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The case of a 66-year-old man with blurred and distorted vision is discussed to better understand neovascular age-related macular degeneration (AMD). The different treatment methodologies and management regime for the same including Ranibizumab therapy are highlighted.

Although age-related macular degeneration is the most prevalent macular disease in the world, numerous discoveries regarding the molecular bases of vision have been made through genetic association studies of rare inherited maculopathies. In this issue of the JCI, Yang et al. present a functional genetics study that identifies a role for prominin 1 (PROM1), best known as a stem cell and/or progenitor cell marker, in the biogenesis of retinal photoreceptor disk arrays (see the related article beginning on page 2908). This study supports an established model in which disk morphogenesis occurs through membrane evagination and extends other recent studies assigning PROM1 important functions outside of the stem cell niche., Essentials of photoreceptor organization More than 50 years ago, the first ultrastructural evidence of photoreceptor disk organization was published by noted electron microscopist Fritiof Sjostrand (1). Subsequent studies provided more [...]

Macular degeneration is a type of blindness that develops after the age of 50 years and is irreversible. The symptoms, diagnosis and management of the problem are discussed.

We apply the life-span theory of control proposed by Heckhausen and Schulz to study the change in use of control strategies related to age-related macular degeneration (AMD). A mixed-model approach considers nonlinear relations of rate of change in the use of control strategies with time since diagnosis and functional ability. Data stem from a sample of 90 individuals with AMD (age, M = 79.5 years at Time 1), of whom 71 were assessed two times over 1 year. Compensatory primary control strategies increased shortly after the diagnosis, whereas the increase in compensatory secondary control strategies was related to functional loss in instrumental daily activities. Findings provide support for the critical role of compensatory control strategies in the event that individuals with AMD are faced with anticipated or real functional loss.

OBJECTIVE: To determine whether either of the gene variants associated with age-related macular degeneration is associated with coronary artery disease (CAD). PATIENTS AND METHODS: This study consisted of 493 patients [...]

Macular degeneration is a large group of conditions that are collectively the most common cause of irreversible vision loss in the developed world and many forms of macular degeneration have a considerable genetic component. A lot of progress is made in understanding the genes involved while in future, genetic testing might allow specific preventive treatments to be administered to individuals at risk, decades before the disease would normally become noticeable.

A study of adaptation in affective well-being under a prevalent chronic health condition was studied using age-related macular degeneration as a case model in which measures of positive and negative affect were analyzed in older adults diagnosed with age-related macular degeneration (AMD). Results showed an initial decline in affective well-being after disease outbreak followed by a turnaround into a restorative phase of increase for positive affect but not for negative affect.

ABSTRACT Background Age-related macular degeneration (AMD) is the leading cause of blindness in people over 50 y of age in at least three continents. Choroidal neovascularization (CNV) is the process [...]

Mutations in VMD2, encoding bestrophin (best-1), cause Best vitelliform macular dystrophy (BMD), adult-onset vitelliform macular dystrophy (AVMD), and autosomal dominant vitreoretinochoroidopathy (ADVIRC). BMD is distinguished fl-om AVMD by a diminished electrooculogram light peak (LP) in the absence of changes in the flash electroretinogram. Although the LP is thought to be generated by best-l, we find enhanced LP luminance responsiveness with normal amplitude in Vmd[2.sup.-/-] mice and no differences in cellular [Cl.sup.-] currents in comparison to Vmd[2.sup.+/+] littermates. The putative [Ca.sup.2+] sensitivity of best-l, and our recent observation that best-1 alters the kinetics of voltage-dependent [Ca.sup.2+] channels (VDCC), led us to examine the role of VDCCs in the LR Nimodipine diminished the LP, leading us to survey VDCC [beta]-subunit mutant mice. Lethargic mice, which harbor a loss of function mutation in the [[beta]sub.4] subunit of VDCCs, exhibited a significant shift in LP luminance response, establishing a role for [Ca.sup.2+] in LP generation. When stimulated with ATE which increases [[[Ca.sup.++]].sub.l], retinal pigment epithelial cells derived from Vmd[2.sup.- /-] mice exhibited a fivefold greater response than Vmd[2.sup.+/+] littermates, indicating that best-1 can suppress the rise in [[[Ca.sup.2+]].sub.1] associated with the LR We conclude that VDCCs regulated by a [[beta].sub.4] subunit are required to generate the LP and that best-1 antagonizes the LP luminance response potentially via its ability to modulate VDCC function. Furthermore, we suggest that the loss of vision associated with BMD is not caused by the same pathologic process as the diminished LP, but rather is caused by as yet unidentified effects of best-1 on other cellular processes.