Taipei Medical University

A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
Lee JT
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------>journal_name=J Cell Biol
------>paper_name=Amyloid-beta peptide induces oligodendrocyte death by activating the neutral sphingomyelinase-ceramide pathway.
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------>fullAbstract=Amyloid-beta peptide (Abeta) accumulation in senile plaques, a pathological hallmark of Alzheimer~s disease (AD), has been implicated in neuronal degeneration. We have recently demonstrated that Abeta induced oligodendrocyte (OLG) apoptosis, suggesting a role in white matter pathology in AD. Here, we explore the molecular mechanisms involved in Abeta-induced OLG death, examining the potential role of ceramide, a known apoptogenic mediator. Both Abeta and ceramide induced OLG death. In addition, Abeta activated neutral sphingomyelinase (nSMase), but not acidic sphingomyelinase, resulting in increased ceramide generation. Blocking ceramide degradation with N-oleoyl-ethanolamine exacerbated Abeta cytotoxicity; and addition of bacterial sphingomyelinase (mimicking cellular nSMase activity) induced OLG death. Furthermore, nSMase inhibition by 3-O-methyl-sphingomyelin or by gene knockdown using antisense oligonucleotides attenuated Abeta-induced OLG death. Glutathione (GSH) precursors inhibited Abeta activation of nSMase and prevented OLG death, whereas GSH depletors increased nSMase activity and Abeta-induced death. These results suggest that Abeta induces OLG death by activating the nSMase-ceramide cascade via an oxidative mechanism.
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------>authors2=Xu J
------>authors3=Lee JM
------>authors4=Han X
------>authors5=Yang DI
------>authors6=Chen S, Hsu CY
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------>authors=Lee JT
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------>updateTitle=Amyloid-beta peptide induces oligodendrocyte death by activating the neutral sphingomyelinase-ceramide pathway.
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------>publish_year=2004
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A B C D E F G H I J K L M N O P Q R S T U V W X Y Z