Issn Print: 0893-0341
Publication Date: 2003/04/01
Amyloid-β Binding Molecule: Potential Role in the Pathogenesis and Treatment of Alzheimer Disease
Excerpt
The neuropathology of Alzheimer disease (AD) is marked by selective vulnerability of neurons and neuron connections in the entorhinal cortex, hippocampus, and associated areas of the neocortex, changes that are probably the final substrate for the dementia that is the hallmark of this disorder. In addition, AD is characterized by the development of diffuse neuritic and cerebrovascular plaques in the brain. The buildup of plaques, which are composed primarily of the protein amyloid-beta (Aβ), is a key feature of AD. During the past several years, researchers have investigated how the Aβ peptide is converted from a soluble form to an insoluble one, because strong evidence now suggests that the conversion of Aβ to its insoluble form is an important initiating factor in AD. Although much is known about the production of Aβ, far less is known about its conversion to insoluble forms, which is facilitated by endogenous Aβ binding molecules.
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