PMID- 27082952 OWN - NLM STAT- MEDLINE DCOM- 20170406 LR - 20220318 IS - 1791-3004 (Electronic) IS - 1791-2997 (Linking) VI - 13 IP - 6 DP - 2016 Jun TI - Ginsenoside Rg1 ameliorates hippocampal long-term potentiation and memory in an Alzheimer's disease model. PG - 4904-10 LID - 10.3892/mmr.2016.5103 [doi] AB - The complex etiopathogenesis of Alzheimer's disease (AD) has limited progression in the identification of effective therapeutic agents. Amyloid precursor protein (APP) and presenilin‑1 (PS1) are always overexpressed in AD, and are considered to be the initiators of the formation of beta‑amyloid plaques and the symptoms of AD. In the present study, a transgenic AD model, constructed via the overexpression of APP and PS1, was used to verify the protective effects of ginsenoside Rg1 on memory performance and synaptic plasticity. AD mice (6‑month‑old) were treated via intraperitoneal injection of 0.1‑10 mg/kg ginsenoside Rg1. Long‑term memory, synaptic plasticity, and the levels of AD‑associated and synaptic plasticity‑associated proteins were measured following treatment. Memory was measured using a fear conditioning task and protein expression levels were investigated using western blotting. All the data was analyzed by one-way analysis of variance or t‑test. Following 30 days of consecutive treatment, memory in the AD mouse model was ameliorated in the 10 mg/kg ginsenoside Rg1 treatment group. As demonstrated by biochemical experiments, ginsenoside Rg1 treatment reduced the accumulations of beta‑amyloid 1‑42 and phosphorylated (p)‑Tau in the AD model. Additionally, brain-derived neurotrophic factor (BDNF) and p‑TrkB synaptic plasticity‑associated proteins were upregulated following ginsenoside Rg1 application. Correspondingly, long‑term potentiation (LTP) was restored following ginsenoside Rg1 application in the AD mice model. Taken together, ginsenoside Rg1 repaired hippocampal LTP and memory, likely through facilitating the clearance of AD‑associated proteins and through activation of the BDNF‑TrkB pathway. Therefore, ginsenoside Rg1 may be a candidate drug for the treatment of AD. FAU - Li, Fengling AU - Li F AD - Department of Neurology, The Affiliated Hospital of Weifang Medical University, Weifang, Shandong 261031, P.R. China. FAU - Wu, Xiqing AU - Wu X AD - Medical Imaging Center, Weifang Traditional Chinese Medicine Hospital, Weifang, Shandong 261041, P.R. China. FAU - Li, Jing AU - Li J AD - Department of Orthopaedics Rehabilitation, Weifang Traditional Chinese Medicine Hospital, Weifang, Shandong 261041, P.R. China. FAU - Niu, Qingliang AU - Niu Q AD - Medical Imaging Center, Weifang Traditional Chinese Medicine Hospital, Weifang, Shandong 261041, P.R. China. LA - eng PT - Journal Article DEP - 20160412 PL - Greece TA - Mol Med Rep JT - Molecular medicine reports JID - 101475259 RN - 0 (Biomarkers) RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Ginsenosides) RN - 0 (Membrane Glycoproteins) RN - EC 2.7.10.1 (Ntrk2 protein, mouse) RN - EC 2.7.10.1 (Protein-Tyrosine Kinases) RN - PJ788634QY (ginsenoside Rg1) SB - IM MH - Alzheimer Disease/drug therapy/*metabolism/*psychology MH - Animals MH - Biomarkers MH - Brain-Derived Neurotrophic Factor/metabolism MH - Disease Models, Animal MH - Ginsenosides/administration & dosage/*pharmacology MH - Hippocampus/*drug effects/*metabolism MH - Long-Term Potentiation/*drug effects MH - Male MH - Membrane Glycoproteins/metabolism MH - Memory/*drug effects MH - Mice MH - Protein-Tyrosine Kinases/metabolism MH - Signal Transduction/drug effects EDAT- 2016/04/16 06:00 MHDA- 2017/04/07 06:00 CRDT- 2016/04/16 06:00 PHST- 2015/04/24 00:00 [received] PHST- 2016/03/02 00:00 [accepted] PHST- 2016/04/16 06:00 [entrez] PHST- 2016/04/16 06:00 [pubmed] PHST- 2017/04/07 06:00 [medline] AID - 10.3892/mmr.2016.5103 [doi] PST - ppublish SO - Mol Med Rep. 2016 Jun;13(6):4904-10. doi: 10.3892/mmr.2016.5103. Epub 2016 Apr 12.