Titlebook: Retinal Degenerative Diseases; Mechanisms and Exper John D. Ash,Robert E. Anderson,Christian Grimm Conference proceedings 2018 Springer Int

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Toll-Like Receptors and Age-Related Macular Degeneration implicated in disease progression, but while polymorphisms in genes associated with the immune system have been identified as risk factors for disease, the underlying pathways and mechanisms involved in disease progression remain incompletely characterised. Typically inflammatory responses are medi

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Alterations in Extracellular Matrix/Bruch’s Membrane Can Cause the Activation of the Alternative Comrtunately, the design of therapies for early stages of the disease is limited by our understanding of the mechanisms involved in the formation of basal deposits and drusen, the first clinical signs of AMD. During the last decade, the identification of common and rare alleles in complement genes as r

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MicroRNA as Therapeutics for Age-Related Macular Degenerationne expression. While miRNAs were only identified in humans as recently as the turn of this century, some miRNA-based agents are already in Phase 2 clinical trials (Christopher et al. .). This rapid progress from initial discovery to drug development reflects the effectiveness of miRNAs as therapeuti

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Anaphylatoxin Signaling in Retinal Pigment and Choroidal Endothelial Cells: Characteristics and Releh an increased risk for AMD, and it has been hypothesized that an overactive complement system is partially responsible for the pathology of AMD. AMD is classified as early, intermediate, or late AMD, depending on the degree of the associated pathologies. Late AMD can be characterized as either lesi

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Co-Expression of Wild-Type and Mutant S163R C1QTNF5 in Retinal Pigment Epitheliumresence of thick extracellular sub-RPE deposits, similar histopathologically to those found in AMD patients. We have previously shown that the S163R C1QTNF5 mutant forms globular aggregates within the RPE in vivo following its AAV-mediated expression in the RPE and exhibits a reversely polarized dis

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Mutation-Independent Gene Therapies for Rod-Cone Dystrophiesns using adeno-associated virus (AAV) as viral vector. However, inherited retinal degenerative diseases showcase a broad genetic and mechanistic heterogeneity, challenging the development of mutation-specific therapies for each specific mutation. Mutation-independent approaches must be developed to