The deposition of amyloid beta (Abeta) protein is a key pathological feature in 
Alzheimer's disease (AD). In murine models of AD, both active and passive 
immunization against Abeta induce a marked reduction in amyloid brain burden and 
an improvement in cognitive functions. Preliminary results of a prematurely 
terminated clinical trial where AD patients were actively vaccinated with 
aggregated Abeta bear resemblance to those documented in murine models. Passive 
immunization of AD patients with anti-Abeta antibodies, in particular human 
antibodies, is a strategy that provides a more cautious management and control 
of any undesired side effects. Sera of all healthy adults contain anti-Abeta IgG 
autoimmune antibodies. Hence antigen-committed human B-cells are easily 
immortalized by Epstein-Barr virus (EBV) into anti-Abeta secreting cell lines. 
Two anti-Abeta human monoclonal antibodies which we recently prepared bind to 
the N-terminus of Abeta peptide and were shown to stain amyloid plaques in 
non-fixed brain sections from an AD patient. It is anticipated that specifically 
selected anti-Abeta human monoclonal antibodies could reduce and inhibit 
deposits of amyloid in brain while avoiding the cognitive decline that 
characterizes AD. In the future, this type of antibody may prove to be a 
promising immune therapy for the disease.