The Effect Of Amyloid-β On Neural Stem Cells Migration And Relevant Signaling Protein Research

Alzheimer’s disease (AD) is becoming a serious social problem alongwith the aging of society. Amyloid-β (Aβ) accumulation, a hallmark ofAlzheimer’s disease, promotes the disease progress in multiple facets andis regarded as a key pivot in AD onset. With the discovery of adult neuralstem cells (NSCs), the usage of stem cells to fix injuries has attractedwide and increasing attention. However, the irreversible loss of neuronsin the brain of AD patients suggests that activities of neural stem cellswould be inhibited. Our previous research found that incubation of Aβ onNSCs influenced their migration and changed levels of some signalingmolecules. Here we are verifying the effect of Aβ on NSCs migration andexploring the potential mechanism.We used the original neural stem cells taken from embryos of SD Ratsand incubated with different concentration of Aβ. The wound healingassay and neurosphere assay was used to measure the distance of NSCsmigration. Western blot was conducted to investigate levels of GRK2andMAPK. Our results demonstrate that Aβ decreases NSCs migration in time-andconcentration-dependent manners, and also increases GRK2levelssignificantly. Up-regulation of GRK2can be provoked by formyl peptidereceptor (FPR) activation, yet there are still other pathways existing, bywhich Aβ enhances GRK2levels, to be continued exploration.