Abstract
Age-related macular degeneration (ARMD) is the leading cause of central vision loss in individuals over the age of 50 in the Western hemisphere.1 ARMD is characterized by the accumulation of debris (drusen) within Bruch’s membrane during the early stages of the disease, with the subsequent development of choroidal neovascularization or atrophy of the choriocapillaris and retinal pigment epithelium (RPE) at later stages. The latter events are thought to be causally involved in the death of macular photoreceptors. While the ophthalmological changes during the progression of the various forms of ARMD have been described, and end-stage histopathological descriptions of ARMD are available, little is known about the cellular mechanisms associated with the normal maintenance and turnover of Bruch’s membrane, the events that lead to drusen formation, or the cause of subretinal neovascularization and atrophy of the RPE and choriocapillaris.
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© 1997 Springer Science+Business Media New York
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Kamei, M., Apte, S.S., Rayborn, M.E., Lewis, H., Hollyfield, J.G. (1997). TIMP-3 Accumulation in Bruch’s Membrane and Drusen in Eyes From Normal and Age-Related Macular Degeneration Donors. In: LaVail, M.M., Hollyfield, J.G., Anderson, R.E. (eds) Degenerative Retinal Diseases. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5933-7_2
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DOI: https://doi.org/10.1007/978-1-4615-5933-7_2
Publisher Name: Springer, Boston, MA
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