NDLI: Chemical Hypoxia Facilitates Alternative Splicing of EAAT2 in Presymptomatic APP23 Transgenic Mice

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Chemical Hypoxia Facilitates Alternative Splicing of EAAT2 in Presymptomatic APP23 Transgenic Mice

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Chemical Hypoxia Facilitates Alternative Splicing of EAAT2 in Presymptomatic APP23 Transgenic Mice

Content Provider	Springer Nature Link
Author	Münch, Christoph Zhu, Bing gen Mink, Andreas Seefried, Ulrich Riepe, Matthias W. Ludolph, Albert C. Meyer, Thomas
Copyright Year	2007
Abstract	Hypoxia is one of the major common components of vascular risk factors for pathogenesis of Alzheimer’s disease. This study investigated the possible relationship between hypoxia and alternative splicing of the excitatory amino acid transporter 2 (EAAT2) in a transgenic model for Alzheimer’s disease. We used an APP23 mouse model prior to amyloid deposition and subjected it to chemical hypoxia treatment as induced by 3-nitropropionic acid. One hour after administration of 3-nitropropionic acid changes in the expression of the 5′-splice forms mEAAT2/5UT3, mEAAT2/5UT4, and mEAAT2/5UT5 were found in the frontal cortex, hippocampus and cerebellum of the APP23 model. In untreated APP23 animals the expression of EAAT2 splice variants was unchanged. Our results demonstrate that hypoxia facilitates alternative splicing of EAAT2 in the APP23 model. This may be a molecular mechanism linking vascular factors to early pathophysiology of Alzheimer’s disease.
Starting Page	1005
Ending Page	1010
Page Count	6
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	33
Issue Number	6
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2007-11-13
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Alzheimer’s disease Hypoxia Excitatory amino acid transporter 2 Alternative splicing 3-Nitropropionic acid Mouse model Neurology Biochemistry Neurosciences
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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