Impact of Gold Nanoparticles on Amyloid β-Induced Alzheimer's Disease in a Rat Animal Model: Involvement of STIM Proteins

Alzheimer's disease (AD) is the most common type of neurodegenerative amyloid disorder causing progressive cognitive decline and memory loss. A considerable number of therapies for AD rely on inhibition/delay/ dissociation of amyloid beta (A beta) oligomers and fibrils. In this case, nanoparticles (NPs) demonstrated substantial effects on the A beta fibrillation process; however, their effects on progressive cognitive decline and memory have been poorly investigated in vivo. In this study, acquisition and retention of spatial learning and memory are studied in a rat animal model of AD after intrahippocampal (IH) and intraperitoneal (IP) injections of a model NP, i.e., gold NPs (AuNPs). The outcomes revealed that the AuNPs could improve the acquisition and retention of spatial learning and memory in A beta treated rats as indicated by decreased time (A beta: 39.60 +/- 3.23 s vs A beta+AuNPs: 25.78 +/- 2.80 s) and distance (A beta: 917.98 +/- 50.81 cm vs A beta+AuNPs: 589.09 +/- 65.96 cm) of finding the hidden platform during training days and by increased time spent in the target quadrant (A beta: 19.40 +/- 0.98 s vs Afi+AuNPs: 29.36 +/- 1.14 s) in the probe test in Morris water maze (MWM). Expression of brain-derived neurotrophic factor, BDNF, cAMP response element binding protein, CREB, and stromal interaction molecules, e.g., STIM1 and STIM2 was also increased, supporting improved neural survival. Our outcomes may pave a way for mechanistic insights toward the role of NPs on retrieval of the deteriorated behavioral functions in brain tissue after AD outbreak.