An investigation into pro-apoptotic targets in experimental glaucoma and the neuroprotective effects of Ginkgo biloba in retinal ganglion cells

Ginkgo biloba has been advocated as a neuroprotective agent for several years in glaucoma. In this study, immunohistochemistry was used to identify known potential molecular targets of Ginkgo biloba related to retinal ganglion cell (RGC) apoptosis in experimental glaucoma, including amyloid precursor protein (APP), Aß, cytochrome c, caspase-3 and tumor necrosis factor receptor-1 (TNF-R1). Furthermore, using apoptotic inducers related to mechanisms implicated in glaucoma, namely Dimethyl sulphoxide (DMSO), ultraviolet C (UVC) and Sodium Azide (NaN3), the effects of the terpenoid fraction of Ginkgo biloba (Ginkgolide A, Ginkgolide B and Bilobalide) were investigated separately in cultured retinal ganglion cells (RGC-5). Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and morphological analysis of DMSO treated RGC-5 was performed using Hoechst 33342 stain. Immunohistochemistry showed a strong inverse correlation between Aß and APP in ocular hypertension (OHT) animals, with APP and Aß accumulation peaking at 1 and 12 weeks after intraocular pressure (IOP) elevation respectively. Cytochrome c and TNF-R1 expression peaked at 3 weeks, and active caspase 3 activity at 12 weeks after IOP elevation. 1% DMSO, UV40, 1mM NaN3 and 50μM Aβ25-35 dose dependently reduced RGC-5 survival at 24 hours by 27%, 20%, 35% and 27% respectively. These effects were inhibited by Ginkgolide A, Ginkgolide B and Bilobalide in different assays at different levels. In these experiments, all three compounds showed a dose-related response although some intrinsic toxicity was observed with Ginkgolide A. Ginkgolide B had the most profound neuroprotective effects in the majority of assays at a concentration range of 0.5-5μg/ml, whereas Ginkgolide A and Bilobalide had variable activity. Although the effect of simultaneous administration of all three fractions was not assessed, work in this thesis suggest that Ginkgolide B can be neuroprotective to RGCs in preventing apoptosis and cell death, therefore may be of use as a neuroprotective strategy in glaucoma management

Vogt-Koyanagi-Harada syndrome - current perspectives

Vogt-Koyanagi-Harada syndrome is a cause of noninfectious panuveitis, leading to significant vision loss in many patients. It is an autoimmune disease occurring in genetically susceptible individuals and clinically presents as bilateral panuveitis with serous retinal detachments and hyperemic, swollen optic discs, which are associated with neurological and auditory manifestations. Early diagnosis and prompt and adequate treatment with immunosuppressive agents (corticosteroids and other immunosuppressive drugs) may halt disease progression and prevent recurrences and vision loss. This review summarizes the current knowledge on the variable clinical aspects of this disease, highlighting diagnostic and treatment strategies

White Eyelashes and Red Eyes in a 7‐Year‐Old Boy

A 7‐year‐old boy presented to Paediatric Dermatology with a history of white tinges within his eyelashes, followed 2 weeks later by patchy scalp hair hypopigmentation and loss and an area of cutaneous hypopigmentation on the lower back

Examining the Choroid in Ocular Inflammation: A Focus on Enhanced Depth Imaging

The choroid is the vascular layer that supplies the outer retina and is involved in the pathogenesis of several ocular conditions including choroidal tumors, age related macular degeneration, central serous chorioretinopathy, diabetic retinopathy, and uveitis. Nevertheless, difficulties in the visualization of the choroid have limited our understanding of its exact role in ocular pathology. Enhanced depth imaging optical coherent topography (EDI-OCT) is a novel, noninvasive technique that is used to evaluate choroidal thickness and morphology in these diseases. The technique provides detailed objective in vivo visualization of the choroid and can be used to characterize posterior segment inflammatory disorders, monitor disease activity, and evaluate efficacy of treatment. In this review we summarize the current application of this technique in ocular inflammatory disorders and highlight its utility as an additional tool in monitoring choroidal involvement in ocular inflammation

Vogt–Koyanagi–Harada syndrome – current perspectives

Abeir Baltmr,1 Sue Lightman,1,2 Oren Tomkins-Netzer1–3 1Uveitis Service, Moorfields Eye Hospital, London, UK; 2Department of Clinical Ophthalmology, UCL Institute of Ophthalmology, London, UK; 3Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel Abstract: Vogt–Koyanagi–Harada syndrome is a cause of noninfectious panuveitis, leading to significant vision loss in many patients. It is an autoimmune disease occurring in genetically susceptible individuals and clinically presents as bilateral panuveitis with serous retinal detachments and hyperemic, swollen optic discs, which are associated with neurological and auditory manifestations. Early diagnosis and prompt and adequate treatment with immunosuppressive agents (corticosteroids and other immunosuppressive drugs) may halt disease progression and prevent recurrences and vision loss. This review summarizes the current knowledge on the variable clinical aspects of this disease, highlighting diagnostic and treatment strategies. Keywords: multifocal choroiditis, serous retinal detachment, panuveitis, sunset glow fundus, starry sky, corticosteroi