Mechanisms of Abeta clearance and catabolism.
Mutations that result in an increased generation of amyloid beta peptide (Abeta) account for less than 5% of Alzheimer's disease (AD). Data suggesting that late onset AD risk factors play a role in Abeta turnover in the brain have shifted some of the research focus to the study of Abeta clearance and degradation and the impact of these processes on the etiology of Alzheimer's disease (AD). This review will examine the data obtained from studies performed in knockout and transgenic mice on the proteases; the cells and the physiological mechanisms that play a part in the removal of Abeta from the brain.
Guénette
Suzanne Y
SY
Mass General Institute for Neurodegenerative Disease, Massachusetts General Hospital East, 114 16th St., Charlestown, MA 02129-4404, USA. guenette@helix.mgh.harvard.edu
D000544:Alzheimer Disease / Q000235:genetics / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology; D010450:Endopeptidases / Q000378:metabolism*; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D051379:Mice; D018345:Mice, Knockout
D016229:Amyloid beta-Peptides; D010450:Endopeptidases