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背景说明：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.
In Vitro：未检测
参考文献：[1] E.Portelius et al., Neurodegener. Dis., 10, 138 (2012);
[2]E.Portelius et al., Curr. Pharm. Des., 17, 2594 (2011);
[3]E.Portelius et al., Alzheimer Res. Ther., 2, 7 (2010).
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