Journal
NEURON
Volume 75, Issue 1, Pages 26-39Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2012.06.018
Keywords
-
Categories
Funding
- National Eye Institute (NEI)/National Institutes of Health (NIH) [R01EY018350, R01EY018836, R01EY020672, R01EY022238, R21EY019778, RC1EY020442]
- Doris Duke Distinguished Clinical Scientist Award
- Burroughs Wellcome Fund Clinical Scientist Award in Translational Research
- Dr. E. Vernon Smith and Eloise C. Smith Macular Degeneration Endowed Chair
- NIH [T32HL091812, UL1RR033173]
Ask authors/readers for more resources
Age-related macular degeneration (AMD), a progressive condition that is untreatable in up to 90% of patients, is a leading cause of blindness in the elderly worldwide. The two forms of AMD, wet and dry, are classified based on the presence or absence of blood vessels that have disruptively invaded the retina, respectively. A detailed understanding of the molecular mechanisms underlying wet AMD has led to several robust FDA-approved therapies. In contrast, there are no approved treatments for dry AMD. In this review, we provide insight into the critical effector pathways mediating each form of the disease. A recurring theme that spans most aspects of AMD pathogenesis is defective immune modulation in the classically immune-privileged ocular haven. Interestingly, the latest advances in AMD research also highlight common molecular disease pathways with other neurodegenerative disorders. Finally, the therapeutic potential of intervening at known mechanistic steps of AMD pathogenesis is discussed.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available