Aims and Purpose The aim of this study was to describe the prevalence and characteristics of drusen and pigmentary changes in a middle-aged population. Methods Retinal images from 500 individuals aged 18-54 years were included. The source of participants was two UK optometry practices. Retinal images were graded using the Wisconsin Age-Related Maculopathy Grading System. However, owing to the relatively young age of the population studied, a new category of drusen of smaller size (o31.5 mm) was introduced. Results Drusen were identified within the central macular grid in 91.48% of all gradable eyes and in 444 subjects. Drusen sized o31.5 mm were present in 89.7% of eyes, drusen sized 431.5 mm and o63 mm were present in 45.9% of all eyes and drusen 463 mm and o125 mm were present in only 1.7% of eyes. No eye had drusen larger or equal to 125 mm. Very few eyes (1.2%) showed pigmentary changes within the grid. Drusen load increased with increasing age, P o0.001. Conclusions The frequency of drusen in a younger Caucasian population aged 18-54 years is high, with 91.48% of all gradable eyes having drusen. The most frequent drusen subtype was hard distinct drusen o31.5 mm. No druse greater or equal in size to 125 mm was seen. Pigmentary changes are rare.

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PURPOSE.To characterize in vivo dendritic changes in retinal ganglion cells (RGCs) after acute (optic nerve transection, ONT) and chronic (experimental glaucoma, EG) optic nerve injury. METHODS.ONT and EG (microbead model) were carried out in Thy1-YFP mice in which the entire RGC dendritic arbor was imaged with confocal fluorescence scanning laser ophthalmoscopy over two weeks in the ONT group and over two and six months, respectively, in two (groups 1 and 2) EG groups. Sholl analysis was used to quantify dendritic structure with the parameters: area under the curve (AUC), radius of the dendritic field, peak number of intersections (PI), and distance to the PI (PD).RESULTS. Dendritic changes were observed after three days post-ONT with significant decreases in all parameters at two weeks. In group 1 EG mice, mean (SD) intraocular pressure (IOP) was 15.2 (1.1) and 9.8 (0.3) mmHg in the EG and untreated contralateral eyes, respectively, with a significant corresponding decrease in AUC, PI, and PD, but not radius. In group 2 mice, the respective IOP was 13.1 (1.0) and 8.8 (0.1) mmHg, peaking at two months before trending towards baseline. Over the first two months, AUC, PI, and PD decreased significantly, with no further subsequent changes. The rates of change of the parameters after ONT was 5 to 10 times faster than in EG. CONCLUSIONS.Rapid dendritic changes occurred after ONT, while changes in EG were slower and associated with level of IOP increase. The earliest alterations were loss of inner neurites without change in dendritic field.

Glaucoma is a multifactorial neurodegenerative disease that leads to the progressive loss of retinal ganglion cells (RGCs) and their axons resulting in visual field damage and retinal and optic nerve head changes. Progression is generally slow but, in some patients, can lead to a ‘catastrophic’ reduction of visual function and in advanced cases may lead to blindness. Glaucoma is, in fact, the leading cause of irreversible blindness worldwide. Finding a model of retinal ganglion cell (RGC) loss or experimental glaucoma which accurately mimics human disease has been a challenge for researchers. There have been many attempts to produce a model of studying RGC pathophysiology or death longitudinally to study pharmacological treatments or neuroprotective interventions. There are many methods, both acute and chronic, that have been used to induce retinal ganglion cell death. Some methods made a direct injury to the optic nerve which causes rapid RGC death, while others are models try to increase the IOP with mechanical damage or injection of different agents into the anterior chamber to block aqueous humour outflow. Several models of chronic glaucoma, primarily in non‐human primates and rodents, in which IOP is elevated has been described. However, most of these animal models due to the opacification of the ocular medias as a result of the inflammation or intraocular pression increase only allow to perform a single time point for many different time ex vivo analysis of the RGCs. So, longitudinal changes in the number of RGCs in the same animal can only be performed in vivo. This is an important way to remove the between‐subject variability, but any aging effects will be compounded to those due to disease progression. A novel glaucoma model using a cross‐linking polymer result in a consistent and sustained elevation of IOP with preservation of optical media clarity for long term. This model is based on in situ temperature sensitive cross‐linking of a mixture of two components (hyaluronic acid functionalized with vinyl sulfone (HA‐VS) and thiol groups (HA‐SH)). When the mixture is injected into the anterior chamber, the higher temperature of aqueous humour compared to air causes the gel to solidify within the anterior chamber angle thereby blocking aqueous outflow through the trabecular meshwork and increasing the IOP. Furthermore, the hydrogel is localized to the anterior chamber angle with no noticeable media opacities, thereby allowing repeated in vivo imaging. It has been shown that the increased IOP and the optical media clarity produced in this animal model of glaucoma allows for in vivo study with the Confocal Scanning Laser Ophthalmoscope of the density and structural loss of RGCs, as well as functional loss of RGCs with electroretinography for more than 4 weeks after the hydrogel injection.