Age-Related Macular Degeneration Halted by Blocking
Protein to Stop Blood Vessel Growth
Protein CCR3 a new target for diagnosis and treatment
of AMD, the most common cause of blindness in senior citizens.
June 15, 2009 The battle to prevent millions of
senior citizens from going blind from age-related macular degeneration
(AMD) appears to have received an important boost from researchers that
have demonstrated that blocking the activity of a specific protein -
called CCR3 - can reduce the abnormal blood vessel growth that leads to
macular degeneration.
Furthermore, targeting this new protein may prove
to be safer and more effective than the current treatment for the
disease, which is directed at a protein called vascular endothelial
growth factor or VEGF.
Age-related macular degeneration is the most common
cause of blindness in older Americans. AMD affects 30 to 50 million
people globally, and that number is expected to double in the next
decade as the baby boomer generation ages.
The discovery - made in mouse models and cultured
human cells - may also enable physicians to catch the disease in its
earliest stages, before blood vessels have fully infiltrated and
destroyed the central portion of the eyes retina - an area known as the
macula - to cause vision loss.
About Cataract
A cataract is a clouding of the lens in your eye. It affects
your vision. Cataracts are very common in older people. By age
80, more than half of all people in the United States either
have a cataract or have had cataract surgery.
Common symptoms are
● Blurry vision
● Colors that seem faded
● Glare
● Not being able to see well at night
● Double vision
● Frequent prescription changes in your eye wear
Cataracts usually develop slowly. New glasses, brighter
lighting, anti-glare sunglasses or magnifying lenses can help at
first. Surgery is also an option. It involves removing the
cloudy lens and replacing it with an artificial lens. Wearing
sunglasses and a hat with a brim to block ultraviolet sunlight
may help to delay cataracts.
Also called: Age-related macular degeneration, AMD
Macular degeneration, or age-related macular degeneration (AMD)
is a leading cause of vision loss in Americans 60 and older. It
is a disease that destroys your sharp, central vision. You need
central vision to see objects clearly and to do tasks such as
reading and driving.
AMD affects the macula, the part of the eye that allows you to
see fine detail. It does not hurt, but it causes cells in the
macula to die. In some cases, AMD advances so slowly that people
notice little change in their vision. In others, the disease
progresses faster and may lead to a loss of vision in both eyes.
Regular comprehensive eye exams can detect macular degeneration
before the disease causes vision loss. Treatment can slow vision
loss. It does not restore vision.
The lead investigator was Jayakrishna Ambati, M.D.,
professor of ophthalmology and visual sciences and of physiology at the
University of Kentucky. Ambati is a Doris Duke Charitable Foundation
Distinguished Clinical Scientist and a Burroughs Wellcome Fund Clinical
Scientist in Translational Research. His laboratory is also supported by
the National Eye Institute of the NIH, Research to Prevent Blindness,
and American Health Assistance Foundation.
It would be much better to prevent the disease in
the first place, said study co-author and principal investigator of the
UNC study site,
Mary Elizabeth Hartnett, M.D., a professor of ophthalmology in the
UNC School of Medicine.
An exciting implication of this study was that the
CCR3 protein could be detected in early abnormal blood vessel growth,
giving us the opportunity to prevent structural damage to the retina and
preserve vision.
The disease is currently treated with drugs that
block the effects of VEGF, a growth factor that promotes the growth of
abnormal blood vessels. However, because this factor is also involved in
the growth and health of normal blood vessels, concerns have been raised
about the safety of its long-term use. To date, however, these anti-VEGF
agents have been found to be safe.
Thus, the investigators sought to identify a new
target for treatment that is specific to AMD. They detected the presence
of the CCR3 protein in eye tissue from humans with AMD but not in that
of individuals of similar age who did not have the disease.
When they blocked CCR3, either with drugs or
through genetic engineering, they saw a decrease in the generation of
abnormal blood vessels. Drugs targeting CCR3 were significantly more
effective than those targeting VEGF, meaning this could represent a new
therapy for the two-thirds of patients that do not respond to current
treatment.
The researchers now may look to see if levels of
the protein can be detected in the bloodstream in order to identify
people who are at risk of developing the disease. They also plan to
search for genetic changes in the CCR3 gene in patients with AMD to
better understand its causes.
UNC study co-authors along with Hartnett include
Steven J. Budd, technician and Pete Geisen, former technician, both from
the Hartnett laboratory; and John D. Wright, Jr., M.D., associate
professor of ophthalmology.
Other sites include Nagoya City University,
University of Cincinnati, University of Utah, Veterans Affairs of Salt
Lake City, Kyushu University, Harvard Medical School, Oregon Health and
Science University and University of Luebeck.
Keep up with the latest news for senior citizens, baby
boomers
June 15, 2009 The battle to prevent millions of
senior citizens from going blind from age-related macular degeneration
(AMD) appears to have received an important boost from researchers that
have demonstrated that blocking the activity of a specific protein -
called CCR3 - can reduce the abnormal blood vessel growth that leads to
macular degeneration.