ArticleExperimental and therapeutic medicine2021
Ginseng gintonin attenuates the disruptions of brain microvascular permeability and microvascular endothelium junctional proteins in an APPswe/PSEN-1 double-transgenic mouse model of Αlzheimer's disease.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 11 citations in OpenAlex.
- Neo-gintonin: production of high concentrations of lysophosphatidic acids from Korean Red ginseng marc.Journal of ginseng research · 2026Article
- Ginseng Nanosizing: The Second Spring of Ginseng Therapeutic Applications.Antioxidants (Basel, Switzerland) · 2025Review
- Gintonin Binds to Reduced LPA4 Receptor Subtype in Human Cortical Neurons in Alzheimer's Disease Brains.Biomolecules · 2025Article
- Non-saponin fromJournal of ginseng research · 2025Article
- Emerging evidence that ginseng components improve cognition in subjective memory impairment, mild cognitive impairment, and early Alzheimer's disease dementia.Journal of ginseng research · 2024Review
- Review
- Antioxidants in Alzheimer's Disease: Current Therapeutic Significance and Future Prospects.Biology · 2022Review
- Applications of Phyto-Nanotechnology for the Treatment of Neurodegenerative Disorders.Materials (Basel, Switzerland) · 2022Review
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11 authors at 4 institutions in 1 country.
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Abstract
It has been previously indicated that gintonin, which is a novel exogenous ginseng-derived lysophosphatidic acid (LPA) receptor ligand, restores memory dysfunctions in an APPswe/PSEN-1 double-transgenic mouse model of Alzheimer's disease (AD Tg mice) by attenuating β-amyloid plaque deposition, recovering cholinergic dysfunctions and upregulating hippocampal neurogenesis in the cortex and hippocampus. Although β-amyloid plaque depositions in AD is accompanied with disruptions of brain microvessels, including the brain-blood barrier (BBB), it is unknown whether gintonin exerts protective effects on brain microvascular dysfunctions in AD Tg mice. In the present study, the effects of gintonin-enriched fraction (GEF) on the changes in β-amyloid plaque depositions, brain permeability of Evans blue, and microvascular junctional proteins were investigated in AD Tg mice. Long-term oral administration of GEF reduced β-amyloid plaque depositions in the cortex and hippocampus of AD Tg mice. GEF treatment also reduced the permeability of Evans blue through BBB and decreased immunoreactivity of platelet endothelial cell adhesion molecule-1 (a marker of BBB disruption) in the cortex and hippocampus of AD Tg mice in a dose-dependent manner. However, GEF elevated the protein expression of occludin, claudin-5 and zonula occludens-1, which are tight-junction proteins. The present results demonstrated that long-term oral GEF treatment not only attenuates β-amyloid plaque depositions in the brain but also exhibits protective effects against microvascular disruptions in AD Tg mice. Finally, GEF exhibits anti-AD effects through attenuation of β-amyloid plaque depositions and protection against brain microvascular damage in an AD animal model.
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