Amyloid beta-peptide is produced by cultured cells during normal metabolism: a reprise.
In the twenty years since George Glenner identified the amyloid beta-protein (Abeta), 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 anti-amyloid agents. The ability to study Abeta dynamically in cultured cells and in vivo derives from the recognition in 1992 that Abeta 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.
Selkoe
Dennis J
DJ
Center for Neurologic Diseases, Harvard Institutes of Medicine, Rm 730, 77 Avenue Louis Pasteur, Boston MA 02115, USA. dselkoe@rics.bwh.harvard.edu
D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology* / Q000517:prevention & control; D016229:Amyloid beta-Peptides / Q000276:immunology / Q000378:metabolism*; D000906:Antibodies / Q000276:immunology; D001921:Brain / Q000378:metabolism* / Q000473:pathology*; D002478:Cells, Cultured; D006801:Humans; D047468:Immunoprecipitation; D058225:Plaque, Amyloid / Q000473:pathology
D016229:Amyloid beta-Peptides; D000906:Antibodies