Publications
226 results found
Jutley G, Luk SMH, Dehabadi MH, et al., 2017, Management of glaucoma as a neurodegenerative disease, NEURODEGENERATIVE DISEASE MANAGEMENT, Vol: 7, Pages: 157-172, ISSN: 1758-2024
Balendra SI, Shah PA, Jain M, et al., 2017, Glaucoma: Hot Topics in Pharmacology, CURRENT PHARMACEUTICAL DESIGN, Vol: 23, Pages: 596-607, ISSN: 1381-6128
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- Citations: 6
Kang S, Luk S, Han H, et al., 2016, Refractive outcome of combined phacoemulsification and endoscopic cyclophotocoagulation, International Ophthalmology, Vol: 37, Pages: 1311-1317, ISSN: 0165-5701
Purpose:To compare the refractive outcome of eyes that underwent phacoemulsification combined with endoscopic cyclophotocoagulation (phaco-ECP) with the eyes that underwent phacoemulsification alone.Methods:A retrospective case series review of 103 consecutive eyes that underwent phaco-ECP and 62 eyes that underwent phacoemulsification between January 2006 and August 2012 was conducted. Post-operative refractive outcomes were obtained by subjective refraction or autorefraction. Demographic data, best corrected visual acuity, intraocular pressure, number of glaucoma agents and mean deviation of the Humphrey visual field test (MD) were also analysed.Results:The total number of eyes included in the study was 62 eyes for the phaco-ECP group and 62 eyes for the control group who underwent phacoemulsification alone. More than 90% of eyes (n = 56) in phaco-ECP group achieved post-operative refraction within ±1 dioptre (D) of the target refraction. In the control group, 100% of eyes achieved post-operative refraction within ±1D of the target refraction. When comparing the difference between the target and the actual refractive outcome between the phaco-ECP and the control group, there was no statistically significant difference.Conclusions:Refractive outcome after phaco-ECP is comparable to phacoemulsification alone. This study suggests that the intraocular lens power can be selected for cataract surgery alone and that ECP does not change the effective lens position significantly; therefore, no modification of biometry formulae is required. Phaco-ECP should be considered as an effective, safe and predictable surgical treatment option for glaucoma patients with co-existing cataract.
Nizari S, Guo L, Davis BM, et al., 2016, Non-amyloidogenic effects of alpha 2 adrenergic agonists: implications for brimonidine-mediated neuroprotection, Cell Death and Disease, Vol: 7, ISSN: 2041-4889
The amyloid beta (Aβ) pathway is strongly implicated in neurodegenerative conditions such as Alzheimer’s disease and more recently, glaucoma. Here, we identify the α2 adrenergic receptor agonists (α2ARA) used to lower intraocular pressure can prevent retinal ganglion cell (RGC) death via the non-amyloidogenic Aβ-pathway. Neuroprotective effects were confirmed in vivo and in vitro in different glaucoma-related models using α2ARAs brimonidine (BMD), clonidine (Clo) and dexmedetomidine. α2ARA treatment significantly reduced RGC apoptosis in experimental-glaucoma models by 97.7% and 92.8% (BMD, P<0.01) and 98% and 92.3% (Clo, P<0.01)) at 3 and 8 weeks, respectively. A reduction was seen in an experimental Aβ-induced neurotoxicity model (67% BMD and 88.6% Clo, both P<0.01, respectively), and in vitro, where α2ARAs significantly (P<0.05) prevented cell death, under both hypoxic (CoCl2) and stress (UV) conditions. In experimental-glaucoma, BMD induced ninefold and 25-fold and 36-fold and fourfold reductions in Aβ and amyloid precursor protein (APP) levels at 3 and 8 weeks, respectively, in the RGC layer, with similar results with Clo, and in vitro with all three α2ARAs. BMD significantly increased soluble APPα (sAPPα) levels at 3 and 8 weeks (2.1 and 1.6-fold) in vivo and in vitro with the CoCl2 and UV-light insults. Furthermore, treatment of UV-insulted cells with an sAPPα antibody significantly reduced cell viability compared with BMD-treated control (52%), co-treatment (33%) and untreated control (27%). Finally, we show that α2ARAs modulate levels of laminin and MMP-9 in RGCs, potentially linked to changes in Aβ through APP processing. Together, these results provide new evidence that α2ARAs are neuroprotective through their effects on the Aβ pathway and sAPPα, which to our knowledge, is the first description. Studies have identified the need for &alph
Davis BM, Crawley L, Pahlitzsch M, et al., 2016, Glaucoma: the retina and beyond, Acta Neuropathologica, Vol: 132, Pages: 807-826, ISSN: 1432-0533
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.
Cordeiro MF, 2016, Eyeing the brain, Acta Neuropathologica, Vol: 132, Pages: 765-766, ISSN: 1432-0533
Balendra SI, Davies B, Guo L, et al., 2016, Eye-drop formulation and Evaluation of Miceliar Curcumin for the treatment of glaucoma, Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology (ARVO), Publisher: ASSOC RESEARCH VISION OPHTHALMOLOGY INC, ISSN: 0146-0404
Davis B, Guo L, Brenton J, et al., 2016, Measuring Primary and Secondary Degeneration of Retinal Ganglion Cells in the Rodent Partial Optic Nerve Transection Model, Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology (ARVO), Publisher: ASSOC RESEARCH VISION OPHTHALMOLOGY INC, ISSN: 0146-0404
Normando EM, Davis B, Brenton J, et al., 2016, Retinal Neuroprotective Effect of a Liposomal Formulation of Rosiglitazone in a Rat Model of Parkinson's Disease, Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology (ARVO), Publisher: ASSOC RESEARCH VISION OPHTHALMOLOGY INC, ISSN: 0146-0404
Normando EM, Davis BM, De Groef L, et al., 2016, The retina as an early biomarker of neurodegeneration in a rotenone-induced model of Parkinson's disease: evidence for a neuroprotective effect of rosiglitazone in the eye and brain, Acta Neuropathologica Communications, Vol: 4, ISSN: 2051-5960
Parkinson’s Disease (PD) is the second most common neurodegenerative disease worldwide, affecting 1 % of the population over 65 years of age. Dopaminergic cell death in the substantia nigra and accumulation of Lewy bodies are the defining neuropathological hallmarks of the disease. Neuronal death and dysfunction have been reported in other central nervous system regions, including the retina. Symptoms of PD typically manifest only when more than 70 % of dopaminergic cells are lost, and the definitive diagnosis of PD can only be made histologically at post-mortem, with few biomarkers available.In this study, a rotenone-induced rodent model of PD was employed to investigate retinal manifestations in PD and their usefulness in assessing the efficacy of a novel therapeutic intervention with a liposomal formulation of the PPAR-γ (Peroxisome proliferator-activated receptor gamma) agonist rosiglitazone.Retinal assessment was performed using longitudinal in vivo imaging with DARC (detection of apoptosing retinal cells) and OCT (optical coherence tomography) technologies and revealed increased RGCs (Retinal Ganglion Cells) apoptosis and a transient swelling of the retinal layers at day 20 of the rotenone insult. Follow-up of this model demonstrated characteristic histological neurodegenerative changes in the substantia nigra and striatum by day 60, suggesting that retinal changes precede the “traditional” pathological manifestations of PD. The therapeutic effect of systemic administration of different formulations of rosiglitazone was then evaluated, both in the retina and the brain. Of all treatment regimen tested, sustained release administration of liposome-encapsulated rosiglitazone proved to be the most potent therapeutic strategy, as evidenced by its significant neuroprotective effect on retinal neurons at day 20, and on nigrostriatal neurons at day 60, provided convincing evidence for its potential as a treatment for PD.Our results demonstrate
Davis BM, Guo L, Brenton J, et al., 2016, Towards maximising information extraction from rodent models of ocular disease, Cell Death and Disease, Vol: 7, ISSN: 2041-4889
Stalmans I, Oddone F, Cordeiro MF, et al., 2016, Comparison of preservative-free latanoprost and preservative-free bimatoprost in a multicenter, randomized, investigator-masked cross-over clinical trial, the SPORT trial, GRAEFES ARCHIVE FOR CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY, Vol: 254, Pages: 1151-1158, ISSN: 0721-832X
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- Citations: 9
Davis BM, Guo L, Brenton J, et al., 2016, Automatic quantitative analysis of experimental primary and secondary retinal neurodegeneration: implications for optic neuropathies., Cell Death Discovery, Vol: 2, ISSN: 2058-7716
Secondary neurodegeneration is thought to play an important role in the pathology of neurodegenerative disease, which potential therapies may target. However, the quantitative assessment of the degree of secondary neurodegeneration is difficult. The present study describes a novel algorithm from which estimates of primary and secondary degeneration are computed using well-established rodent models of partial optic nerve transection (pONT) and ocular hypertension (OHT). Brn3-labelled retinal ganglion cells (RGCs) were identified in whole-retinal mounts from which RGC density, nearest neighbour distances and regularity indices were determined. The spatial distribution and rate of RGC loss were assessed and the percentage of primary and secondary degeneration in each non-overlapping segment was calculated. Mean RGC number (82 592±681) and RGC density (1695±23.3 RGC/mm(2)) in naïve eyes were comparable with previous studies, with an average decline in RGC density of 71±17 and 23±5% over the time course of pONT and OHT models, respectively. Spatial analysis revealed greatest RGC loss in the superior and central retina in pONT, but significant RGC loss in the inferior retina from 3 days post model induction. In comparison, there was no significant difference between superior and inferior retina after OHT induction, and RGC loss occurred mainly along the superior/inferior axis (~30%) versus the nasal-temporal axis (~15%). Intriguingly, a significant loss of RGCs was also observed in contralateral eyes in experimental OHT. In conclusion, a novel algorithm to automatically segment Brn3a-labelled retinal whole-mounts into non-overlapping segments is described, which enables automated spatial and temporal segmentation of RGCs, revealing heterogeneity in the spatial distribution of primary and secondary degenerative processes. This method provides an attractive means to rapidly determine the efficacy of neuroprotective therapies with impl
Javaid FZ, Brenton J, Guo L, et al., 2016, Visual and ocular manifestations of Alzheimer's Disease and their use as biomarkers for diagnosis and progression, Frontiers in Neurology, Vol: 7, Pages: 1-11, ISSN: 1664-2295
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.
Ameen S, Javaid F, Cordeiro MF, 2016, Risk calculators in glaucoma, EXPERT REVIEW OF OPHTHALMOLOGY, Vol: 11, Pages: 21-27, ISSN: 1746-9899
Normando EM, Brodie JT, Francesca Cordeiro M, 2016, Animal models in neuro ophthalmology, OCT in Central Nervous System Diseases: The Eye as a Window to the Brain, Pages: 239-263, ISBN: 9783319240831
Neuro-ophthalmology is the branch of ophthalmology dedicated to the study of neurological conditions which affect the visual system. An adequate understanding of the aetiology and pathophysiology of neuro-ophthalmic conditions is fundamental for establishing successful therapeutic strategies. Animal models are therefore considered crucial for understanding and investigating pathological events. Several animal models have been developed for studying neuro-ophthalmic disorders. However, their validity is closely related to the level of similarity with the human pathology. Rodent models are extensively used due to their accessibility and cost efficiency. In particular, mouse models are recognised as among the best genetic models due to the ability to easily alter their genome. Rats are easy to breed and mostly used for toxic/pharmacological and surgical models. Nevertheless, rodent models are still suboptimal for human neuro-ophthalmic conditions because of anatomical differences between species. Primate models have the obvious advantage of sharing vast anatomical and genomic similarities with humans. However, monkeys are expensive, difficult to breed and can only be handled by qualified personnel, all of which limits their suitability. Hence, there is no perfect species for studying neuro-ophthalmic conditions. This chapter will focus on the most common animal models of neuro-ophthalmic conditions.
Tian K, Shibata-Germanos S, Pahlitzsch M, et al., 2015, Current perspective of neuroprotection and glaucoma, CLINICAL OPHTHALMOLOGY, Vol: 9, Pages: 2109-2118, ISSN: 1177-5483
Glaucoma is the second leading cause of blindness worldwide and is most notably characterized by progressive optic nerve atrophy and advancing loss of retinal ganglion cells (RGCs). The main concomitant factor is the elevated intraocular pressure (IOP). Existing treatments are focused generally on lowering IOP. However, both RGC loss and optic nerve atrophy can independently occur with IOP at normal levels. In recent years, there has been substantial progress in the development of neuroprotective therapies for glaucoma in order to restore vital visual function. The present review intends to offer a brief insight into conventional glaucoma treatments and discuss exciting current developments of mostly preclinical data in novel neuroprotective strategies for glaucoma that include recent advances in noninvasive diagnostics going beyond IOP maintenance for an enhanced global view. Such strategies now target RGC loss and optic nerve damage, opening a critical therapeutic window for preventative monitoring and treatment.
Galvao J, Elvas F, Martins T, et al., 2015, Adenosine A<sub>3</sub> receptor activation is neuroprotective against retinal neurodegeneration, EXPERIMENTAL EYE RESEARCH, Vol: 140, Pages: 65-74, ISSN: 0014-4835
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- Citations: 42
Balendra SI, Normando EM, Bloom PA, et al., 2015, Advances in retinal ganglion cell imaging, EYE, Vol: 29, Pages: 1260-1269, ISSN: 0950-222X
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- Citations: 29
Cordeiro MF, Goldberg I, Schiffman R, et al., 2015, Efficacy of a preservative-free formulation of fixed-combination bimatoprost and timolol (Ganfort PF) in treatment-naive patients vs previously treated patients, Clinical Ophthalmology, Vol: 9, Pages: 1605-1611, ISSN: 1177-5467
Purpose: To evaluate, using subgroup analysis, the effect of treatment status on the intraocular pressure (IOP)-lowering efficacy of a preservative-free formulation of fixed-combination bimatoprost 0.03%/timolol 0.5% (FCBT PF).Methods: A primary, multicenter, randomized, double-masked, 12-week study compared the efficacy and safety of FCBT PF with preserved FCBT (Ganfort®) in 561 patients diagnosed with glaucoma or ocular hypertension. For this analysis, eligible patients were treatment-naïve or had inadequate IOP lowering and underwent a washout of previous treatment. IOP (8 am, 10 am, and 4 pm) was measured at baseline and weeks 2, 6, and 12. Subgroup analysis of the FCBT PF arm assessed changes in average eye IOP from baseline in treatment-naïve vs previously treated patients. To evaluate the effect of treatment status at baseline (treatment-naïve vs previously treated) on IOP reduction in the FCBT PF treatment group, an analysis of covariance model was used with treatment status and investigator as fixed effects, and baseline average eye IOP, age, glaucoma diagnosis, and baseline average eye corneal thickness as covariates. P-values and the 95% confidence intervals were determined using the model.Results: In the FCBT PF arm, IOP mean changes from baseline ranged from -8.7 mmHg to -9.8 mmHg in treatment-naïve patients (N=50), compared with -7.3 mmHg to -8.5 mmHg in previously treated patients (N=228). Baseline IOP, age, glaucoma diagnosis, and corneal thickness significantly affected IOP reduction in the FCBT PF group. Adjusting for these covariates, FCBT PF had a greater IOP-lowering effect (0.8–1.7 mmHg) in treatment-naïve patients than previously treated patients, which was statistically significant (P≤0.05) at seven of nine time points.Conclusion: In this subgroup analysis, FCBT PF reduced IOP more effectively in treatment-naïve than in previously treated patients possibly due, in part, to altered responsiveness or t
Ghaffar M-A, Davis B, Turner L, et al., 2015, New method for semi-automated identification of changes in DARC-labelled cells in the same eye at different time points in vivo, Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology (ARVO), Publisher: ASSOC RESEARCH VISION OPHTHALMOLOGY INC, ISSN: 0146-0404
Normando EM, Davis B, Nizari S, et al., 2015, Neuroprotective Effect of Rosiglitazone on Retinal Changes in a Rat Model of Parkinson's Disease, Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology (ARVO), Publisher: ASSOC RESEARCH VISION OPHTHALMOLOGY INC, ISSN: 0146-0404
Bono V, Normando EM, Davis B, et al., 2015, Cluster visual field progression and its relationship with optic disc changes, Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology (ARVO), Publisher: ASSOC RESEARCH VISION OPHTHALMOLOGY INC, ISSN: 0146-0404
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- Citations: 1
Shi H, Williams JA, Guo L, et al., 2015, Exposure to the complement C5b-9 complex sensitizes 661W photoreceptor cells to both apoptosis and necroptosis, Apoptosis, Vol: 20, Pages: 433-443, ISSN: 1573-675X
The loss of photoreceptors is the defining characteristic of many retinal degenerative diseases, but the mechanisms that regulate photoreceptor cell death are not fully understood. Here we have used the 661W cone photoreceptor cell line to ask whether exposure to the terminal complement complex C5b-9 induces cell death and/or modulates the sensitivity of these cells to other cellular stressors. 661W cone photoreceptors were exposed to complete normal human serum following antibody blockade of CD59. Apoptosis induction was assessed morphologically, by flow cytometry, and on western blotting by probing for cleaved PARP and activated caspase-3. Necroptosis was assessed by flow cytometry and Sirtuin 2 inhibition using 2-cyano-3-[5-(2,5-dichlorophenyl)-2-furyl]-N-5-quinolinylacrylamide (AGK2). The sensitivity of 661W cells to ionomycin, staurosporine, peroxide and chelerythrine was also investigated, with or without prior formation of C5b-9. 661W cells underwent apoptotic cell death following exposure to C5b-9, as judged by poly(ADP-ribose) polymerase 1 cleavage and activation of caspase-3. We also observed apoptotic cell death in response to staurosporine, but 661W cells were resistant to both ionomycin and peroxide. Interestingly, C5b-9 significantly increased 661W sensitivity to staurosporine-induced apoptosis and necroptosis. These studies show that low levels of C5b-9 on 661W cells can induce apoptosis, and that C5b-9 specifically sensitizes 661W cells to certain apoptotic and necroptotic pathways. Our observations provide new insight into the potential role of the complement system in photoreceptor loss, with implications for the molecular aetiology of retinal disease.
Heaton GR, Davis BM, Turner LA, et al., 2015, Ocular biomarkers of Alzheimer's disease., Cent Nerv Syst Agents Med Chem, Vol: 15, Pages: 117-125
Alzheimer's disease (AD) is a devastating neurodegenerative disease characterised clinically by a progressive decline in executive functions, memory and cognition. Classic neuropathological hallmarks of AD include intracellular hyper-phosphorylated tau protein which forms neurofibrillary tangles (NFT), and extracellular deposits of amyloid β (Aβ) protein, the primary constituent of senile plaques (SP). The gradual process of pathogenic amyloid accumulation is thought to occur 10-20 years prior to symptomatic manifestation. Advance detection of these deposits therefore offers a highly promising avenue for prodromal AD diagnosis. Currently, the most sophisticated method of 'probable AD' diagnosis is via neuroimaging or cerebral spinal fluid (CSF) biomarker analysis. Whilst these methods have reported a high degree of diagnostic specificity and accuracy, they fall significantly short in terms of practicality; they are often highly invasive, expensive or unsuitable for large-scale population screening. In recent years, ocular screening has received substantial attention from the scientific community due to its potential for non-invasive and inexpensive central nervous system (CNS) imaging. In this appraisal we build upon our previous reviews detailing ocular structural and functional changes in AD (Retinal manifestations of Alzheimer's disease, Alzheimer's disease and Retinal Neurodegeneration) and consider their use as biomarkers. In addition, we present an overview of current advances in the use of fluorescent reporters to detect AD pathology through non-invasive retinal imaging.
Normando EM, Dehabadi MH, Guo L, et al., 2015, Real-Time Imaging of Retinal Cell Apoptosis by Confocal Scanning Laser Ophthalmoscopy, NEURONAL CELL DEATH: METHODS AND PROTOCOLS, Editors: Lossi, Merighi, Publisher: HUMANA PRESS INC, Pages: 227-237, ISBN: 978-1-4939-2151-5
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- Citations: 6
Agarwal N, Hanumunthadu D, Afrasiabi M, et al., 2015, Clinical update in optic nerve disorders, EXPERT REVIEW OF OPHTHALMOLOGY, Vol: 10, Pages: 145-166, ISSN: 1746-9899
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- Citations: 5
Salt TE, Nizari S, Cordeiro MF, et al., 2014, Effect of the Aβ Aggregation Modulator MRZ-99030 on Retinal Damage in an Animal Model of Glaucoma, NEUROTOXICITY RESEARCH, Vol: 26, Pages: 440-446, ISSN: 1029-8428
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- Citations: 16
Guo L, Davis B, Nizari S, et al., 2014, Direct optic nerve sheath (DONS) application of Schwann cells prolongs retinal ganglion cell survival in vivo, Cell Death and Disease, Vol: 5, ISSN: 2041-4889
Cell-based therapies are increasingly recognized as a potential strategy to treat retinal neurodegenerative disease. Their administration, however, is normally indirect and complex, often with an inability to assess in real time their effects on cell death and their migration/integration into the host retina. In the present study, using a partial optic nerve transection (pONT) rat model, we describe a new method of Schwann cell (SC) delivery (direct application to injured optic nerve sheath, SC/DONS), which was compared with intravitreal SC delivery (SC/IVT). Both SC/DONS and SC/IVT were able to be assessed in vivo using imaging to visualize retinal ganglion cell (RGC) apoptosis and SC retinal integration. RGC death in the pONT model was best fitted to the one-phase exponential decay model. Although both SC/DONS and SC/IVT altered the temporal course of RGC degeneration in pONT, SC/DONS resulted in delayed but long-lasting effects on RGC protection, compared with SC/IVT treatment. In addition, their effects on primary and secondary degeneration, and axonal regeneration, were also investigated, by histology, whole retinal counting, and modelling of RGC loss. SC/DONS was found to significantly reduce RGC apoptosis in vivo and significantly increase RGC survival by targeting secondary rather than primary degeneration. Both SC/DONS and SC/IVT were found to promote RGC axonal regrowth after optic nerve injury, with evidence of GAP-43 expression in RGC somas and axons. SC/DONS may have the potential in the treatment of optic neuropathies, such as glaucoma. We show that SC transplantation can be monitored in real time and that the protective effects of SCs are associated with targeting secondary degeneration, with implications for translating cell-based therapies to the clinic.
Liu M, Guo L, Salt TE, et al., 2014, Dendritic Changes in Rat Visual Pathway Associated with Experimental Ocular Hypertension, CURRENT EYE RESEARCH, Vol: 39, Pages: 953-963, ISSN: 0271-3683
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- Citations: 14
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