Major strides in ophthalmologists’ understanding of dry AMD

[caption id="attachment_9383" align="alignright" width="1024"] Frank Holz MD[/caption] Major strides are being made in our collective understanding of dry AMD. This was apparent during the EURETINA symposium “New Insights into Dry AMD”, which took place on the first day of the 17th Annual EURETINA Congress in Barcelona, Spain. The symposium featured six researchers who are on the cutting edge of research into dry AMD. “Bio-energetics are compromised in the retinal pigment epithelium of AMD,” said Professor Phil Luthert, University College London, England. He addressed the contribution of Bruch’s membrane alterations and RPE degeneration to the pathophysiology of dry AMD. Impaired bio-energetics, which refers to the degeneration of cellular energy production, drives many phenomena leading to dry AMD. For example, Prof Luthert shared substantial evidence of problems in RPE cells’ mitochondria in AMD. This “energy failure” is associated with reactive oxygen species and a pro-inflammatory state. This understanding offers new potential substrates for therapy. Dr Christine Curcio, University of Alabama, USA, spoke next, sharing her insights into the entities known as subretinal drusenoid deposits (SDD). These are extracellular deposits leading to the same AMD end-stages of atrophy and neovascularisation as drusen. “Because drusen and SDD are plausibly part of the same outer retinal lipid recycling system, progress on drusen gives hope for progress on SDD,” said Dr Curcio. Indeed, they have a very high prevalence in geographic atrophy. She referred to the CAT trial, which taught us that confluent SDD are a risk factor for geographic atrophy, while non-confluent, or “dot” SDD more often lead to neovascular AMD. Moving an ocular layer or two deeper, Professor Leopold Schmetterer, Singapore Eye Research Institute, gave delegates insight into the current ability of OCT-angiography (OCT-A) to evaluate the choriocapillaris. Despite great challenges in imaging the choroid, such as light scattering within the overlying RPE and motion artefacts, this modality, and particularly its ability to differentiate between the various choroidal layers, has allowed us to detect alterations in choroidal microvasculature early in the disease process. Dr Catherine Cukras, National Eye Institute, Bethesda, USA, told delegates how we might move beyond visual acuity to assess macular function in AMD. Dr Cukras focused on microperimetry and dark adaptation, both of which have their relative pros and cons. “Microperimetry can accommodate non-central fixators, allows us to investigate structure-function correlations and enables longitudinal follow-up of non-foveal points,” said Dr Cukras. Similarly, dark adaptation, which decreases significantly in dry AMD, might also be used as an outcome measure in the future. Which biomarkers are of prognostic and diagnostic value in geographic atrophy? This question was tackled by Professor Steffen Schmitz-Valckenberg, University of Bonn, Germany. “There is a multitude of risk-markers for increased progression of geographic atrophy,” he said. These include genetic variants, characteristics of the fellow eye and lesion- and eye-specific morphological characteristics such as abnormal fundus autofluorescence (FAF) markers. On FAF, “small lesion size, unifocality and foveal location are associated with slower progression,” said Prof Schmitz-Valckenberg. Professor Sascha Fauser, University Hospital Cologne, Germany, closed the symposium with maybe the most important topic for patients: emerging therapeutic approaches for geographic atrophy. Although there is currently no approved treatment, “lampalizumab is the first drug to show evidence of efficacy in a phase 2 trial for geographic atrophy”, said Prof Fauser.