The Alzheimer's Aβ-peptide is deposited at sites of complement activation in pathologic deposits associated with aging and age-related macular degeneration

• DOI: 10.1073/pnas.192203399
• Publication Date: 2002-09-03T19:58:55Z
• Authors: Lincoln V. Johnson; William P. Leitner; Alexander J. Rivest; Michelle K. Staples; Monte J. Radeke; Don H. Anderson
• Keywords: Drusen; Pathogenesis

Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss in older individuals worldwide. The disease characterized by abnormal extracellular deposits, known as drusen, that accumulate along the basal surface retinal pigmented epithelium. Although drusen deposition common individuals, large numbers and/or extensive areas confluent represent significant risk factor for AMD. Widespread associated with epithelial cell dysfunction and photoreceptor cells neural retina. Recent studies have shown contain variety immunomodulatory molecules, suggesting process formation involves local inflammatory events, including activation complement cascade. Similar observations Alzheimer's (AD) lead to hypothesis chronic localized inflammation an important element AD pathogenesis, neurodegenerative consequences. Accordingly, amyloid beta (Aβ) peptide, major constituent neuritic plaques AD, has been implicated primary activator AD. Here we show Aβ substructural vesicular component within drusen. colocalizes activated components these “amyloid vesicles,” thereby identifying them potential sites activation. Thus, could be events contribute atrophy epithelium, biogenesis, pathogenesis