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- W2897624132 abstract "Alzheimer's disease (AD) is a progressive neurodegenerative disorder. Synaptic loss correlates strongly with disease severity, but the pathological mechanism remains elusive. During the pathological progression of AD, Aβ oligomers can induce the disruption of glutamate receptors in the macromolecules of the Shank-network located in the postsynaptic density (PSD). Shank proteins show distinct pathological changes which contribute to N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor loss at the PSD in AD. Aβ oligomers also can induce the loss of Na/K-ATPase activity at synapse, which lead to synaptic dysfunction. we used Ginsenosides to remove Aβ oligomers and protect synaptic function to prevent AD development at early stage. When APP/PS1 AD mice at 3 months old were treated 10mg/Kg Ginsenosides each day for consecutive 3 months, multiple methods including water Maze and fear conditioning test, westernblot, immunocytochemistry were used to examine memory change of these mice and the relevant mechanism. The results showed Ginsenosides can increase space memory function of APP/PS1 mice to obviously decrease the time for finding safe platform, the levels of Aβ oligomers were significantly decrease and the levels of dentridic spines and Shank3 proteins were significantly increased in the brains of APP/PS1 mice to rescue the homeostasis of synapse, compared with these levels in brains of APP/PS1 mice without treatment, respectively, and Ginsenosides can increase immunological function and neuronal autophage to clean Aβ oligomers, and protect Na/K-ATPases to restore synaptic homeostasis, preventing AD development. Ginsenosides could be used to protect synaptic dysfunction in the early of AD." @default.
- W2897624132 created "2018-10-26" @default.
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- W2897624132 date "2018-07-01" @default.
- W2897624132 modified "2023-10-16" @default.
- W2897624132 title "P3‐143: GINSENOSIDES PROTECT NA/K‐ATPASE ACTIVITY PREVENTING SYNAPTIC DYSFUNCTION IN APP/PS1 MICE" @default.
- W2897624132 doi "https://doi.org/10.1016/j.jalz.2018.06.1500" @default.
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