pseudoginsenoside-f11 and Cognitive-Dysfunction

pseudoginsenoside-f11 has been researched along with Cognitive-Dysfunction* in 2 studies

Other Studies

2 other study(ies) available for pseudoginsenoside-f11 and Cognitive-Dysfunction

ArticleYear
Pseudoginsenoside-F11 attenuates cognitive dysfunction and tau phosphorylation in sporadic Alzheimer's disease rat model.
    Acta pharmacologica Sinica, 2021, Volume: 42, Issue:9

    Topics: Alzheimer Disease; Animals; Calpain; Chromosome Pairing; Cognitive Dysfunction; Disease Models, Animal; Ginsenosides; Glycogen Synthase Kinase 3 beta; Hippocampus; Insulin Receptor Substrate Proteins; Male; Maze Learning; Morris Water Maze Test; Proto-Oncogene Proteins c-akt; Rats; Rats, Wistar; Streptozocin; tau Proteins

2021
Pseudoginsenoside-F11 alleviates cognitive deficits and Alzheimer's disease-type pathologies in SAMP8 mice.
    Pharmacological research, 2019, Volume: 139

    Alzheimer's disease (AD) is a common neurodegenerative disease which is characterized by aggregation of amyloid beta (Aβ) and hyperphosphorylated tau. We previously reported that pseudoginsenoside-F11 (PF11), an ocotillol-type saponin, improved cognitive function and reduced Aβ aggregation in APP/PS1 mice, a familial AD model. Here, we chose senescence-accelerated mouse prone 8 (SAMP8) mice, a widely used model of aging, to investigate the effect of PF11 on sporadic AD. PF11 was orally administered to male 6-month-old SAMP8 mice for 3 months. Consistent with previous studies, SAMP8 mice showed several AD-type pathologies including cognitive impairment, Aβ deposition and tau hyperphosphorylation. We found increased protein levels of cytoplasmic amyloid precursor protein (APP) and β-site APP cleavage enzyme 1 (BACE1) in the hippocampus and cortex of SAMP8 mice. The protein level of demethylated protein phosphatase 2A (PP2A) was elevated in SAMP8 animals and the protein level of leucine carboxyl methyltransferase 1 (LCMT-1) was reduced. PF11 attenuated learning and memory impairments in the novel object recognition test and Morris water maze. PF11 promoted the transport of APP from cytoplasm to plasma membrane and decreased the abnormally high expression of BACE1 in hippocampus and cortex of SAMP8 mice. The elevated protein level of demethylated PP2A and the reduced expression of LCMT-1 in hippocampus and cortex of SAMP8 were also attenuated by PF11. Together, our findings indicate that PF11 has beneficial effects on AD-like pathological changes in SAMP8 mice and may act by inhibiting amyloidogenic processing of APP and attenuating tau hyperphosphorylation.

    Topics: Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Amyloid Precursor Protein Secretases; Animals; Aspartic Acid Endopeptidases; Cerebral Cortex; Cognitive Dysfunction; Disease Models, Animal; Ginsenosides; Hippocampus; Locomotion; Male; Maze Learning; Mice; Protein O-Methyltransferase; Protein Phosphatase 2; tau Proteins

2019