| Literature DB >> 22326868 |
Yoon Ki Hong1, Soojin Lee, Seung Hwan Park, Jang Ho Lee, Seung Yeop Han, Sang Tae Kim, Young-Kyoon Kim, Songhee Jeon, Byung-Soo Koo, Kyoung Sang Cho.
Abstract
Amyloid-β-42 (Aβ42) has been implicated in the pathogenesis of Alzheimer's disease (AD). Neuronal Aβ42 expression induces apoptosis and decreases survival and locomotive activity in Drosophila. However, the mechanism by which Aβ42 induces these neuronal impairments is unclear. In this study, we investigated the underlying pathway in theses impairments. JNK activity was increased in Aβ42-expressing brains, and the Aβ42-induced defects were rescued by reducing JNK or caspase activity through genetic modification or pharmacological treatment. In addition, these impairments were restored by Drosophila forkhead box subgroup O (dFOXO) deficiency. These results suggest that the JNK/dFOXO pathway confers a therapeutic potential for AD.Entities:
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Year: 2012 PMID： 22326868 DOI： 10.1016/j.bbrc.2012.01.122
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN： 0006-291X Impact factor: 3.575