| First Author | Lee S | Year | 2018 |
| Journal | Biochem Biophys Res Commun | Volume | 506 |
| Issue | 3 | Pages | 492-497 |
| PubMed ID | 30361088 | Mgi Jnum | J:271773 |
| Mgi Id | MGI:6280071 | Doi | 10.1016/j.bbrc.2018.10.118 |
| Citation | Lee S, et al. (2018) Endogenous amyloid-beta mediates memory forgetting in the normal brain. Biochem Biophys Res Commun 506(3):492-497 |
| abstractText | Amyloid beta (Abeta) 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 Abeta play in the normal brain. In this study, we report that Abeta is required for memory forgetting in the normal brain. We monitored object recognition memory, and in order to quench soluble Abeta, we microinjected anti-Abeta antibody (4G8) into the ventricles after memory acquisition. Microinjection of anti-Abeta 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 Fcgamma receptor II-b (FcgammaRIIb), a receptor for soluble Abeta oligomers. Taken together, these findings suggest that endogenous Abeta is involved in memory forgetting in the normal brain. |
