Courtesy of the National Institute on Aging
Amyloid β is the cleavage product of Amyloid Precursor Protein (APP). Long suspected a culpable player in Alzheimer disease progression due to the plaques it forms, Aβ may have a physiological role depressing neuronal function.
Recent work has revealed a potential physiological role for amyloid β, often considered a major culprit in Alzheimer disease (AD) pathology. This suggests that Aβ, an ordinarily upstanding protein, turns bad as the result of a mob-type effect, when the physical buildup into plaques promotes neuronal damage and loss. "There's been a growing awareness over the last three or four years that it's not just a toxic peptide," says Hugh Pearson from the University of Leeds, UK.
Pearson used specific enzyme inhibitors to block β- and γ-secretase, which produce Aβ through the sequential cleavage of amyloid precursor protein (APP).1 Death occurred in neuronal cell lines but not in ...
