Mechanisms of Aβ 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.