Secretases as targets for the treatment of Alzheimer's disease.
Alzheimer's disease (AD) is the major cause of dementia in most developed countries. Treatment to modify this disease is currently unavailable, but needed urgently. The amyloid-cascade hypothesis proposes that amyloid beta-peptide (Abeta), found in the plaques characteristic of AD, plays an early, critical role in the disease process. It follows that preventing the generation of Abeta could be therapeutically useful in all cases of AD. Inhibition of the secretases that produce Abeta from a large precursor protein is the main approach to achieve this goal.
Citron
M
M
Dept of Neuroscience, M/S 29-2-B, Amgen Inc., One Amgen Center Drive, 91320, Thousand Oaks, CA, USA. mcitron@amgen.com
D000544:Alzheimer Disease / Q000201:enzymology* / Q000473:pathology / Q000628:therapy*; D053829:Amyloid Precursor Protein Secretases; D016564:Amyloid beta-Protein Precursor / Q000096:biosynthesis*; D016282:Aspartic Acid Endopeptidases; D010450:Endopeptidases / Q000378:metabolism*; D006801:Humans; D058225:Plaque, Amyloid / Q000473:pathology; D011480:Protease Inhibitors / Q000627:therapeutic use*
D016564:Amyloid beta-Protein Precursor; D011480:Protease Inhibitors; D053829:Amyloid Precursor Protein Secretases; D010450:Endopeptidases; D016282:Aspartic Acid Endopeptidases; C509280:BACE1 protein, human