Clearing the brain's amyloid cobwebs.
Elevated cerebral levels of amyloid beta-protein occur universally in Alzheimer's disease, yet only a few patients show evidence of increased Abeta production. Therefore, defects in proteases that degrade Abeta could underlie some or many cases of familial and sporadic AD. This previously neglected topic has begun receiving serious attention. Understanding how proteolysis regulates Abeta levels in the cerebral cortex has implications for both the pathogenesis and the treatment of this protean disorder.
Selkoe
D J
DJ
Center for Neurologic Diseases, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115, USA. selkoe@cnd.bwh.harvard.edu
D000544:Alzheimer Disease / Q000201:enzymology / Q000235:genetics; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000201:enzymology*; D010450:Endopeptidases / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007339:Insulysin / Q000378:metabolism; D009154:Mutation; D015260:Neprilysin / Q000378:metabolism
D016229:Amyloid beta-Peptides; D010450:Endopeptidases; D015260:Neprilysin; D007339:Insulysin