Immunotherapeutic Study for Altzheimer's Disease
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Accession number;04A0022334
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| Title;Immunotherapeutic Study for Altzheimer's Disease |
| Author;
OKUDA KENJI
(Yokohama City Univ., School of Medicine, JPN)
HAMAJIMA KENJI
(Yokohama City Univ., School of Medicine, JPN)
XIN K-Q
(Yokohama City Univ., School of Medicine, JPN)
MATSUI KIYOHIKO
(Yokohama City Univ., School of Medicine, JPN)
TAJIMA NOBUYOSHI
(Yokohama City Univ., School of Medicine, JPN)
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Journal Title;Shokuniku ni kansuru Josei Kenkyu Chosa Seika Hokokusho
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Journal Code:X0296A
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ISSN:
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VOL.21;NO.;PAGE.112-116(2003)
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| Figure&Table&Reference;FIG.1, TBL.1, REF.8 |
| Pub. Country;Japan |
| Language;Japanese |
| Abstract;Immunotherapy for Alzheimer's disease(AD) has been the subject of intense investigation. Both active and passive immunization against amyloid-.BETA.(A.BETA.) in mouse models reduce levels of A.BETA., prevent and clear amyloid plaques, and improve cognitive behavior. However, signs of inflammation the central nervous system were reported in human trials. The goal of this study is to treat and prevent AD without any side effects. We prepared short length of A.BETA. peptide and applied to a Tg2576 transgenic mouse model, which exhibits the age-related development of amyloid plaques and neurodegeneration. We found that Tg2576 mice immunized with various length of A.BETA. peptide maintained serum antibody titers against each peptide greater than 1:10000. On the other hand, we constructed recombinant vaccinia virus(rvirus) expressing A.BETA. antigen. Immunization with A.BETA. protein-expressing vaccinia virus induced certain extent antibody titer. We are now examining if these resulting antibody can reduce the deposit of A.BETA. protein in the brain. We also have established anti-A.BETA.1-42/A.BETA.1-13IgG1-mAb-producing hybridomas. This mAb was directly applied to the brains of 15-month-old Tg2576 mice and we realized that F(ab')2 fragments of this mAb potent to clearance of A.BETA.-deposit forming. Fc' fragment didn't showed these clearance effect. These result indicate that the passive immunization with antibodies against A.BETA.-peptide reduce amyloid burden without complement and Fc receptor-mediated clearance. (author abst.) |
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