Iowa Reference Algorithm for automated retinal layer segmentation. The average thickness of 10 intra-retinal layers was then corrected for ocular magnification using axial length measurements, and pairwise comparisons were made using multivariable linear regression models adjusted for gender and race. In DM no DR eyes, significant thinning was evident in the ganglion cell layer (GCL; p < 0.001), inner nuclear layer (INL; p = 0.001), and retinal pigment epithelium (RPE; p = 0.014) compared to normal eyes. Additionally, mild DR eyes exhibited a thinner inner plexiform layer (IPL; p = 0.008) than DM no DR eyes. Conversely, moderate DR eyes displayed thickening in the INL, outer nuclear layer, IPL, and retinal nerve fiber layer (all p ≤ 0.002), with notably worse vision. These findings highlight distinctive patterns: early diabetic eyes experience thinning in specific retinal layers, while moderate DR eyes exhibit thickening of certain layers and slightly compromised visual acuity, despite the absence of macular edema. Understanding these structural changes is crucial for comprehending diabetic eye complications.

Modulating amacrine cell-derived dopamine signaling promotes optic nerve regeneration and preserves visual function.

As part of the central nervous system, the optic nerve, composed of axons from retinal ganglion cells (RGCs), generally fails to regenerate on its own when injured in adult mammals. An innovative approach to promoting optic nerve regeneration involves manipulating the interactions between amacrine cells (ACs) and RGCs. Here, we identified a unique AC subtype, dopaminergic ACs (DACs), that responded early after optic nerve crush by down-regulating neuronal activity and reducing retinal dopamine (DA) release. Activating DACs or augmenting DA release with levodopa demonstrated neuroprotective effects and modestly enhanced axon regeneration. Within this context, we pinpointed the DA receptor D1 (DRD1) as a critical mediator of DAC-derived DA and showed that RGC-specific Drd1 overexpression effectively overcame subtype-specific barriers to regeneration. This strategy markedly boosted RGC survival and axon regeneration after crush and preserved vision in a glaucoma model. This study unveils the crucial role of DAC-derived DA signaling in optic nerve regeneration, holding promise for therapeutic insights into neural repair.

A cross-sectional study on the impact of hemodialysis duration on retinal nerve fiber layer thinning in hemodialysis patients.

This study aimed to investigate the relationship between hemodialysis duration (HDD) and retinal nerve fiber layer (RNFL) thickness. A total of 60 patients receiving maintenance hemodialysis and 67 healthy controls were analyzed. Spectral domain optical coherence tomography (SD-OCT) was employed to measure annular RNFL thicknesses. The hemodialysis group exhibited reduced temporal and inferior RNFL thicknesses relative to the control group. In hemodialysis patients, the inferior RNFL thickness was negatively correlated with HDD and positively correlated with intraocular pressure (IOP). Moreover, IOP was positively correlated with HDD. Mediation analysis showed that the negative correlation between HDD and inferior RNFL thickness was mediated by IOP. In conclusion, hemodialysis leads to temporal and inferior RNFL thinning, and the thickness reduction is proportional to hemodialysis duration. However, such changes are not induced by an increase in IOP.

Independent Effects of Blood Pressure on Intraocular Pressure and Retinal Ganglion Cell Degeneration: A Mendelian Randomization Study.

Purpose: To investigate the causal effect of elevated blood pressure on primary open-angle glaucoma (POAG) and POAG endophenotypes. Methods: Two-sample Mendelian randomization (MR) was performed to investigate the causal effect of elevated systolic blood pressure (SBP) (N = 757,601) and diastolic blood pressure (DBP) (N = 757,601) on intraocular pressure (IOP) (N = 139,555), macular retinal nerve fiber layer (mRNFL) thickness (N = 33,129), ganglion cell complex (GCC) thickness (N = 33,129), vertical cup-to-disc ratio (VCDR) (N = 111,724), and POAG liability (Ncases = 16,677, Ncontrols = 199,580). The primary analysis was conducted using the inverse-variance weighted approach. Sensitivity analyses were performed to investigate robustness to horizontal pleiotropy, winner's curse, and collider bias. Multivariable MR was performed to investigate whether any effect of blood pressure on retinal ganglion cell degeneration was mediated through increased IOP. Results: Increased genetically predicted SBP and DBP associated with an increase in IOP (0.17 mm Hg [95% CI = 0.11 to 0.24] per 10 mm Hg higher SBP, P = 5.18 × 10-7, and 0.17 mm Hg [95% CI = 0.05 to 0.28 mm Hg] per 10 mm Hg higher DBP, P = 0.004). Increased genetically predicted SBP associated with a thinner GCC (0.04 µm [95% CI = -0.07 to -0.01 µm], P = 0.018) and a thinner mRNFL (0.04 µm [95% CI = -0.07 to -0.01 µm], P = 0.004), an effect that arises independently of IOP according to our mediation analysis. Neither SBP nor DBP associated with VCDR or POAG liability. Conclusions: These findings support a causal effect of elevated blood pressure on retinal ganglion cell degeneration that does not require intermediary changes in IOP. Targeted blood pressure control may help preserve vision by lowering IOP and, independently, by preventing retinal ganglion cell degeneration, including in individuals with a normal IOP.

Optimization-Based Pairwise Interaction Point Process (O-PIPP): A Precise and Universal Retinal Mosaic Modeling Approach.

Purpose: A retinal mosaic, the spatial organization of a population of homotypic neurons, is thought to sample a specific visual feature into the feedforward visual pathway. The purpose of this study was to propose a universal modeling approach for precisely generating retinal mosaics and overcoming the limitations of previous models, especially in modeling abnormal mosaic patterns under disease conditions. Methods: Here, we developed the optimization-based pairwise interaction point process (O-PIPP). It incorporates optimization techniques into previous simulation approaches, enabling directional control of the simulation process according to the user-designed optimization target. For the convenience of the community, we implemented the O-PIPP approach into a Python package and a website application. Results: We showed that the O-PIPP can generate more precise neural spatial patterns of healthy and diseased mosaics compared to previous phenomenological approaches. Notably, through modeling the retinal neural circuitry with O-PIPP-simulated retinitis pigmentosa cone mosaics, we elucidated how the cone mosaic rearrangement impacted the information processing of ganglion cells. Conclusions: The O-PIPP provides a precise and universal tool to simulate realistic mosaics, which could help to investigate the function of retinal mosaics in vision.

ASSOCIATIONS BETWEEN CHOROIDAL ALTERATIONS AND EARLY NEURODEGENERATION IN DIABETES WITHOUT DIABETIC RETINOPATHY: Insights From Ultra-Widefield Optical Coherence Tomography Angiography Imaging.

PURPOSE: To identify associations between choroidal alterations and the reduction of peripapillary retinal nerve fiber layer (pRNFL) thickness in diabetes without diabetic retinopathy (nondiabetic retinopathy, NDR). METHODS: This retrospective cross-sectional study included 143 eyes from 83 patients with NDR and 124 eyes from 82 matched healthy controls. Ultra-widefield swept-source optical coherence tomography angiography was used to automatically measure retinal and choroidal thickness (ChT), retinal vascular density, and choroidal vascular metrics. Data were analyzed using Student's t-tests, generalized estimating equations, and generalized linear mixed models. RESULTS: Patients with NDR exhibited significant reductions in perifoveal ChT (e.g., perifoveal inferior region: 253.42 ± 86.59 µm vs. 281.01 ± 80.25 µm, P = 0.026 in GEE test) compared with the controls. The NDR group showed a significant decrease in the choroidal vascular index (P = 0.012 in GEE test), and an increase in the choroidal stromal index (P = 0.012 in GEE test). The average pRNFL thickness significantly decreased in patients with NDR (114.58 ± 11.88 µm vs. 120.25 ± 16.36 µm, P = 0.005 in GEE test). The thickness of the outer nuclear layer and total retina significantly decreased in patients with NDR (P < 0.05). In multivariate models, ChT was significantly correlated with pRNFL thickness (ß = 0.041, P = 0.001), even after adjusting by confounding factors (ß = 0.056, P = 0.001). CONCLUSION: In NDR, there were decreases in ChT, choroidal vascular index, pRNFL thickness, and outer nuclear layer thickness. The reduction in ChT was independently associated with the reduction in pRNFL thickness, suggesting that ChT could serve as a predictor of retinal neurodegeneration in NDR.

Analysis of macular thickness and peripapillary retinal nerve fiber layer thickness in various ABO and Rh blood groups.

PURPOSE: To determine the association between ABO and Rh blood groups with retinal structural indices including macular thickness and peripapillary retinal nerve fiber layer (RNFL) thickness. METHODS: This cross-sectional study was conducted using convenience sampling in a tertiary referral eye hospital in Tehran, Iran. Study participants were referred to the hospital laboratory to test their blood group. Ocular examinations were performed including measurement of visual acuity, auto-refraction, subjective refraction, and slit-lamp biomicroscopy. Retinal imaging was carried out using Spectral-domain OCT under dilated papillary conditions. RESULTS: Three hundred and twenty-eight individuals were recruited in this study. Of these, 219 (60.7%) were female and the mean age of the participants was 63.29 ± 5.57 years (range: 56 to 83 years). According to the multiple linear regression model, the global peripapillary RNFL thickness [coefficient: -3.05 (95% CI: -5.30 to -0.74); P = 0.010] and peripapillary RNFL thickness in the superior [coefficient: -4.65 (95% CI: -8.40 to -0.89), P < 0.001] and inferior [coefficient: -4.00 (95% CI: -7.81 to -0.19); P = 0.040] quadrants were significantly thinner in individuals with blood type B compared to those with other ABO blood groups. The average [coefficient: 12.69 (95% CI: 4.12-21.64); P = 0.004) and central [coefficient: 16.21 (95%: 6.44-25.97); P = 0.001) macular thicknesses were significantly thicker in AB group compared to other blood groups. The average macular thickness was significantly thinner in Rh + compared to the Rh- group [coefficient: -8.33 (95% CI: -15.4 to -1.25); P = 0.021]. CONCLUSION: Retinal structural indices may be related to blood groups implying a genetic linkage. Considering the lack of consistency among various studies, larger trials are needed to explore the effect of ABO and Rh grouping on peripapillary RNFL and macular thicknesses.

Temporal pattern recognition in retinal ganglion cells is mediated by dynamical inhibitory synapses.

A fundamental task for the brain is to generate predictions of future sensory inputs, and signal errors in these predictions. Many neurons have been shown to signal omitted stimuli during periodic stimulation, even in the retina. However, the mechanisms of this error signaling are unclear. Here we show that depressing inhibitory synapses shape the timing of the response to an omitted stimulus in the retina. While ganglion cells, the retinal output, responded to an omitted flash with a constant latency over many frequencies of the flash sequence, we found that this was not the case once inhibition was blocked. We built a simple circuit model and showed that depressing inhibitory synapses were a necessary component to reproduce our experimental findings. A new prediction of our model is that the accuracy of the constant latency requires a sufficient amount of flashes in the stimulus, which we could confirm experimentally. Depressing inhibitory synapses could thus be a key component to generate the predictive responses observed in the retina, and potentially in many brain areas.

Characterization of a monkey model with experimental retinal damage induced by N-methyl-D-aspartate.

N-methyl-D-aspartate (NMDA)-induced retinal damage has been well studied in rodents, but the detailed mechanisms have not yet been characterized in nonhuman primates. Here, we characterized the retinal degenerative effects of NMDA on rhesus monkeys in vivo. NMDA saline or saline-only control was injected intravitreally to the randomly assigned eyes and contralateral eyes of four rhesus monkeys, respectively. The structural and functional changes of retina were characterized by optical coherence tomography and electroretinography on days 0, 4, 30 and 60 post injection. Both optic discs and macular areas of the NMDA-injected eyes initially presented with a transient retinal thickening, followed by continued retinal thinning. The initial, transient retinal thickening has also been observed in glaucoma patients, but this has not been reported in rodent NMDA models. This initial response was followed by loss of retina ganglion cells (RGCs), which is similar to glaucomatous optic neuropathy and other RGC-related retinal degenerations. The amplitudes of both the photopic negative response and pattern electroretinogram decreased significantly and remained low until the end of the study. Thus, the NMDA monkey model may serve as a more clinically relevant animal model of retinal damage.

Creation of an Isogenic Human iPSC-Based RGC Model of Dominant Optic Atrophy Harboring the Pathogenic Variant c.1861C>T (p.Gln621Ter) in the OPA1 Gene.

Autosomal dominant optic atrophy (ADOA) is a rare progressive disease mainly caused by mutations in OPA1, a nuclear gene encoding for a mitochondrial protein that plays an essential role in mitochondrial dynamics, cell survival, oxidative phosphorylation, and mtDNA maintenance. ADOA is characterized by the degeneration of retinal ganglion cells (RGCs). This causes visual loss, which can lead to legal blindness in many cases. Nowadays, there is no effective treatment for ADOA. In this article, we have established an isogenic human RGC model for ADOA using iPSC technology and the genome editing tool CRISPR/Cas9 from a previously generated iPSC line of an ADOA plus patient harboring the pathogenic variant NM_015560.3: c.1861C>T (p.Gln621Ter) in heterozygosis in OPA1. To this end, a protocol based on supplementing the iPSC culture media with several small molecules and defined factors trying to mimic embryonic development has been employed. Subsequently, the created model was validated, confirming the presence of a defect of intergenomic communication, impaired mitochondrial respiration, and an increase in apoptosis and ROS generation. Finally, we propose the analysis of OPA1 expression by qPCR as an easy read-out method to carry out future drug screening studies using the created RGC model. In summary, this model provides a useful platform for further investigation of the underlying pathophysiological mechanisms of ADOA plus and for testing compounds with potential pharmacological action.

[Ophthalmological traits in older adult and risk of Alzheimer's disease: results from a French geriatric cohort]. / Caractéristiques ophtalmologiques chez la personne âgée et risque de maladie d'Alzheimer : résultats d'une cohorte française gériatrique.

Ophthalmological changes have been reported in Alzheimer's patients. Our objectives were to determine whether: i) GCC (ganglion cell complex) and RNFL (retinal nerve fibre layer) thickness were associated with different stages of AD (i.e., no AD, prodromal AD, dementia-stage AD), and ii) GCC and RNFL thickness predicted disease progression in older non-demented patients with subjective memory complaints followed for four years. Ninety-one French older community-dwellers with memory complaint and without open-angle glaucoma or age-related macular degeneration (mean, 71.60 ± 4,73 years; 44% women) from the GAIT study underwent examination with HD-OCT, measuring the thickness of the macula, the macular GCC and the RNFL. They also had a complete cognitive diagnosis (i.e., cognitively healthy, prodromal AD, or dementia AD), and a cognitive follow-up 4 years later looking for a possible conversion. Age, sex, body mass index (BMI), number of comorbidities, and Instrumental activities of daily living (IADL) score were considered as potential confounders. At baseline, 37 (40.7%) patients were diagnosed as cognitively healthy, 47 (51.6%) as MCI, and 7 (7.7%) as AD. Mean GCC thickness was higher in cognitively healthy patients than in MCI patients (79.23 vs. 76.27 µm, p = 0.023), particularly in the inferior and nasal fields (p = 0.023 and p = 0.005, respectively). This difference was also found between cognitively healthy patients and others (MCI and AD) in the superior, inferior and nasal fields (p = 0.030, p = 0.014 and p = 0.002, respectively). There was no difference in RNFL thickness between the different cognitive statuses. After 4 years of follow-up, 12 patients (70.6%) of the 17 followed had not changed their cognitive status, while 5 (29.4%) had converted to a more advanced stage of AD. There were no significant differences between the two groups in either GCC thickness (p = 0.429) or RNFL thickness (p = 0.286). We found decreased CGG thicknesses in Alzheimer's patients at prodromal and dementia stages, compared with cognitively healthy participants. There was no association between RNFL thickness and cognitive status, nor between CCG or RNFL thicknesses and the risk of progressing to AD stages after 4 years of follow-up.

Optical coherence tomography of the macular ganglion cell layer in children with neurofibromatosis type 1 is a useful tool in the assessment for optic pathway gliomas.

BACKGROUND: Optic pathway glioma (OPG) is a feared complication to neurofibromatosis type 1 (NF1) since it can cause visual impairment in young children. The main goal of screening is to detect symptomatic OPGs that require treatment. Optical coherence tomography (OCT) has been suggested as a tool for detection of neuro-retinal damage. AIMS: To investigate whether the ganglion cell layer assessed by OCT is a reliable measure to identify and detect relapses of symptomatic OPGs in children with NF1. METHODS: Children (3-6 years) with NF1, with and without known OPG and children with sporadic OPG (S-OPG) resident in the Stockholm area, were invited and followed in a prospective study during a three-year period. Brain magnetic resonance tomography (MRI) had been performed in children with symptoms of OPG. Outcome measures were VA in logMAR, visual field index (VFI), average thicknesses of the ganglion cell-inner plexiform layer (GC-IPL), and peripapillary retinal nerve fiber layer (pRNFL). RESULTS: There were 25 children with MRI-verified OPG and 52 with NF1 without symptomatic OPG. Eyes from NF1 patients without symptoms of OPG showed significantly better results in all four analyzed parameters compared to eyes with NF1-associated OPG. Mean GC-IPL measurements seemed stable and reliable, significantly correlated to pRNFL (correlation coefficient (r) = 0.662, confidence interval (CI) = .507 to .773 p<0.001), VA (r = -0.661, CI = -7.45 to -.551, p<0.001) and VFI (r = 0.644, CI = .452 to .774, p<0.001). GC-IPL measurements were easy to obtain and acquired at considerably younger age than pRNFL (5.6±1.5 vs 6.8±1.3; p<0.001). CONCLUSIONS: The mean GC-IPL thickness could distinguish well between eyes with OPG and eyes without symptomatic OPG in children with NF1. As thinning of GC-IPL assessed with OCT could indicate underlying OPG, it should be included in the screening protocol of children with questionable VA measurements and in particular in children with NF1.

The Prodrug DHED Delivers 17ß-Estradiol into the Retina for Protection of Retinal Ganglion Cells and Preservation of Visual Function in an Animal Model of Glaucoma.

We report a three-pronged phenotypic evaluation of the bioprecursor prodrug 10ß,17ß-dihydroxyestra-1,4-dien-3-one (DHED) that selectively produces 17ß-estradiol (E2) in the retina after topical administration and halts glaucomatous neurodegeneration in a male rat model of the disease. Ocular hypertension (OHT) was induced by hyperosmotic saline injection into an episcleral vein of the eye. Animals received daily DHED eye drops for 12 weeks. Deterioration of visual acuity and contrast sensitivity by OHT in these animals were markedly prevented by the DHED-derived E2 with concomitant preservation of retinal ganglion cells and their axons. In addition, we utilized targeted retina proteomics and a previously established panel of proteins as preclinical biomarkers in the context of OHT-induced neurodegeneration as a characteristic process of the disease. The prodrug treatment provided retina-targeted remediation against the glaucomatous dysregulations of these surrogate endpoints without increasing circulating E2 levels. Collectively, the demonstrated significant neuroprotective effect by the DHED-derived E2 in the selected animal model of glaucoma supports the translational potential of our presented ocular neuroprotective approach owing to its inherent therapeutic safety and efficacy.

Identification and Characterization of ATOH7-Regulated Target Genes and Pathways in Human Neuroretinal Development.

The proneural transcription factor atonal basic helix-loop-helix transcription factor 7 (ATOH7) is expressed in early progenitors in the developing neuroretina. In vertebrates, this is crucial for the development of retinal ganglion cells (RGCs), as mutant animals show an almost complete absence of RGCs, underdeveloped optic nerves, and aberrations in retinal vessel development. Human mutations are rare and result in autosomal recessive optic nerve hypoplasia (ONH) or severe vascular changes, diagnosed as autosomal recessive persistent hyperplasia of the primary vitreous (PHPVAR). To better understand the role of ATOH7 in neuroretinal development, we created ATOH7 knockout and eGFP-expressing ATOH7 reporter human induced pluripotent stem cells (hiPSCs), which were differentiated into early-stage retinal organoids. Target loci regulated by ATOH7 were identified by Cleavage Under Targets and Release Using Nuclease with sequencing (CUT&RUN-seq) and differential expression by RNA sequencing (RNA-seq) of wildtype and mutant organoid-derived reporter cells. Additionally, single-cell RNA sequencing (scRNA-seq) was performed on whole organoids to identify cell type-specific genes. Mutant organoids displayed substantial deficiency in axon sprouting, reduction in RGCs, and an increase in other cell types. We identified 469 differentially expressed target genes, with an overrepresentation of genes belonging to axon development/guidance and Notch signaling. Taken together, we consolidate the function of human ATOH7 in guiding progenitor competence by inducing RGC-specific genes while inhibiting other cell fates. Furthermore, we highlight candidate genes responsible for ATOH7-associated optic nerve and retinovascular anomalies, which sheds light to potential future therapy targets for related disorders.

Comparative Analysis of Retinal Structural and Angiographic Parameters in Diabetic Patients, Alzheimer's Disease Patients, and Healthy Controls: An OCT-Based Study.

Objective: This study aimed to investigate the potential connections between Alzheimer's Disease (AD) and diabetes. Methods: This is a cross-sectional study in which AD and diabetes patients sent by the Psychiatry and Diabetes Departments for ophthalmological screening were observed for inclusion/exclusion criteria. Patients were divided into two comparison groups. The first group (n=3) consisted of the age-matched normal and diabetic patient of the stage 3 AD disease participant. The second group (n=3) was for the stage 5 AD patient with diabetes and normal age-matched controls. Each patient underwent a full ophthalmological examination and SS-OCT (Swept Source-Ocular Computer Tomography) for retinal evaluation. Results: A total of 6 patients (12 eyes) were obtained, three men and three women. In the early AD group, the patient with diabetes showed lower macular thickness compared to other groups. In the nasal-inferior (NI) and temporal-superior (TS) ganglion cell layer (GCL), the AD patient showed statistically significant lower values compared to the other patients. In the moderately severe AD group, we found that the AD patient had lower retinal nerve fiber layer (RNFL) thickness on the temporal side compared to the rest of the patients and both the AD patient and diabetes patient showed lower RNFL thickness in the nasal-superior (NS) quadrant. Also, the foveal avascular zone (FAZ) area was statistically significantly lower for both the diabetes and AD patients compared to the healthy control. Conclusions: In conclusion, distinct retinal findings associated with AD and diabetes in young and elderly patients were revealed in our study. The clinical implications and potential interplay between these conditions need to be elucidated by further research. Abbreviations: AD = Alzheimer's Disease, SS-OCT = Swept Source - Ocular Computer Tomography, GCL = Ganglion cell layer, RNFL = Retinal nerve fiber layer, FAZ = foveal avascular zone.

Wide-Field Optical Coherence Tomography Imaging Improves Rate of Change Detection in Progressing Glaucomatous Eyes Compared With Standard-Field Imaging.

Purpose: To compare rates of retinal nerve fiber layer change over time in healthy, eyes with nonprogressing glaucoma and eyes with progressing glaucoma using single wide-field (SWF) and optic nerve head (ONH) cube scan optical coherence tomography (OCT) images. Methods: Forty-five eyes of 25 healthy individuals and 263 eyes of 161 glaucoma patients from the Diagnostic Innovations in Glaucoma Study were included. All eyes underwent 24-2 visual field testing and OCT (Spectralis SD-OCT) ONH and macular imaging. SWF images (up to 43° × 28°) were created by stitching together ONH cube scans centered on the optic disc and macular cube scans centered on the fovea. Visual field progression was defined as guided progression analysis likely progression and/or a significant (P < 0.01) mean deviation slope of less than -1.0 dB/year. Mixed effects models were used to compare rates of change. Highly myopic eyes were included. Results: Thirty glaucomatous eyes were classified as progressing. In eyes with glaucoma, mean global rate of change was -1.22 µm/year (P < 0.001) using SWF images and -0.83 µm/year (P = 0.003) using ONH cube scans. Rate of change was significantly greater in eyes with progressing glaucoma compared with eyes with nonprogressing glaucoma (-1.51 µm/year vs. -1.24 µm/year; P = 0.002) using SWF images and was similar using ONH cube scans (P = 0.27). Conclusions: In this cohort that includes eyes with and without high axial myopia, the mean rate of retinal nerve fiber layer thinning measured using SWF images was faster in eyes with progressing glaucoma than in eyes with nonprogressing glaucoma. Wide-field OCT images including the ONH and macula can be effective for monitoring glaucomatous progression in patients with and without high myopia.

Comparative analysis of changes in retinal layer thickness following femtosecond laser-assisted cataract surgery and conventional cataract surgery.

BACKGROUND: To investigate the influence of femtosecond laser-assisted cataract surgery (FLACS) on macula by examining changes in retinal layers after FLACS and to compare these changes with those after conventional cataract surgery (CCS). METHODS: This study included 113 unrelated Korean patients with age-related cataract who underwent CCS or FLACS in Severance Hospital between September 2019 and July 2021. Optical coherence tomography was performed before and 1 month after surgery. The total retinal layer (TRL) was separated into the inner retinal layer (IRL) and outer retinal layer (ORL); moreover, the IRL was subdivided into the retinal nerve fiber layer, ganglion cell layer, inner plexiform layer, inner nuclear layer (INL), outer plexiform layer, and outer nuclear layer. We performed between-group comparisons of the postoperative thickness in each retinal layer and the postoperative differences in retinal thickness. The average retinal thickness of the four inner macular ring quadrants was used for comparative analysis. RESULTS: Compared with the CCS group, the FLACS group exhibited a thicker ORL (P = 0.004) and a thinner INL (P = 0.007) after surgery. All retinal layer thickness values showed significant postoperative changes regardless of the type of surgery (P < 0.05). The postoperative increase in TRL and IRL thickness was significantly smaller in the FLACS group than in the CCS group (P = 0.027, P = 0.012). CONCLUSIONS: The 1-month postoperative retinal changes were less pronounced in the FLACS group than in the CCS group.