Plasmalogen Improves Memory Function by Regulating Neurogenesis in a Mouse Model of Alzheimer's Diseases

Adult hippocampal neurogenesis (AHN) is associated with hippocampus-dependent cognitive function, and its initiation is attributed to neural stem cells (NSCs). Dysregulated AHN has been identified in Alzheimer's disease (AD) and may underlie impaired cognitive function in AD. Modulating the function of NSCs and stimulating AHN are potential ways to manipulate AD. Plasmalogen (PLA) are a class of cell membrane glycerophospholipids which exhibit neuroprotective properties. However, the effect of PLA on altered AHN in AD has not been investigated. In our study, PLA(10 & mu;g/mL) -attenuated A & beta; (1-42) (5 & mu;M) induced a decrease in NSC viability and neuronal differentiation of NSCs, partially through regulating the Wnt/& beta;-catenin pathway. Additionally, AD mice were supplemented with PLA (67mg/kg/day) for 6 weeks. PLA treatment improved the impaired AHN in AD mice, including increasing the number of neural stem cells (NSCs) and newly generated neurons. The memory function of AD mice was also enhanced after PLA administration. Therefore, it was summarized that PLA could regulate NSC differentiation by activating the Wnt/& beta;-catenin pathway and ameliorate AD-related memory impairment through up-regulating AHN.