Text Size Normal Text Sizing Button Medium Text Sizing Button Large Text Sizing Button Text Contrast Normal Contrast Button Reverse Contrast Button Switch to Spanish Language Contact Us Sitemap Sign In Register
Link to Homepage About AHAF
Donate Now Get Involved  
Alzheimer's Disease Research Macular Degeneration Research National Glaucoma Research


Sign up for Email Notifications
If you would like to be notified when submission deadlines are announced please click on the link below.

Sign up for new RFP announcements and submission deadline notifications.

This email list is not sold or distributed, and serves only as an annual reminder of the availability of research funding through the American Health Assistance Foundation (www.ahaf.org). Please follow instructions on the notification emails for removal requests.
 

Researchers:
Have you heard a story, statistic, or discovery that might interest the public? Let us know about it!
 
AHAF Research Grants Funding
Grant Funding for Alzheimer's Research
Grant Funding for Macular Degeneration Research
Grant Funding for Glaucoma Research
 

  

Macular Degeneration Research - Current Award

Dr. Roxanna Radu

Roxana Radu, M.D.

UCLA - Jules Stein Eye Institute
Los Angeles, CA

Title: Analysis of A2E-degradation and Complement Activation in Two New Animals Models for Age-related Macular Degeneration
Non-Technical Title: The Role of Lipofuscin Pigments and Chronic Inflammation as a Cause of Macular Degeneration

Duration: April 1, 2008 - June 28, 2010
Award Type: Standard
Award Amount: $100,000


Summary:

This project will test the hypothesis that abnormal metabolism of vitamin A and its derivatives could lead to overt activation of the immune complement system. It will test this hypothesis using a well established animal model of macular defects. They will investigate the biochemical and molecular mechanisms used by the retina to deal with abnormal build-up of vitamin A-based toxic compounds.

Details:

A pathologic feature of AMD is accumulation of toxic lipofuscin pigments, derived from vitamin A, in cells of the retinal pigment epithelium (RPE). This layer of cells is critical to the normal function and survival of rods and cones. Lipofuscin is a natural byproduct of photoreceptor turnover, and slowly accumulates in everyone's RPE. However, patients with AMD may have biochemical defects leading to accelerated accumulation or delayed clearance of lipofuscin pigments. When these pigments rise, the RPE loses its ability to support the photoreceptors. In time, this leads to photoreceptor death and subsequent blindness. Recent research showed that the gene for complement factor H (CFH), a component of the innate immune system, is a strong susceptibility locus for AMD. However, it is not known how dysfunction of CFH causes AMD. The study will test whether abnormal metabolism of vitamin A and its derivatives could lead to overt activation of the complement system. Studying mouse models will help us to understand the relationship between lipofuscin accumulation, complement activation, and retinal degeneration in AMD.