CTF1-51, a truncated carboxyl-terminal fragment of amyloid precursor protein, suppresses the effects of Aβ42-lowering γ-secretase modulators

Haruhiko Watahiki, Sosuke Yagishita, Eugene Futai, Shoichi Ishiura

    研究成果: Article査読

    抄録

    The pathogenesis of Alzheimer's disease (AD) is correlated with the toxicity of amyloid β-peptide (Aβ), especially Aβ42. γ-Secretase modulators (GSMs) are compounds that alter production of Aβ42 without interfering with the physiological function of γ-secretase. Aβ42-lowering GSMs have been studied with the hope of using them as therapeutic or prophylactic drugs for AD. However, the mechanism of action of GSMs is not well defined. We examined the effect of Aβ42-lowering GSMs on model cells producing large amounts of Aβ42: CHO cells expressing CTF1-51, a precursor peptide of Aβ that is mainly cleaved into Aβ42. Our results indicate that the effect of GSM in the model was weak. Thus, we conclude that CTF1-51 cleavage mainly yields Aβ42 and suppresses the effects of some GSMs, a phenomenon that may be related to their mechanism of action.

    本文言語English
    ページ(範囲)96-99
    ページ数4
    ジャーナルNeuroscience Letters
    526
    2
    DOI
    出版ステータスPublished - 2012 9月 27

    ASJC Scopus subject areas

    • 神経科学(全般)

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