期刊名称:Proceedings of the National Academy of Sciences
印刷版ISSN:0027-8424
电子版ISSN:1091-6490
出版年度:2001
卷号:98
期号:15
页码:8850-8855
DOI:10.1073/pnas.151261398
语种:English
出版社:The National Academy of Sciences of the United States of America
摘要:Active immunization with the amyloid {beta} (A{beta}) peptide has been shown to decrease brain A{beta} deposition in transgenic mouse models of Alzheimer's disease and certain peripherally administered anti-A{beta} antibodies were shown to mimic this effect. In exploring factors that alter A{beta} metabolism and clearance, we found that a monoclonal antibody (m266) directed against the central domain of A{beta} was able to bind and completely sequester plasma A{beta}. Peripheral administration of m266 to PDAPP transgenic mice, in which A{beta} is generated specifically within the central nervous system (CNS), results in a rapid 1,000-fold increase in plasma A{beta