Molecular pathology of age-related macular degeneration

Age-related macular degeneration (AMD) is a leading cause of irreversible blindness in the world. Although the etiology and pathogenesis of AMD remain largely unclear, a complex interaction of genetic and environmental factors is thought to exist. AMD pathology is characterized by degeneration invol...

Full description

Saved in:
Bibliographic Details
Published in:Progress in retinal and eye research 2009-01, Vol.28 (1), p.1-18
Main Authors: Ding, Xiaoyan, Patel, Mrinali, Chan, Chi-Chao
Format: Article
Language:English
Subjects:
Age-related macular degeneration
Animals
Bruch's membrane
Disease Models, Animal
Drusen
Genetics
Humans
Inflammation
Macular Degeneration - genetics
Macular Degeneration - pathology
Molecular pathology
Polymorphism, Single Nucleotide
Retina - pathology
Retinal photoreceptors
Retinal pigment epithelium
Single nucleotide polymorphism
Vascular endothelial growth factor
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Age-related macular degeneration (AMD) is a leading cause of irreversible blindness in the world. Although the etiology and pathogenesis of AMD remain largely unclear, a complex interaction of genetic and environmental factors is thought to exist. AMD pathology is characterized by degeneration involving the retinal photoreceptors, retinal pigment epithelium, and Bruch's membrane, as well as, in some cases, alterations in choroidal capillaries. Recent research on the genetic and molecular underpinnings of AMD brings to light several basic molecular pathways and pathophysiological processes that might mediate AMD risk, progression, and/or response to therapy. This review summarizes, in detail, the molecular pathological findings in both humans and animal models, including genetic variations in CFH, CX3CR1, and ARMS2/HtrA1, as well as the role of numerous molecules implicated in inflammation, apoptosis, cholesterol trafficking, angiogenesis, and oxidative stress.
ISSN:1350-9462
1873-1635
DOI:10.1016/j.preteyeres.2008.10.001