Conclusion
The application of EGb effectively treats SCO-induced memory impairments probably by suppressing miR-1-3p/miR-206-3p and elevating the expression of PSD95.
Methods
Scopolamine (SCO)-induced rats were used to mimic AD-like memory deficits. Morris water maze test and fear conditioning test were conducted to evaluate the memory status of rats in response to different treatments. Then, the synapse alterations were assessed by Golgi staining, and Western blotting was conducted to assess the protein expression of PSD95, GluN2B, synapsin-1, and synaptophysin. Reverse transcription quantitative polymerase chain reaction was applied to detect the mRNA expression of PSD95 and the levels of miR-1-3p/miR-206-3p.
Objective
Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder. Emerging evidence suggests that synaptic dysfunction is associated with the onset and progression of AD. Interestingly, Ginkgo biloba extract (EGb) is one of the most frequently investigated herbal medicines for enhancing cognition and alleviating neurodegenerative dementia. This study aimed to investigate the effect and the mechanism of EGb on AD-like synaptic disorders.
Results
EGb supplement alleviated the learning and memory deficits induced by SCO in behavioral experiments. Moreover, EGb treatment attenuated synaptic damage elicited by SCO, manifested as increased dendritic spine density and the proportion of mushroom-type spines in hippocampal neurons. Further investigation indicated that EGb rescued the expression of synaptic-related proteins, especially PSD95, and decreased the levels of miR-1-3p/miR-206-3p in the rat hippocampus.