| Literature DB >> 27423265 |
Bradley D Gelfand1, Jayakrishna Ambati2.
Abstract
Age-related macular degeneration (AMD) afflicts one out of every 40 individuals worldwide, causing irreversible central blindness in millions. The transformation of various tissue layers within the macula in the retina has led to competing conceptual models of the molecular pathways, cell types, and tissues responsible for the onset and progression of AMD. A model that has persisted for over 6 decades is the hemodynamic, or vascular theory of AMD progression, which states that vascular dysfunction of the choroid underlies AMD pathogenesis. Here, we re-evaluate this hypothesis in light of recent advances on molecular, anatomic, and hemodynamic changes underlying choroidal dysfunction in AMD. We propose an updated, detailed model of hemodynamic dysfunction as a mechanism of AMD development and progression.Entities:
Mesh:
Year: 2016 PMID: 27423265 PMCID: PMC4969140 DOI: 10.1016/j.molmed.2016.06.009
Source DB: PubMed Journal: Trends Mol Med ISSN: 1471-4914 Impact factor: 11.951