Amyloid-β immunization enhances neurogenesis and cognitive ability in neonatal mice.

Whether Aβ actually has a physiological as well as a pathological role is not known. In order to investigate the effect of endogenous Aβ, wild type C57BL/6 mice were immunized with human or mouse derived Aβ1-42. The anti-Aβ antibody concentrations were increased in both treated groups. Compared to the human Aβ1-42 treated group, level of serum Aβ significantly decreased in mouse Aβ1-42 treated group. Western blot results revealed that these two derived Aβ1-42 had no cross-reaction. The new dentate granule survival cells increased in Aβ1-42 immunization groups, indicated by more BrdU+/NeuN+ and BrdU+/DCX+ cells as compared to PBS-treated group, accompanied by behavioral performance improving in a hippocampus-dependent learning task. Immunohistochemical analysis showed that BrdU+/Iba1+ cells also increased, however new born astrocytes (BrdU+/GFAP+) were unaffected in all treated mice. Interestingly, according the results of ELISA analysis both vaccines up-regulated IL-4 and IFN-γ levels in the brains and sera, but the TNF-α level did not changed. Of note, human Aβ1-42 immunization in neonatal mice enhanced neurogenesis and cognitive ability, might via Aβ immune response rather than cleaning endogenous Aβ.