Modulation of Alzheimer's pathology by cerebro-ventricular grafting of hybridoma cells expressing antibodies against Abeta in vivo.
Accumulation in brain of the beta-amyloid peptide (Abeta) is considered as crucial pathogenic event causing Alzheimer's disease (AD). Anti-Abeta immune therapy is a powerful means for Abeta clearance from the brain. We recently showed that intravenous injections of anti-Abeta antibodies led to reduction, elevation or no change in brain Abeta42 concentrations of an AD mouse model. We report here, in a second passive immunization protocol, a different bioactivity of same antibodies to alter brain Abeta42 concentrations. Comparing the bioactivity of anti-Abeta antibodies in these two passive immunization paradigms underscores the potential of immune therapy for AD treatment and suggests that both the epitope recognized by the antibody and the mode of antibody administration are crucial for its biological activity.
Gaugler
Meret N M
MN
Division of Psychiatry Research, University of Zurich, August Forel Str. 1, 8008 Zurich, Switzerland.
Tracy
Jay
J
Kuhnle
Katrin
K
Crameri
Arames
A
Nitsch
Roger M
RM
Mohajeri
M Hasan
MH
D000544:Alzheimer Disease / Q000276:immunology / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000276:immunology*; D000818:Animals; D000906:Antibodies / Q000008:administration & dosage* / Q000276:immunology; D002552:Cerebral Ventricles / Q000276:immunology / Q000473:pathology*; D006825:Hybridomas / Q000276:immunology*; D051379:Mice; D008822:Mice, Transgenic
D016229:Amyloid beta-Peptides; D000906:Antibodies