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.
journal_name
Neurochem Resjournal_title
Neurochemical researchauthors
Münch C,Zhu BG,Mink A,Seefried U,Riepe MW,Ludolph AC,Meyer Tdoi
10.1007/s11064-007-9540-5subject
Has Abstractpub_date
2008-06-01 00:00:00pages
1005-10issue
6eissn
0364-3190issn
1573-6903journal_volume
33pub_type
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