Alt text
Figure 1: Immune response induced by different Aβ vaccines. (a) Vaccines having the Aβ N-terminal region (A ) as an immunogen induced the production of antibodies (orange) that while binding to Aβ monomers and AβOs, are not protective. Similar to the ineffective mAbs that bound A , these antibodies cannot neutralize the cytotoxic AβOs, and protect neural cells from death. That these antibodies release toxic AβOs, which were immobilized as plaque, increase their harmful levels in the brain. Use of proinflammatory adjuvants in these vaccines, induces a systemic Th1/Th17 immunity, which increases the damage associated with AD. (b) Vaccines having AβOs as an immunogen and a sole Th2 adjuvant, elicit an anti-inflammatory immunity characterized by the production of antibodies against the Aβ N-terminal region (black) and AβOs cytotoxic conformational epitopes (red). Different from previous AD vaccines, which only induced production of anti-A antibodies (orange), the antibodies against the AβOs’ cytotoxic epitopes will be neutralizing ones (green), thus protecting the neural cells from death. Since the elicited neutralizing antibodies are against different conformational epitopes, it is feasible to expect some cooperative effects among the different antibodies. A synergism that would increase their protective effects on neural cells. Stimulation of a sole systemic anti-inflammatory immunity will prevent and/or delay some of the AD pathological changes associated with inflammation.