4.6 Review

A Revised Hemodynamic Theory of Age-Related Macular Degeneration

Journal

TRENDS IN MOLECULAR MEDICINE
Volume 22, Issue 8, Pages 656-670

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2016.06.009

Keywords

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Funding

  1. NIH [DP1GM114862, R01EY018350, R01EY018836, R01EY020672, R01EY022238, R01EY024068]
  2. Doris Duke Distinguished Clinical Scientist Award
  3. Burroughs Wellcome Fund Clinical Scientist Award in Translational Research
  4. Ellison Medical Foundation Senior Scholar in Aging Award
  5. Foundation Fighting Blindness Individual Investigator Research Award
  6. Harrington Discovery Institute Scholar-Innovator Award
  7. John Templeton Foundation
  8. Dr. E. Vernon Smith and Eloise C. Smith Macular Degeneration Endowed Chair
  9. American Heart Association
  10. International Retinal Research Foundation
  11. National Center for Research Resources, National Institutes of Health [UL1TR000117]
  12. National Center for Advancing Translational Sciences, National Institutes of Health [UL1TR000117]

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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.

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