| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5815659 | Neuropharmacology | 2012 | 9 Pages |
Abstract
⺠PREGS prevented Aβ25-35-induced cognitive deficit and apoptosis of pyramidal cells. ⺠The PREGS-neuroprotection in Aβ25-35-mice depended on activation of α7nAChR and Ï1R. ⺠PI3K-Akt and ERK were involved in α7nAChR and Ï1R-mediated PREGS-neuroprotection. ⺠The anti-amnesic effect of PREGS in Aβ25-35-mice depended on its neuroprotection.
Keywords
PI3KAβERKMLASigma-1 receptor (σ1R)NMDARα7nAChRDMXBLY294002U0126MAPKβ-Amyloidβ-Amyloid (Aβ)γ-aminobutyric acid type A receptorPREGSAlzheimer's diseasepregnenolonepregnenolone sulfatephosphatidylinositol-3-kinasemethyllycaconitinePREGextracellular signal-related kinaseGABAARN-methyl-d-aspartate receptorα7 nicotinic acetylcholine receptor
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Authors
Rong Yang, Lei Chen, Haofei Wang, Bingzhong Xu, Hidekazu Tomimoto, Ling Chen,