Biofeedback training has been used to improve fixation stability in subjects with central vision loss, but the psychophysiological mechanisms underlying the functional improvements resulted was not reported. The aim of this study was to investigate the effects of microperimetric biofeedback training on different visual functions and self-reported quality of vision in subjects with age-related macular degeneration. This case-control study included six subjects (72.0 ± 6.1 years of age) diagnosed with age-related macular degeneration (wet or dry) with low vision (best corrected visual acuity ranging from 0.5 to 0.1 in the study eye) and five healthy volunteers (64.2 ± 3.7 years of age). Ophthalmological and functional examinations were obtained from all subjects twice with an approximately 3-month interval. Subjects with central vision loss performed 12 sessions (10 min each) of biofeedback training between the two examinations. Functional evaluation included: microperimetry, spatial luminance contrast sensitivities, color vision thresholds, visual acuity, and reading speed. Visual performance during daily activities was also assessed using a standardized questionnaire. The ratio (2nd/1st examination) of the spatial luminance contrast sensitivity at lower spatial frequencies were much higher for the training subjects compared with the controls. In addition, self-reported quality of vision improved after the training. The significant improvement of the visual function such as spatial luminance contrast sensitivity may explain the better self-reported quality of vision. Possible structural and physiological mechanisms underlying this neuromodulation are discussed.

In the literature various causes of opacification of hydrophilic lenses have been described. Pronounced opacity is a complication that must be taken seriously because it can lead to explantation or exchange of the intraocular lens (IOL). The calcification of hydrophilic IOLs is often made responsible for an explantation. Despite the rapidly increasing number of intravitreal injections, they have so far not been associated with opacification of lenses. This article reports on a female patient where opacification of the hydrophilic lens was obviously associated with multiple intravitreal injections over several years. It involved a secondary calcification with calcium phosphate deposition directly under the surface of the IOL. Possible pathomechanisms are discussed. Due to the increasing number of intravitreal injections the association with IOL opacity should be further evaluated in the future. Generally, with hydrophilic lens materials it must be taken into consideration that these can become opaque following diverse interventions.

Aim: To present a series of 2 cases of central serous chorioretinopathy and the changes in the macular pigment optical density during the evolution of the disease. Material and methods: A 32-year-old patient presented himself for blurred vision on his LE. The SD OCT imaging revealed serous macular detachment of the neurosensory retina on the LE. The MPOD results were 0.72 on RE and 0.91 on LE. After treatment and resorption of the subretinal fluid, the MPOD values were 0.72 on the RE and 0.82 on the LE. The second patient was a 36-year-old male with metamorphopsia on LE and serous macular detachment on this eye. The MPOD results were 0.43 on RE and 0.58 on the LE and, after treatment, they were 0.38 on the RE and 0.43 on the LE. Conclusions: Central serous chorioretinopathy is a disease of unknown pathophysiology in which we observed a higher MPOD on the eye with CSC than on the fellow eye and a decrease in the MPOD value after the resorption of the subretinal fluid. Abbreviations: L = lutein, Z = zeaxantin, MZ = mezozeaxantin, AMD = age related macular degeneration, MPOD = macular pigment optical density, MP = macular pigment, HFP = Heterochromatic Flicker Photometry, CSC = central serous chorioretinopathy, RE = right eye, LE = left eye.

This report describes a lamellar macular hole formation subsequent to intravitreal bevacizumab injection for the treatment of choroidal neovascularization (CNV) by age-related macular degeneration. A 67-year-old woman with bilateral CNV underwent 3 monthly intravitreal bevacizumab injections in her both eyes. One month after the third bilateral injection, vision loss happened. Optical coherence tomography performed for further evaluation that showed reduction of intra- and sub-retinal fluid associated with lamellar macular hole development in both eyes. Although macular hole formation, especially bilateral form, is a rare complication of intravitreal injections, surgeons should consider macular hole development in cases with vision deterioration following intravitreal bevacizumab injection.

Non-exudative age-related macular degeneration (NE-AMD) represents the leading cause of blindness in the elderly. The macular retinal pigment epithelium (RPE) lies in a high oxidative environment because its high metabolic demand, mitochondria concentration, reactive oxygen species levels, and macular blood flow. It has been suggested that oxidative stress-induced damage to the RPE plays a key role in NE-AMD pathogenesis. The fact that the disease limits to the macular region raises the question as to why this area is particularly susceptible. We have developed a NE-AMD model induced by superior cervical ganglionectomy (SCGx) in C57BL/6J mice, which reproduces the disease hallmarks exclusively circumscribed to the temporal region of the RPE/outer retina. The aim of this work was analyzing RPE regional differences that could explain AMD localized susceptibility. Lower melanin content, thicker basal infoldings, higher mitochondrial mass, and higher levels of antioxidant enzymes, were found in the temporal RPE compared with the nasal region. Moreover, SCGx induced a decrease in the antioxidant system, and in mitochondria mass, as well as an increase in mitochondria superoxide, lipid peroxidation products, nuclear Nrf2 and heme oxygenase-1 levels, and in the occurrence of damaged mitochondria exclusively at the temporal RPE. These findings suggest that despite the well-known differences between the human and mouse retina, it might not be NE-AMD pathophysiology which conditions the localization of the disease, but the macular RPE histologic and metabolic specific attributes that make it more susceptible to choroid alterations leading initially to a localized RPE dysfunction/damage, and secondarily to macular degeneration.

Macular degeneration is hallmarked by retinal accumulation of toxic retinoid species (e.g. A2E) for which there is no endogenous mechanism to eliminate. This ultimately results in progressive dysfunction and loss of vision either in advanced age for genetically normal patients (age-related macular degeneration), or in adolescence for those with inherited genetic mutations (Stargardt's disease). Here, we present a proof-of-concept study for an enzyme-based therapy to remove these retinoids, modeled on traditional enzyme replacement therapy. Recombinant manganese peroxidase (rMnP) is produced in Pichia pastoris. In vitro, we demonstrate that rMnP breaks down A2E and other lipofuscin fluorophores with limited cellular toxicity, and as this enzyme is mannosylated, it can be taken up into cells via mannose receptor-dependent endocytosis. In vivo we demonstrate that rMnP can significantly reduce the A2E burden when administered by intravitreal injections. Together, these data provide encouraging results towards the development of an enzyme-based therapy for macular degeneration and indicate the need for additional work to characterize the molecular mechanism of A2E breakdown and to improve the pharmacological parameters of the enzyme.