In the twenty years since George Glenner identified the amyloid β-protein (Aβ), advances in understanding the biochemical pathology, genetics and cell biology of Alzheimer's disease have led to a detailed molecular hypothesis for the genesis of AD and brought us into human trials of antiamyloid agents. The ability to study Aβ dynamically in cultured cells and in vivo derives from the recognition in 1992 that Aβ is a normal product of cellular metabolism throughout life and circulates as a soluble peptide in biological fluids. Here, I review the background underlying this discovery and then discuss its implications for research on Alzheimer's disease, particularly for the development of disease-modifying therapies.
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