Endogenous amyloid-β mediates memory forgetting in the normal brain.

Amyloid beta (Aβ) is known to be one of the strong candidate molecules for initiating Alzheimer's disease and has been extensively studied in the light of disease pathophysiology. However, it is still elusive what roles Aβ play in the normal brain. In this study, we report that Aβ is required for memory forgetting in the normal brain. We monitored object recognition memory, and in order to quench soluble Aβ, we microinjected anti-Aβ antibody (4G8) into the ventricles after memory acquisition. Microinjection of anti-Aβ antibody prolonged the maintenance of object recognition memory. This effect appeared not to be due to modulation of memory consolidation since antibody injection after memory consolidation still had a similar effect on memory maintenance. Furthermore, the maintenance of object recognition memory was prolonged in Fcgr2b KO mice, which lacks IgG Fcγ receptor II-b (FcγRIIb), a receptor for soluble Aβ oligomers. Taken together, these findings suggest that endogenous Aβ is involved in memory forgetting in the normal brain.