| Summary: | Gangliosides (GLSs), abundant in the mammalian brain, have been shown to affect neuronal plasticity and neurodegenerative diseases, especially Alzheimer’s disease. However, the biological activity and neuroprotective mechanism have not yet been established for sea urchin GLSs (SU-GLSs). Herein, we evaluated the neuroprotective effect of Strongylocentrotus nudus GM4(1S), GD4(1S), GD4(2A), and GD4(2G) in Aβ25-35-induced PC12 cells and in vivo using a GLSs mixture administered to SAMP8 mice. It was established that the pre-treatment of SU-GLSs decreased the loss of cell viability and the levels of Aβ1-40 and Aβ1-42 in the hippocampus significantly, and relieved the cognitive deficiency of SAMP8 mice. Mechanistic studies found that SU-GLSs down regulated the expression of Bax, Caspase-3, and Caspase-9, while it upregulated the expression of Bcl-2, synaptophysin, and GAP-43 significantly. Thus, SU-GLSs promoted resistance to AD in a dose-dependent and structure-selective manner, probably via reducing the loss of neurites and blocking the mitochondrial apoptosis pathway.
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