title: Ginsenoside Rg1 ameliorates hippocampal long-term potentiation and memory in an Alzheimer's disease model.
abstract: 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 β‑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 β‑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.
authors.affiliation: Department of Neurology, The Affiliated Hospital of Weifang Medical University, Weifang, Shandong 261031, P.R. China.
authors.forename: Fengling
authors.initials: F
authors.lastname: Li
authors.affiliation: Medical Imaging Center, Weifang Traditional Chinese Medicine Hospital, Weifang, Shandong 261041, P.R. China.
authors.forename: Xiqing
authors.initials: X
authors.lastname: Wu
authors.affiliation: Department of Orthopaedics Rehabilitation, Weifang Traditional Chinese Medicine Hospital, Weifang, Shandong 261041, P.R. China.
authors.forename: Jing
authors.initials: J
authors.lastname: Li
authors.affiliation: Medical Imaging Center, Weifang Traditional Chinese Medicine Hospital, Weifang, Shandong 261041, P.R. China.
authors.forename: Qingliang
authors.initials: Q
authors.lastname: Niu
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy / Q000378:metabolism* / Q000523:psychology*; D000818:Animals; D015415:Biomarkers; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D004195:Disease Models, Animal; D036145:Ginsenosides / Q000008:administration & dosage / Q000494:pharmacology*; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism*; D017774:Long-Term Potentiation / Q000187:drug effects*; D008297:Male; D008562:Membrane Glycoproteins / Q000378:metabolism; D008568:Memory / Q000187:drug effects*; D051379:Mice; D011505:Protein-Tyrosine Kinases / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D020813:Receptor, trkB
chemical_list: D015415:Biomarkers; D019208:Brain-Derived Neurotrophic Factor; D036145:Ginsenosides; D008562:Membrane Glycoproteins; D011505:Protein-Tyrosine Kinases; C064371:Ntrk2 protein, mouse; D020813:Receptor, trkB; C035054:ginsenoside Rg1