Cerebral amyloid plaques, the characteristic lesions found in Alzheimer's patients, are extracellular deposits of the β-amyloid peptide (Aβ). The peptide is generated by endoproteolysis of the Type I membrane protein APP and its formation involves the sequential cleavage of APP by two proteases: α-secretase and β-secretase.
Two studies in March
Yi Luo and colleagues from Amgen, Thousand Oaks, California, were unable to measure any appreciable levels of Aβ peptide in the brains of transgenic BASE1- mice. This lack of secretion was also observed in mice crossed with a variant that overproduces the APP protein (
Huaibin Cai and colleagues at The Johns Hopkins University School of Medicine show that neurons from BACE1-deficient mice fail to secrete Aβ peptide, even following...