Rare earth ions (Tm3+, Er3+, and Yb3+)-doped cubic Gd2O3 nanocrystals were prepared by a simple sol−gel method. Raman and FT-IR spectra were measured to evaluate the vibrational feature of the samples. Under 980 nm laser excitation, blue (488 nm), green (564 nm), and red (661 nm) upconversion has been recorded in Gd2O3:Tm+Yb and Gd2O3:Er (Gd2O3:Er+Yb), respectively. A great enhancement of red emission and diminishment of green emission of Er3+ in Gd2O3:Er+Yb have been observed. Laser power and doping concentration dependence of the upconverted emissions were studied to understand the upconversion mechanisms. Excited absorption and energy-transfer processes are discussed as the possible mechanisms for the visible emissions.

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The failure of adult hippocampal neurogenesis is increasingly considered as an important factor in the pathological correlates for memory decline in Alzheimer's disease (AD). Loss of adult-born neurons and abnormalities of neural stem/progenitor cells (NSPCs) within the dentate gyrus (DG) of adult hippocampus might contribute to this process. In this study, we showed that amyloid-β1–42 (Aβ42) oligomer triggers senescent phenotype of NSPCs in vitro. Oligomerized Aβ42 induced the production of senescence-associated biomarkers p16 and senescence-associated β-galactosidase (SA-β-gal) in adult mouse hippocampal NSPCs, as well as inhibited cells proliferation and differentiation. In the DG of amyloid precursor protein/presenilin1 (APP/PS1) transgenic mice, the number of senescent NSPCs was significantly increased and senescence-associated protein p16 was upregulated. Formylpeptide receptor 2 (FPR2), one of Aβ42 functional receptors, may be involved in NSPCs senescence. The FPR2 antagonist WRW4 significantly inhibited NSPCs senescence induced by Aβ42. In addition, the activation of p38 mitogen-activated protein kinase (MAPK) in response to the accumulation of reactive oxygen species (ROS) was involved in NSPCs senescence induced by Aβ42. WRW4 inhibited the accumulation of ROS and the activation of p38 MAPK in NSPCs. Our data suggest that Aβ42 accelerates NSPCs senescence via FPR2-dependent activation of its downstream ROS-p38 MAPK signaling, which limits the function of NSPCs and contributes to failure of neurogenesis. This is the first demonstration of NSPCs senescence response to Aβ42.

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