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 Press Room Contact Us Sitemap Sign In Register
Link to Homepage About BrightFocus
BrightFocus
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 funding or meeting opportunities are announced please click on the link below.

Sign up for new announcements.

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

 
 
BrightFocus Research Grants Funding
Grant Funding for Alzheimer's Research
Grant Funding for Macular Degeneration Research
Grant Funding for Glaucoma Research
 

 

Macular Degeneration Research
Completed Award

Photo Pending

Wenchao Song, Ph.D.

University of Pennsylvania
Philadelphia , PA, United States

Title: Complement Activation in RPE Function and AMD Pathogenesis
Non-Technical Title: Establishment of a Mouse Model for Understanding How Plasma Proteins Called Complement May Cause the Dry Form of Age-related Macular Degeneration

Co-PI(s):
Imran Mohammed, Ph.D.
University of Pennsylvania

Duration: July 1, 2011 - June 30, 2013
Award Type: Standard
Award Amount: $100,000

Summary:

To create a mouse model and use it to understand the pathogenesis of age-related macular degeneration caused by complement, a group of plasma proteins involved in inflammation.

Details:

There is no effective treatment available for the early or dry type of age‐related macular degeneration (AMD). One idea for future treatments sprung from the discovery that a group of blood proteins that helps the body to attack “foreign invaders,” called the complement system, may initiate dry AMD. Drs. Wenchao Song, Imran Mohammed, and collaborators will create mice that have had the genetic “brake” removed from the complement system. They suspect that this will cause severe inflammation and damage the retina in a way that will resemble dry AMD. If this is the case, then these mice could then be used as a model for testing new preventions and treatments for dry AMD.

Progress Updates:

Complement is part of the body’s defense system against viral and bacterial infections. Usually, it is controlled precisely so that it does not cause “friendly fire” and injure the body itself. However, if the control mechanism is not working properly, then complement can cause damage and disease. It is now known that improper complement activity contributes to the development of macular degeneration. In this project, Dr. Song’s and Dr. Mohammed’s team is trying to produce a mouse model whereby they disable the complement control mechanism specifically in the eye, in the hope that this will lead to retinal injury that more closely mimics human macular degeneration. The complement control mechanisms are multiple and often redundant, therefore they may need to disable more than one mechanism to be sufficient to cause severe eye disease.

During the past year, the team has achieved disabling one particular control mechanism in a special type of mouse. Preliminary examination showed that the mice exhibited some signs of retinal degeneration, which is really quite exciting to see after disabling only one type of complement control. While they are continuing to observe and study these mice to see if the retinal disease will get worse and resemble the type of macular degeneration seen in humans, they are also disabling a second control mechanism. The team hopes that by concurrently removing these two control mechanisms, complement activity in the retinal cells will be switched into overdrive that will cause severe and fast-developing retinal disease. Such a mouse model of disease will allow testing of new anti-complement drugs, which could eventually be developed and used in human patients with AMD.