Zhancheng Xue

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Amyloid β-protein (Aβ) in the brain of Alzheimer’s disease (AD) potently inhibits the synaptic plasticity subsequently causing the cognitive deficits. Long-term potentiation (LTP) of synaptic transmission is thought to be an important cellular mechanism underlying memory formation. Different NR2 subunits are involved in NMDA receptor-dependent LTP. In the(More)
BACKGROUND VGF (nonacryonimic) and phosphatidylinositol 3-kinase (PI3K)/AKT (also known as protein kinase B, PKB)/mammalian target of rapamycin (mTOR) signaling play pivotal roles in depression. However, whether phosphatidylinositol 3-kinase/AKT/mTOR signaling-mediated VGF participates in rapid-acting antidepressant-like actions of GLYX-13 is unclear. (More)
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