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GSK-3β activation accelerates early-stage consumption of Hip
Custom-Made AAV was used for gene over-expression. (From BrainVTA)
The viruses used in this article from BrainVTA are in the table below
Custom-Made AAV  AAV-EF1α-DIO-GSK-3β-2A-EGFP
Control  AAV-EF1α-DIO-EGFP
Fei Liu, Na Tian, Hua-Qiu Zhang, Shi-Hong Li, Qiu-Zhi Zhou, Ying Yang, Jie Zheng, Jian-Zhi Wang
Pub Date: 2020-08-01, DOI: 10.7150/thno.43829, Email: [email protected]
Adult hippocampal neurogenesis (AHN) deficits contribute to the progression of cognitive impairments during accelerated senescence, with the mechanistic causes poorly understood. Glycogen synthase kinase-3β (GSK-3β) is a critical regulator in prenatal neurodevelopment. The present study aims to study whether and how GSK-3β regulates AHN during the accelerated senescence.
Methods: AHN and AHN-dependent cognition and GSK-3β were evaluated in 3- and 6-month senescence-accelerated mice prone 8 (SAM-P8) and senescence resistant 1 (SAM-R1) mice, respectively. GSK-3β was selectively overexpressed in wild-type mice using adeno-associated virus, or knocked-out by crossbreeding with GSK-3β floxed mice in the neural stem cells (NSCs) of Nestin-Cre mice, or pharmacologically inhibited with SB216763 in SAM-P8 mice. AHN was evaluated by BrdU-, DCX-staining and retrovirus-labeling.
Results: AHN transiently increased at 3-month, but dramatically dropped at 6-month of age in SAM-P8 mice with a simultaneous activation of GSK-3β at 3-month. Selective overexpression of GSK-3β in hippocampal NSCs of wildtype mice induced long-term AHN deficits due to an accelerated depletion of NSC pool, although it transiently increased the proliferation and survival of the newborn neurons. Pharmacologically inhibiting GSK-3β by SB216763 efficiently preserved AHN and improved contextual memory in 6-month SAM-P8 mice, while conditional knock-out of GSK-3β in NSCs impaired AHN.
Conclusion: Early-stage activation of GSK-3β in NSCs impairs AHN by accelerating the depletion of NSC pool, and pharmacological inhibition of GSK-3β is efficient to preserve AHN during the accelerated aging. These results reveal novel mechanisms underlying the AHN impairments during accelerated senescence and provide new targets for pro-neurogenic therapies for related diseases.
In this study, the authors found that GSK-3β activation in hippocampal neural stem cells induced a transient increase of AHN by over-consumption of the NSCs pool in mice with accelerated senescence, which lead to an eventual AHN deficit thus impaired spatial memory, while only partial inhibiting GSK-3β rescues AHN.
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