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Scientists at UCSB link brain plaques in Alzheimer’s disease to eye
disease
Eurekalert, 8 May, 2003 (Santa Barbara, Calif.) –– Scientists at the Center for the Study of Macular Degeneration at the Neuroscience Research Institute of the University of California, Santa Barbara have found a link between the brain plaques that form in Alzheimer’s disease and the deposits in the retina that are associated with age-related macular degeneration (AMD). AMD is a disease that leads to loss of central vision and affects 5 to 10 percent of the population over age 60. Don H. Anderson and
Lincoln V. Johnson, the scientists who head the study, said that both
diseases appear to begin with the development of inflammation and the
appearance of a type of plaque. Yet no one knows their exact causes. "Epidemiological
evidence gathered in Europe suggests that those with advanced AMD are at
somewhat greater risk of developing Alzheimer's disease," said
Anderson. "But, at this point, it is not clear whether the elevated
risk is attributable to common pathogenic factors, or to common risk
factors including smoking and atherosclerosis." The latest findings
were presented at the annual meetings of the Association for Research in
Vision and Ophthalmology (ARVO) in Ft. Lauderdale, Fla. on May 8. The
comparison between these disease processes was first outlined by the
scientists in the Proceedings of the National Academy of Sciences (PNAS)
in September and in an article in the American Journal of Ophthalmology,
also in September. Lincoln Johnson,
senior research biologist who is first author of the PNAS paper, explained
that the protein amyloid beta is thought to stimulate the inflammation
process. He said that many researchers believe it is the culprit in the
Alzheimer’s disease process. Amyloid beta is a toxic protein that tends
to stick together and kill neighboring cells in the brain. The same toxic
protein builds up in the deposits known as drusen that are located
adjacent to the photoreceptor cell layers in the retina. Regarding
age-related macular degeneration, Johnson said, "Many of the pieces
have been identified, we just have to figure out how they go together.
Inflammation seems to be one factor that contributes to vision loss."
Visual perception
begins when light from our surroundings enters our eyes and passes through
the transparent cornea and lens. The curvatures of the cornea and lens
bend the rays of light, like the lens of a camera and bring them into
focus upon a thin, transparent layer of nerve tissue, called the retina,
that lines the inner surface of the eye. The retina is actually part of
the central nervous system. It is connected to the brain by a cable called
the optic nerve that is made up of approximately one million nerve fibers.
Macular degeneration
is a blinding disease caused by the death of the photoreceptor cells in
that part of the retina known as the macula. The macula is a circular
area, approximately 5 millimeters or about 2/10 of an inch in diameter,
that is located next to the optic nerve. In the age-related form of
macular degeneration (AMD), photoreceptor cells within the macula die off
slowly, thus accounting for the progressive loss of vision that usually
begins after the fifth or sixth decade of life. Drusen, a type of
plaque, are regarded by many ophthalmologists as the hallmark clinical
sign of early AMD. The appearance of numerous drusen and/or large drusen,
especially in the macular region, is a significant risk factor for the
subsequent development of the most prevalent type of AMD. Identifying the
origin and molecular composition of these drusen deposits, therefore, has
remained an important but elusive objective for many decades. The presentation at
the ARVO meetings covered how the scientists used electron microscopy to
examine the organization and distribution of amyloid beta and other drusen-associated
molecules. Copyright
© 2002 Global Action on Aging
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