The N-terminal Aβ fragments Aβ1-14, Aβ1-15, and Aβ1-16 are elevated in cell media and in CSF in response to γ-secretase inhibitor treatment. The presence of these small peptides is consistent with a catabolic amyloid precursor protein cleavage pathway by β- followed by α-secretase. It has been shown that Aβ1-14, Aβ1-15, and Aβ1-16 increase dose-dependently in response to γ-secretase inhibitor treatment while Aβ1-42 levels are unchanged.
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