Rapid Cerebral Amyloid Binding by Abeta Antibodies Infused into beta-Amyloid Precursor Protein Transgenic Mice.

Winkler, D.., Abramowski, D., Danner, S., Zurini, M., Paganetti, P., Tolnay, M., Staufenbiel, M.
Journal   Biol Psychiatry.
Species  
Analytes Measured   Abeta 40 , Abeta 42
Matrix Tested   Transgenic mouse plasma, cerebrospinal fluid and brain homogenates
Year   2010
Volume  
Page Numbers  
Application   Alzheimers
Abstract
BACKGROUND: Passive immunization for the treatment of Alzheimer's disease (AD) was rapidly translated into clinical trials. However, basic mechanisms of AD immunotherapy remain only partially understood.

METHODS: We analyzed the dynamic changes of amyloid-β (Aβ) levels in plasma, brain, and cerebrospinal fluid (CSF) as well as cerebral amyloid binding by Aβ antibody after a single β1-antibody infusion into APP(Swedish) and APP(wildtype) transgenic mice at preplaque and plaque-bearing age.

RESULTS: Following intravenous Aβ antibody treatment, plasma Aβ increased rapidly, reaching significantly higher levels in preplaque compared with plaque-bearing mice, whereas cerebral and CSF Aβ remained unchanged. Strikingly, Aβ antibodies exhibited strong cerebral amyloid plaque binding rapidly after intravenous administration in a subset of animals with more severe vascular amyloid.

CONCLUSIONS: Rapid plasma Aβ increase after Aβ antibody infusion results primarily from stabilization of Aβ. Nevertheless, the smaller plasma Aβ increase in plaque-bearing mice might be of diagnostic use. Importantly, intravenously administered antibodies can rapidly bind to cerebral plaques, potentially facilitated by vascular-amyloid-mediated damage of the blood-brain barrier.

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