||15:00 - 16:15
|Diagnostics and Therapy of Dry AMD: Where Are We Now, Where Are We Going?
Despite intense and ground-breaking work on the genetic factors associated with AMD, no efficacious treatment has been found for dry AMD and its late-stage form geographic atrophy. There has been a focus on targeting the alternative complement pathway but clinical trials have failed so far. Extensive genetic as well as epidemiological studies have not revealed promising new targets or treatment strategies. Moreover, the late onset of the disease and the variability in the natural history of patients make disease prediction as well as clinical trial design challenging. This symposium will present a critical discourse on our current understanding of AMD with an emphasis on pathobiology, computational approaches and systems biology. Concepts, ideas and limitations that likely determine future directions for new treatments will be discussed.
Marius Ueffing, Direktor
|Diagnostics, Risks, Pathomechanisms and Clinical Endpoints: Defining risks for AMD onset and progression How can genetics lead us the way to therapy development?|| |
|Diagnostics, Risks, Pathomechanisms and Clinical Endpoints: Defining clinical endpoints and marker signatures for AMD progression Is there a strategy for personalizing therapy development?|| |
To date, there is no effective therapy available to slow down or to halt the progression of dry AMD. Combining novel functional tests for the specific visual deficit in AMD and high-resolution retinal imaging may provide a toolbox to develop and evaluate the efficacy of novel AMD therapies.
|Concepts for rational therapy development: Concepts and limitations for rational clinical trial design; lessons learned from the past?|| |
|Proteasomes and Autophagy as potential therapy targets in dry AMD|| |
The pathogenesis of dry AMD involves impaired protein degradation in RPE cells. Accumulation of lipofuscin and drusen is an indication of disturbed proteostasis in RPE. Decline in RPE proteostasis lead to increased oxidative and <a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/endoplasmic-reticulum-stress" title="Learn more about Endoplasmic Reticulum Stress from ScienceDirect's AI-generated Topic Pages">endoplasmic reticulum stress</a>, mitohondrial damage, and inflammation. The ubiquitin-proteasome pathway and the lysosomal/autophagosomal pathway are the two major clearance systems in cells. Improving their proteolytic capacity dry AMD development might be decelerated.