Physical Activity and Quality of Life in Retinitis Pigmentosa

Purpose. Aerobic exercise has been found to be neuroprotective in animal models of retinal degeneration. This study aims to report physical activity levels in patients with RP and investigate the relationship between physical activity and vision-related quality-of-life (QOL). Materials and Methods. A retrospective study of adult patients with RP examined in 2005–2014. Physical activity levels were assessed using the Godin Exercise Questionnaire. The NEI-Visual Function Questionaire-25 (VFQ-25), SF-36 General Health survey, and Pepper Assessment Tool for Disability (PAT-D) were administered. Results. 143 patients participated. 81 (56.6%) patients were classified as “active” and 62 (43.4%) as “insufficiently active” by Godin score. VFQ-25 revealed statistically significant differences between the active and insufficiently active patients, including overall visual function (53.3 versus 45.1, p=0.010), color vision (73.8 versus 52.9, p<0.001), and peripheral vision (34.3 versus 23.8, p=0.021). The physical component of the SF-36 and the PAT-D survey also demonstrated statistically significant differences (47.2 versus 52.9, p=0.002; 24.3 versus 30.0, p=0.010). Active patients had a higher initial Goldmann visual field (GVF) score (74.8 versus 60.1 degrees, p=0.255) and final GVF score (78.7 versus 47.1 degrees, p=0.069) but did not reach statistical significance. Conclusions. In RP, increased physical activity is associated with greater self-reported visual function and QOL

Inner retinal preservation in rat models of retinal degeneration implanted with subretinal photovoltaic arrays

Photovoltaic arrays (PVA) implanted into the subretinal space of patients with retinitis pigmentosa (RP) are designed to electrically stimulate the remaining inner retinal circuitry in response to incident light, thereby recreating a visual signal when photoreceptor function declines or is lost. Preservation of inner retinal circuitry is critical to the fidelity of this transmitted signal to ganglion cells and beyond to higher visual targets. Post-implantation loss of retinal interneurons or excessive glial scarring could diminish and/or eliminate PVA-evoked signal transmission. As such, assessing the morphology of the inner retina in RP animal models with subretinal PVAs is an important step in defining biocompatibility and predicting success of signal transmission. In this study, we used immunohistochemical methods to qualitatively and quantitatively compare inner retinal morphology after the implantation of a PVA in two RP models: the Royal College of Surgeons (RCS) or transgenic S334ter-line 3 (S334ter-3) rhodopsin mutant rat. Two PVA designs were compared. In the RCS rat, we implanted devices in the subretinal space at 4 weeks of age and histologically examined them at 8 weeks of age and found inner retinal morphology preservation with both PVA devices. In the S334ter-3 rat, we implanted devices at 6-12 weeks of age and again, inner retinal morphology was generally preserved with either PVA design 16-26 weeks post-implantation. Specifically, the length of rod bipolar cells and numbers of cholinergic amacrine cells were maintained along with their characteristic inner plexiform lamination patterns. Throughout the implanted retinas we found nonspecific glial reaction, but none showed additional glial scarring at the implant site. Our results indicate that subretinally implanted PVAs are well-tolerated in rodent RP models and that the inner retinal circuitry is preserved, consistent with our published results showing implant-evoked signal transmission

Lack of cone mediated retinal function increases susceptibility to form-deprivation myopia in mice

© 2018 Elsevier Ltd. This manuscript version is made available under the CC-BY-NC-ND 4.0 license: http://creativecommons.org/licenses/by-nc-nd/4.0/ This author accepted manuscript is made available following 12 month embargo from date of publication (December 2018) in accordance with the publisher’s archiving policyRetinal photoreceptors are important in visual signaling for normal eye growth in animals. We used Gnat2cplf3/cplf3 (Gnat2−/−) mice, a genetic mouse model of cone dysfunction to investigate the influence of cone signaling in ocular refractive development and myopia susceptibility in mice. Refractive development under normal visual conditions was measured for Gnat2−/− and age-matched Gnat2+/+ mice, every 2 weeks from 4 to 14 weeks of age. Weekly measurements were performed on a separate cohort of mice that underwent monocular form-deprivation (FD) in the right eye from 4 weeks of age using head-mounted diffusers. Refraction, corneal curvature, and ocular biometrics were obtained using photorefraction, keratometry and optical coherence tomography, respectively. Retinas from FD mice were harvested, and analyzed for dopamine (DA) and 3,4-dihydroxyphenylacetate (DOPAC) using high-performance liquid chromatography. Under normal visual conditions, Gnat2+/+ and Gnat2−/− mice showed similar refractive error, axial length, and corneal radii across development (p > 0.05), indicating no significant effects of the Gnat2 mutation on normal ocular refractive development in mice. Three weeks of FD produced a significantly greater myopic shift in Gnat2−/− mice compared to Gnat2+/+ controls (−5.40 ± 1.33 D vs −2.28 ± 0.28 D, p = 0.042). Neither the Gnat2 mutation nor FD altered retinal levels of DA or DOPAC. Our results indicate that cone pathways needed for high acuity vision in primates are not as critical for normal refractive development in mice, and that both rods and cones contribute to visual signalling pathways needed to respond to FD in mammalian eyes. Note: Aspects of the article have been presented at the American Academy of Optometry meeting on November 2016 in Anaheim, California, USA

IMI 2021 Yearly Digest

PURPOSE. The International Myopia Institute (IMI) Yearly Digest highlights new research considered to be of importance since the publication of the first series of IMI white papers. METHODS. A literature search was conducted for articles on myopia between 2019 and mid-2020 to inform definitions and classifications, experimental models, genetics, interventions, clinical trials, and clinical management. Conference abstracts from key meetings in the same period were also considered. RESULTS. One thousand articles on myopia have been published between 2019 and mid-2020. Key advances include the use of the definition of premyopia in studies currently under way to test interventions in myopia, new definitions in the field of pathologicmyopia, the role of new pharmacologic treatments in experimental models such as intraocular pressure-lowering latanoprost, a large meta-analysis of refractive error identifying 336 new genetic loci, new clinical interventions such as the defocus incorporated multisegment spectacles and combination therapy with low-dose atropine and orthokeratology (OK), normative standards in refractive error, the ethical dilemma of a placebo control group when myopia control treatments are established, reporting the physical metric of myopia reduction versus a percentage reduction, comparison of the risk of pediatric OK wear with risk of vision impairment in myopia, the justification of preventing myopic and axial length increase versus quality of life, and future vision loss. CONCLUSIONS. Large amounts of research in myopia have been published since the IMI 2019 white papers were released. The yearly digest serves to highlight the latest research and advances in myopia.Peer reviewe

The Diagnosis and Treatment of Early Stage Diabetic Retinopathy

2015 Fall Meeting of the NanoFANS Forum. Presented on October 29, 2015 from 11 a.m.-3 p.m. in the Marcus Nanotechnology Building (Rooms 1116-1118) on the Georgia Tech campus.NanoFANS Fall 2015 - Event Focus: Current Trends in OphthalmologyDr. Machelle T. Pardue is a Professor of Biomedical Engineering at Georgia Tech and Atlanta VA Medical Center.Runtime: 47:10 minutesDiabetic retinopathy (DR) is the leading cause of blindness in adults 20 to 74 years of age. Detecting early stage retinopathy prior to the onset of clinical findings would greatly impact the management and treatment of DR. We have identified several tests that show dysfunction in the retina prior to the onset of clinically‐significant vascular lesions induced by diabetes. We have determine that rod photoreceptor function is most vulnerable to diabetes using novel stimuli with the electroretinogram. Our studies show similar delays in rodent models of diabetes and diabetic patients, prior to clinically diagnosed DR. In addition, we have shown that spatial frequency and contrast sensitivity declines prior to vascular changes when tested with moving gratings. Finally, we have demonstrated that the application of inducible fluorescent tags to detect ROS in the retina, providing another possible screening tool for DR. To determine the mechanisms underlying neuronal dysfunction in early DR, we examined the role of decreased retinal dopamine, a key neuromodulator in the retina. Using our screening tools to detect early disease, we are able to preserve retinal and visual function in diabetic rodents by restoring dopamine levels with L‐DOPA or exercise therapies