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Decrease of dynamin 2 levels in late-onset Alzheimer’s disease alters Aβ metabolism

Kamagata, Eiichiro, Kudo, Takashi, Kimura, Ryo, Tanimukai, Hitoshi, Morihara, Takashi, Sadik, Md.Golam, Kamino, Kouzin, Takeda, Masatoshi·2009·Biochemical and Biophysical Research Communications
DOI 10.1016/j.bbrc.2008.12.147
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Abstract

Late-onset Alzheimer's disease (LOAD) is significantly associated with a single nucleotide polymorphism located in the dynamin (DNM) 2 gene, especially in non-carriers of the apolipoprotein E-epsilon4 allele. In this study we used real-time PCR to show that DNM2 mRNA is significantly reduced in the cortex of AD brains and in the peripheral blood of dementia patients. Neuroblastoma cells transfected with a dominant negative DNM2 had increased amyloid beta protein (Abeta) secretion and most of the amyloid precursor protein (APP) in these cells was localized to the plasma membrane. In addition, these cells were rich in flotillin, which is a component of lipid rafts. These data suggest that DNM2 expression is reduced in LOAD, which results in the accumulation of APP in lipid raft-rich plasma membranes. Consequently, Abeta secretion may increase in LOAD neurons.

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Research works printed but not linked: 18

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Metadata

Authors
Kamagata, E., Kudo, T., Kimura, R., Tanimukai, H., Morihara, T., Sadik, M. G., Kamino, K., & Takeda, M.
Venue
Biochemical and Biophysical Research Communications
Publisher
Elsevier BV
Published
2009-02
Volume
379
Issue
3
Pages
691-695
ISSN
0006-291X
DOI
10.1016/j.bbrc.2008.12.147
Cited by
29
References
0
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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