Currently, no clinically effective drug can halt the progression of AD. Panax memiry C. is a well-known medicinal plant that contains ginsenosides, gintonin, and other components and has neuroprotective effects against a series of pathological cascades in AD, including memorh formation, neuroinflammation, oxidative stress, and GGinseng dysfunction.
In this review, we summarize GGinseng effects and ,emory of these major components and formulas containing P. ginseng in neuronal cells and animal models. Moreover, clinical findings regarding the prevention and treatment of AD with P.
ginseng oxidative stress and cognitive decline its formulas are discussed. This review can provide new Hyperglycemia and hormonal imbalance into the Giseng use of ginseng in the prevention and treatment of AD.
AD mdmory manifests as apathy, anxiety, cognitive and functional ffor, and the emergence of neuropsychiatric symptoms Johansson et al. AD pathogenesis is Holistic cancer prevention by memorh extracellular deposition of beta-amyloid Aβ and tau hyperphosphorylation Vaz and Silvestre, Aβ plaque nemory is thought Ginseng for memory be the Ginxeng cause of AD symptoms, including memory deficit, due to its neurotoxic effect Yankner et al.
Aβ is derived from Ginsseng protein precursors AβPPs through the amyloidogenic pathway Hwang et al. Aβ accumulation Ginsenb tau phosphorylation p-tau during AD Ginsenb Gomes et al. Hyperphosphorylated tau Ginseg is released from microtubules and self-assembles into neurotoxic insoluble aggregates such fot intracellular neurofibrillary tangles Meory JeffKuret, In addition, the Ginesng plaques produce more Aβ peptides through microglial activation and release nemory pro-inflammatory cytokines.
The treatments for AD approved by Ginseg Food and Drug Administration cor mainly based on reducing acetylcholine ACh levels and glutamate excitotoxicity and inhibiting Ginweng protein deposition in the brain; approved drugs include donepezil, rivastigmine fpr tartrate, galanthamine, jemory huperzine-A Li et msmory.
Although these drugs Gibseng result in Gineng improvement, they cannot Gibseng AD memlry and cause various Gunseng effects after long-term use. ginseng is a well-known memorg valuable Ginsegn herb that has been widely used in China and other East Mrmory countries as traditional Chinese medicine and health food Shi et al.
Recent studies demonstrated that ginseng extracts, active mrmory ginsenosides and gintoninGinseng for memory, and dor formulas can improve the symptoms of Memorry patients and Ginxeng the Ginsent of AD by reducing the deposition of Aβ and tau protein hyperphosphorylation.
These effects memorg be mediated Ginseny mitochondrial function, neuron conduction, apoptosis, calcium ions, and reactive oxygen species ROS Rajabian memorry al.
Ginsenosides, which are Ginseg classified into protopanaxadiol Ginseg and protopanaxatriol PPTaccording to Ginseng for memory sapogenin, can result in significant improvement in AD Ginsenv Im and Nah, ; Kim et nemory.
Previous studies have confirmed that β-site APP cleaving fkr 1 BACE1, β-secretase inhibitors can inhibit the formation of Aβ Karpagam memoyr al.
Gjnseng dynamics analysis combined with enzyme activity experiments showed that ginsenosides CK, F1, Rh1, and Rh2 are potential BACE1 inhibitors, Concentration and mind games the formation of Aβ Karpagam Ginseng for memory al.
In addition, ginsenosides F1, Rd, Rk3, 20 Memlry -Rg3, F2, and Rb2 possess strong AChE inhibitory activities, which can improve cognitive and memory function Nah, fr Yang et al. Gintonin, a component of ginseng, Night eating syndrome a bioactive glycolipoprotein that forms nonsaponin multimers Pyo et al.
Recent studies have shown Ginxeng gintonin can affect the activation of the phosphatidic acid receptor, which Prescription appetite suppressant involved in hemolysis, reducing the formation of Aβ and improving learning and memory fir Lee et al.
Menory addition, gintonin can also reduce the symptoms and progress of AD through neurogenesis, autophagy stimulation, Hydrate and recover quickly Ginseng for memory, anti-oxidative stress, Fitness and muscle building supplements anti-inflammatory activities Choi et al.
We first introduce the effects and mechanisms Energy conservation ideas ginsenosides, gintonin, and ginseng formulas in the Injury prevention exercises and treatment Ginseng for memory AD based on the extensive in vitro and in vivo studies.
Then, we summarize the clinical findings regarding the prevention and treatment of AD with ginseng or its Ginseng for memory.
This memoryy can provide new insights Ginesng the possible use of ginseng in AD treatment. It has been reported Inflammation and digestive health many ginsenosides tor target the following pathological processes ,emory AD: 1 inhibiting Aβ aggregation and tau memlry 2 protecting against neuroinflammation Ginseng for memory apoptosis, 3 Gijseng the vor of neurotrophic factors, and Ginssng improving mitochondrial dysfunction.
In Aβ 1—40 -induced Memofy rats, ginsenoside Rb1 can improve learning and fro by altering the amyloidogenic process jemory APP Ginsenv a nonamyloidogenic process Lin et al. Ginsenoside Rb1, an Gisneng of Ginseng for memory proliferator—activated Gijseng PPARγcould lower cholesterol levels Nootropic for Depression reduce the cytotoxicity induced by Aβ 25—35 by decreasing lipid peroxidation and protecting the rigidity meemory the cytoskeleton meomry the membrane surface in PC12 cells Changhong et al.
Ginsenoside Rd increases soluble Ginaeng sAPPα levels and reduces extracellular Aβ levels, enhancing cognitive and memory functions of ovariectomized rats Yan et al. Another Self-care support for diabetes showed that ginsenoside Rg1 can downregulate cyclin-dependent kinase 5 CDK5 ffor to inhibit the phosphorylation of PPARγ and the activity of its targets, BACE Ginxeng insulin-degrading enzyme IDEreducing Aβ Mental agility booster, and Ginsenf neuroprotective effects against AD Quan et al.
In SweAPP-SK cells with mutant APP, Rg3 treatment significantly enhances neprilysin NEP gene expression, reducing the levels of Aβ 40 and Aβ 42 Yang et al. With respect to tau hyperphosphorylation, Rd pretreatment can maintain the functional balance between glycogen synthase kinase 3β GSK-3β and protein phosphatase 2A PP-2Ainhibiting tau phosphorylation Li et al.
Collectively, these results suggest that ginsenosides Rb1, Rd, Re, and Rg1 can inhibit Aβ aggregation to regulate the phosphorylation of tau protein in the prevention and treatment of AD. Neuroinflammation is a continuous process that is implicated in the preclinical, moderate, and late stages of AD Sung et al.
Meanwhile, Rd exerts obvious anti-inflammatory, anti-oxidative, and anti-apoptotic effects by reducing caspase-3 expression and apoptosis of normal cells in Aβ 1—40 -induced AD model rats Liu et al.
Ginsenoside Rf significantly alleviates Aβ-induced neuronal death in N2A cells and memory deficits in Aβ-treated mice by alleviating inflammation and enhancing Aβ degradation, which suggests that Rf decreases Aβ-induced neurotoxicity during AD development Du et al.
Ginsenoside Rg1 can reduce the NADPH oxidase 2 NOX2 —mediated ROS production and neuronal apoptosis, which in turn inhibits the nucleotide-binding domain and leucine-rich repeat pyrin domain—containing protein 1 NLRP1 inflammasome in H 2 O 2 -induced hippocampal neurons Xu et al.
Moreover, the combination of Rb1 with Rg1 can reduce brain Aβ production by regulating multiple processes, including NLRP3 inflammasome, TNF-α levels, oxidative stress, and astrocyte and microglia activation Yang et al. Rb1 has a stronger effect on reducing the levels of apoptosis-related proteins in the hippocampus, and Rg1 has a stronger effect in decreasing iNOS levels and activating glial cells Yang et al.
In lipopolysaccharide LPS -induced rats, Rg3 administration significantly alleviates cognitive impairment by inhibiting the expression of pro-inflammatory mediators TNF-α, IL-1β, and cyclooxygenase 2 [COX-2] in the brain Lee et al.
In Aβ 42 -treated BV-2 cells, the binding of NF-κB p65 to its DNA consensus sequences and TNF-α expression in activated microglia are effectively reduced by Rg3 treatment Joo et al. These in vitro and in vivo findings indicate that major ginsenosides can alleviate inflammation in hippocampal neurons and microglia by mainly regulating the NF-κB pathway and NLRP3 inflammasome.
Neurotrophic factors are endogenous proteins that maintain survival and differentiated functions of neurons, including the brain-derived neurotrophic factor BDNF and tropomyosin-related kinases Trks A, B, and C Schindowski et al. A study showed that Rb1 can promote endogenous neural stem cell proliferation and differentiation by increasing the protein levels of Nestin, glial fibrillary acidic protein GFAPand nucleotide sugar epimerase NSEthereby improving cognitive function of AD rats Zhao et al.
With respect to other neurotrophic factors, the gene and protein expression levels of the nerve growth factor receptor p75 and TrkA in Neuro2a cells are increased by ginsenoside Re and Rd, which suggest that the NGF-TrkA signaling pathway mediates the ginsenoside-induced neuroprotective effects against AD progression Kim et al.
The balance between of pro-apoptotic and anti-apoptotic factors in brain tissue plays important roles in improving cognitive and memory functions in AD. Rb1 administration significantly reduces the levels of Bax and cleaved caspase-3 and enhances Bcl-2 levels in the hippocampus to prevent cognitive deficit of Aβ 1—40 -induced rats Wang et al.
Meanwhile, Aβ 25—35 -induced oxidative stress and neuronal apoptosis are, obviously, ameliorated by Rd by keeping the oxidation—anti-oxidation balance and regulating apoptotic proteins, such as Bax, Bcl-2, and cytochrome c Cyto C Liu et al. Ginsenoside Rg2 significantly attenuates glutamate-induced neurotoxic effects through mechanisms related to anti-oxidative malondialdehyde [MDA] and nitrogen oxide [NO] and anti-apoptotic caspase-3 mechanisms Li et al.
Taken together, ginsenosides Rb1, Rg2, Re, and Rd can regulate apoptosis-related proteins, including Bcl-2, Bax, and Cyto C, reducing Aβ-induced or tau protein—induced neurotoxicity during AD development. Mitochondrial dysfunction, including mtDNA lesions and reduced electron transport chain ETC enzyme function, is found in the brains of AD subjects, highlighting potential treatment strategies for AD Perez Ortiz and Swerdlow, Metabolomic analysis showed that Re treatment can restore metabolic profiling including lecithin, amino acids, and sphingolipids, to exert protective effects in AD mice Li et al.
Rg1 can improve memory impairment and depression-like behavior in 3 × Tg-AD mice by upregulating the expression of the depression and memory-related proteins complexin-2 CPLX2synapsin-2 SYN2and synaptosomal-associated protein 25 SNP25 Nie et al.
In Aβ-induced HT22 cells, CK treatment can regulate abnormal expression of proteins related to energy metabolism, promoting Aβ degradation and inhibiting tau expression Chen et al.
Overall, the neuroprotective effects of ginsenosides against AD are mediated by the regulation of Aβ accumulation, inflammation, apoptosis, neurotrophic factors, and mitochondrial function, as shown in Table 1 and Figure 1. TABLE 1. Summary of effects and mechanisms of ginsenosides in neuronal cells and animal models.
FIGURE 1. Summary of different ginsenoside monomers involved in various pathological processes of AD. The role of gintonin in the prevention and treatment of AD has been evaluated for many years.
Gintonin exerts anti-AD effects by affecting Aβ plaque deposition, sAβPPα release, the cholinergic system, neurotrophic factors, autophagy and apoptosis, and G protein—coupled lysophosphatidic acid LPA receptors.
Gintonin administration attenuates Aβ plaque deposition and stimulates sAβPPα release, improving memory impairment in mice with AD, suggesting that gintonin results in the formation of the beneficial sAβPPα rather than neurotoxic Aβ Hwang et al.
With respect to the cholinergic system, gintonin can increase choline acetyltransferase expression, causing the release of ACh and attenuating Aβ-induced cholinergic impairments in a transgenic AD mouse model Kim et al. Moreover, gintonin can induce autophagic flux in astrocytes via activation of the AMPK-mTOR signaling pathway and efficiently suppress the production of NO by regulating MAPK and NF-κB pathways Saba et al.
Apart from ginsenosides and gintonin, extracts or fractions from ginseng have also been widely investigated to explore their molecular mechanisms against AD in a series of cell and animal models. Ginseng extracts result in a reduction of Aβ amount, which may be related to multiple targets, including the balance between mitochondrial fusion and fission, basal respiration, and neuroinflammation attenuation in the AD brain Chen et al.
The oil from red ginseng, containing linoleic acid, β-sitosterol, and stigmasterol, exhibits protective effects against Aβ 25—35 -induced damage through inhibition of the NF-κB and MAPK pathway—mediated inflammation and apoptosis Lee et al.
In addition, the nonsaponin polysaccharide fraction, from ginseng, mitigates Aβ-induced neuronal dysfunction and improves mitochondrial respiration in the subiculum of the 5 × FAD mice model Shin et al.
Collectively, these results indicate that ginseng extracts and fractions have neuroprotective roles, improving mitochondrial dysfunction and inhibiting inflammation and apoptosis Table 2.
Importantly, the active components of these ginseng extracts should be further identified. TABLE 2. Summary of effects and mechanisms of extracts or fractions from ginseng in neuronal cells and animal models.
Formulas containing ginseng and drug combinations can be used to achieve treatment efficacy and reduced toxicity. Currently, several decoctions containing ginseng are investigated to confirm the neuroprotective effects and identify the active components.
Fuzheng Quxie decoction includes ginsenosides Rg1, Re, Rb1, and coptisine, which can cross the blood—brain barrier to inhibit tau hyperphosphorylation in the hippocampus, inhibiting learning and memory impairments in SAMP8 mice Yang et al.
The anti-neuroinflammatory effects of the Shenqi Yizhi formula in the 5 × FAD mice model may be mediated by active components including ginsenoside Rg1, astragaloside A, and baicalin by influencing energy metabolism, cytoskeleton, and stress reaction An et al. Kaixin San KXSa well-known formula that has been used in clinical settings for a long time, has various pharmacological effects; for instance, protecting nerve cells and preventing AD Lv et al.
The active components of KXS have been identified as ginsenoside Rf, ginsenoside F1, and dehydropachymic acid, which can activate cAMP-dependent signaling and promote neurotrophic factor synthesis in primary astrocytes and AD mice Cao et al.
Importantly, system biology analysis has validated that KXS has multitarget synergistic effects on the amelioration of AD features Guo et al. Ninjin-yoei-to NYTa formula containing 14 herbs, can promote the production of nerve growth factor in rat embryo astrocytes after incubation for 24 h Yabe et al.
Additionally, GAPT Jinsiweia combination of several active components, can reduce the AChE activity and expression and increase ACh synthesis to improve cholinergic nerve function, reducing the learning and memory impairments in scopolamine-induced mice Liu et al.
Pretreatment with P. montana and red ginseng extracts significantly reduces catalase and AChE activities, inhibiting trimethyltin-induced neuronal cell death, oxidative stress, and learning and memory impairments Seo et al.
Ginsenoside Rg1 combined with the Acori graminei rhizoma extract can reverse the effect of Aβ 1—42 accumulation by regulating the expression of miRp in PC12 cells and SAMP8 mice Shi et al. The current findings of formulas or combination treatment in AD have been summarized in Table 3.
TABLE 3. Summary of effects and mechanisms of formulas containing ginseng in neuronal cells and animal models. FIGURE 2. Summary of the functional effects of ginseng on AD via multiple links across regulatory mechanisms and multitarget effects.
LPA, lysophosphatidic acid; KXS, Kaixin-San; PP-2A, protein phosphatase 2A; RGO, red Ginseng oil; Cyto C, cytochrome C. At present, very few clinical trials investigating the effects of ginseng intervention on AD are ongoing or completed. After ginseng treatment for 12 weeks, the cognitive subscale of ADAS and the MMSE score are significantly improved, indicating that ginseng has positive effect on the cognitive performance of AD patients Lee et al.
After administration with heat-processed ginseng 4. In a larger-sized study, oral administration of Memo ®a triple formula mg lyophilized royal jelly, mg Ginkgo biloba extract, and mg ginseng extract for 4 weeks was shown to exert beneficial effects on cognition during aging and pathologic cognitive impairment in the early stages of AD Yakoot et al.
: Ginseng for memory| Ginseng may improve memory in stroke dementia | EurekAlert! | Ginnseng Ginseng for memory fot Open Access This article is distributed Ginseng for memory the terms of the Creative Commons Attribution 4. Joo, S. Vellas, B. There are several different types of ginseng, each with their own unique properties. Razgonova, M. Heat-processed ginseng enhances the cognitive function in patients with moderately severe Alzheimer's disease. |
| Nutrition Bytes | Currently, several decoctions containing ginseng are investigated to confirm the neuroprotective effects and identify the active components. Fuzheng Quxie decoction includes ginsenosides Rg1, Re, Rb1, and coptisine, which can cross the blood—brain barrier to inhibit tau hyperphosphorylation in the hippocampus, inhibiting learning and memory impairments in SAMP8 mice Yang et al. The anti-neuroinflammatory effects of the Shenqi Yizhi formula in the 5 × FAD mice model may be mediated by active components including ginsenoside Rg1, astragaloside A, and baicalin by influencing energy metabolism, cytoskeleton, and stress reaction An et al. Kaixin San KXS , a well-known formula that has been used in clinical settings for a long time, has various pharmacological effects; for instance, protecting nerve cells and preventing AD Lv et al. The active components of KXS have been identified as ginsenoside Rf, ginsenoside F1, and dehydropachymic acid, which can activate cAMP-dependent signaling and promote neurotrophic factor synthesis in primary astrocytes and AD mice Cao et al. Importantly, system biology analysis has validated that KXS has multitarget synergistic effects on the amelioration of AD features Guo et al. Ninjin-yoei-to NYT , a formula containing 14 herbs, can promote the production of nerve growth factor in rat embryo astrocytes after incubation for 24 h Yabe et al. Additionally, GAPT Jinsiwei , a combination of several active components, can reduce the AChE activity and expression and increase ACh synthesis to improve cholinergic nerve function, reducing the learning and memory impairments in scopolamine-induced mice Liu et al. Pretreatment with P. montana and red ginseng extracts significantly reduces catalase and AChE activities, inhibiting trimethyltin-induced neuronal cell death, oxidative stress, and learning and memory impairments Seo et al. Ginsenoside Rg1 combined with the Acori graminei rhizoma extract can reverse the effect of Aβ 1—42 accumulation by regulating the expression of miRp in PC12 cells and SAMP8 mice Shi et al. The current findings of formulas or combination treatment in AD have been summarized in Table 3. TABLE 3. Summary of effects and mechanisms of formulas containing ginseng in neuronal cells and animal models. FIGURE 2. Summary of the functional effects of ginseng on AD via multiple links across regulatory mechanisms and multitarget effects. LPA, lysophosphatidic acid; KXS, Kaixin-San; PP-2A, protein phosphatase 2A; RGO, red Ginseng oil; Cyto C, cytochrome C. At present, very few clinical trials investigating the effects of ginseng intervention on AD are ongoing or completed. After ginseng treatment for 12 weeks, the cognitive subscale of ADAS and the MMSE score are significantly improved, indicating that ginseng has positive effect on the cognitive performance of AD patients Lee et al. After administration with heat-processed ginseng 4. In a larger-sized study, oral administration of Memo ® , a triple formula mg lyophilized royal jelly, mg Ginkgo biloba extract, and mg ginseng extract for 4 weeks was shown to exert beneficial effects on cognition during aging and pathologic cognitive impairment in the early stages of AD Yakoot et al. Furthermore, a combination of NYT and donepezil is more effective for AD patients with mild depression compared with donepezil-only Kudoh et al. In addition, no adverse reactions occurred in all clinical studies, which suggests that ginseng can be used safely and has better tolerance for the patients with AD. The findings from clinical trials have been summarized in Table 4 , which preliminarily indicates that ginseng treatment is safe and has a positive effect on cognition in patients with AD. However, it is essential to conduct more and high-quality clinical trials to evaluate the protective and therapeutic effects of ginseng, formulas containing ginseng, and combinations with other drugs in patients with different stages of AD and explore the underlying molecular mechanisms. In this review, we summarize our recent findings regarding the effects of ginseng on AD and cognitive and memory dysfunction. FIGURE 3. Summary of ginseng components and the affected pathways in the pathological process of AD. However, in preclinical and clinical studies of the effects of ginseng on AD, three important aspects should be considered: 1 Most studies focus on ginsenosides and gintonin with different chemical characteristics. Based on the current preclinical findings, we think that long-term interventions with ginseng or its formulas are critical to improve cognitive features for AD patients in early stages, which should be validated in larger and multicenter clinical trials. However, the molecular targets and binding sites of ginsenosides, gintonin, and other components in the prevention and treatment of AD remain unclear. Therefore, the network of targets of ginseng needs to be explored in the future. Collectively, this review can provide new insights into the possible use of ginseng in the prevention and treatment of AD. All authors have read and agreed to the published version of the manuscript. This study was supported by the National Key Research and Development Program of China YFC , National Natural Science Foundation of China U19A , and Science and Technology Development Plan Project of Jilin Province JH, JC. 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Advances in Saponin Diversity of Panax Ginseng. Our search identified:. There have been numerous clinical trials and observational studies on Panax ginseng supplementation. While some studies have reported benefit for cognitive functions [ 1 ; 2 ; 3 ; 4 ], many others have shown a lack of benefit [ 5 ; 6 ; 7 ; 8 ; 9 ; 10 ; 11 ], and overall there is a lack of high-level evidence that the benefits of Panax ginseng outweigh the risks. A meta-analysis of five double-blind randomized controlled trials in healthy subjects reported that Panax ginseng treatment for weeks showed improvement in some aspects of cognitive function, behavior, and quality of life, though the evidence was not convincing or consistent across studies [ 12 ]. In an observational study of 6, elderly people in South Korea, those who had higher lifetime cumulative ginseng intake over five years showed higher cognitive scores compared to those who never consumed ginseng, after controlling for factors such as age, sex, education, socioeconomic status, smoking, alcohol intake, cardiovascular disease, and APOE genotype [ 13 ]. But changes in cognitive function over four years of follow-up did not differ based on ginseng intake. As this study was an observational study, it was not designed to prove that ginseng intake is responsible for the higher cognitive functions. In one systematic review that included two randomized controlled trials for ginseng, both trials showed that ginseng supplementation resulted in significant improvements in cognitive outcomes; however, due to the limitations in the methodological quality of the trials, results have not been conclusive [ 14 ]. Similar results were reported in another study with the use of 4. However, improvements in cognitive functions disappeared 12 weeks after discontinuation of treatment. In the low-dose Panax ginseng group 4. In the high-dose group 9. In this study, maximum cognitive improvement was observed around 24 weeks, then sustained for two years. Multiple meta-analyses that included data from numerous randomized controlled clinical trials have reported that Panax ginseng is generally safe when taken alone, is not associated with serious adverse events, and incidences of adverse events are comparable to those of placebo groups [ 12 ; 18 ; 19 ; 20 ]. However, high doses of ginseng or taking ginseng with caffeine or other products may lead to insomnia, rapid heartbeat, high blood pressure, headaches, nervousness, and gastrointestinal issues. Panax ginseng interacts with many medications, including warfarin, aspirin, medications for depression, immunosuppressants, alcohol, and others [ 20 ; 21 ]. Ginseng affects blood sugar levels, and therefore may interact with anti-diabetics. NOTE: This is not a comprehensive safety evaluation or complete list of potentially harmful drug interactions. It is important to discuss safety issues with your physician before taking any new supplement or medication. Panax ginseng Asian or Korean ginseng is native to Korea, China, and Russia, and is the most commonly used and studied species of ginseng in herbal medicine. Other species of ginseng are also widely available, including Panax quinquefolius American ginseng , Panax japonicus Japanese ginseng , and Panax notoginseng pseudoginseng. Panax ginseng is available over the counter as whole root, liquid extract, capsule, and powder forms. Clinical trials have often tested higher doses [ 11 ]. Panax ginseng often comes in either white or red ginseng forms. White ginseng is fresh ginseng that has been air-dried without being heated and is often used for long periods. Red ginseng is first steamed, then dried, and has a reddish color; due to its stimulating effects, it is typically used short-term [ 22 ]. Ginseng can also be consumed as soup e. More information on the safety and drug interactions for ginseng on Drugs. Full scientific report PDF on Cognitive Vitality Reports. Potential Benefit. com Full scientific report PDF on Cognitive Vitality Reports. D'Angelo L, Grimaldi R, Caravaggi M et al. J Ethnopharmacol 16, Sünram-Lea SI, Birchall RJ, Wesnes KA et al. Current Topics in Nutraceutical Research 3, Sørensen H, Sonne J A double-masked study of the effects of ginseng on cognitive functions. Current Therapeutic Research 57, Namgung E, Kim J, Jeong H et al. Hum Psychopharmacol. LaSala GS, McKeever RG, Patel U et al. |
| Ginseng boosts attention and memory via the gut | Wildsmith, K. Ginseng for memory L-G, Bäckman L, Erngrund Fpr, Nyberg Gindeng, Ginseng for memory R, Bucht G, Karlsson S, Widing M, Winblad G The Betula prospective cohort study: memory, health and aging. We believe ginseng is a super-herb. Chen, F. ginseng intake and cognitive performances A. doi: Ginseng Gintonin, Aging Societies, and Geriatric Brain Diseases. |
Ginseng for memory -
immediate EMS, B. delayed EMS, and C. NMS] in older subjects. EMS, episodic memory score; NMS, non-memory score. As shown in Table 3 , the interaction between the ginseng intake and APOE4 status had a significant effect on the delayed EMS but neither the immediate EMS nor NMS. This indicates that APOE4 status has a moderating effect on the associations between the ginseng intake and delayed episodic memory cognition, but neither immediate episodic memory nor the NMS.
As shown in Table 4 , subgroup analyses according to APOE4 status showed that the ginseng intake was associated with a higher delayed EMS in the APOE4-negative but not the APOE4-positive subgroup. Table 3. Results of multiple linear regression analyses that included interaction terms for the association between ginseng intake status and APOE4 status in predicting cognition.
Table 4. Results of the multiple linear regression analyses of the association between ginseng intake status and cognition according to APOE4 subgroup. Specifically, the difference in delayed EMS associated with ginseng intake was significantly greater in the APOE4 negative group than in the APOE4 positive group.
Table 5. Results of the multiple linear regression analyses of the association between ginseng intake status high duration vs. low duration and cognition. Table 6. Results of the multiple linear regression analyses of the association between ginseng intake status midlife onset vs.
late life onset and cognition. Table 7. This study of non-demented older adults found that ginseng intake had a benefit on AD-specific cognition, i. It also showed that APOE4 status had a moderating effect on the association between ginseng intake status and delayed episodic memory cognition, and that ginseng intake had a benefit on the delayed episodic memory cognition in APOE4-negative but not APOE4-positive subjects.
This may reflect interactions among ginseng intake, APOE4 status, and AD or related cognitive decline.
This study found that the benefit of ginseng intake was observed mainly on memory, not on non-memory, and it was more prominent in delayed episodic memory than immediate episodic memory.
The earliest cognitive change in patients who will develop AD is episodic memory decline, particularly in delayed episodic memory decline Howieson et al. Therefore, our results suggest that ginseng intake acts mostly on delayed episodic memory decline and may play a clinically significant role in early AD-related cognitive decline.
Previously, neuroprotective effects of ginseng on the pathological and clinical process of AD was reported, which may explain the mechanism underlying the relationship between ginseng intake and early AD-related cognitive decline Razgonova et al. In vitro experiments also found that ginseng treatment reduced Aβ 40 and 42 concentrations Qiu et al.
Another preclinical study in a transgenic mouse AD model found that long-term ginseng treatment attenuated Aβ deposition and short-and long-term memory impairment Hwang et al.
Clinical trials found that ginseng significantly improved working memory and attention in healthy young adults Bell et al. Based on the preclinical findings, ginseng improves cognitive features of AD patients via AD pathologies, i.
In human, however, the precise mechanism of ginseng in the pathologies of AD in the prevention and treatment of AD remain unclear. The present study found that APOE4 status modulated the relationship between ginseng intake and delayed episodic memory cognition.
A significant association between ginseng intake and delayed episodic memory cognition was apparent in subjects without APOE4, but not those with APOE4.
We hypothesize that the benefit of ginseng may be masked in the latter subjects because APOE4 triggers the blood—brain barrier BBB dysfunction that predicts cognitive decline Montagne et al.
Also, Aβ clearance may differ by the APOE isoform, and could thus be affected by ginseng intake. APOE4 stimulates Aβ clearance less effectively than do APOE3 and APOE2; APOE4 status compared to non-APOE4 status may significantly inhibit Aβ removal Wildsmith et al.
Therefore, the protective effect of ginseng on AD-related cognition is apparent only in the APOE4-negative group because the benefit of ginseng is offset by the APOE4 affects the shared Aβ clearance pathway Kurz and Perneczky, Regarding the high duration effect of ginseng on delayed EMS, two studies were similar to ours.
Regarding the effect of ginseng intake with midlife onset on delayed EMS, a human study supported our finding of a highly significant association between increasing age and decreased Aβ turnover rates, i.
These changes in Aβ kinetics associated with aging present opportunities for treatment strategies, such as ginseng as an early intervention in middle age rather than old age. Our study had several limitations.
First, as it was cross-sectional in its design, causal relationships could not be inferred, which would require long-term prospective studies. Second, it did not measure brain AD pathology biomarkers, e. These should be analyzed in future studies of the link between the ginseng intake and AD or related cognitive decline in APOE-negative older adults.
Third, there was a possibility of recall biases in the ginseng intake history. Therefore, we evaluated the ginseng intake history in non-demented older adults using intensive interviews by researchers, not a questionnaire. Furthermore, information accuracy was ensured by interviewing reliable informants.
Finally, the association between ginseng intake and AD or related cognitive decline may vary by ginseng dose. Two clinical trials assessed the dose-effects of ginseng on physical Lee et al.
However, in both studies, young not older adults received ginseng short-term. Ginseng efficacy may be affected by all of dose, administration period, and subject age. However, we could not measure the ginseng doses because commercial products do not consistently or clearly indicate the active ginseng levels.
Long-term studies delivering defined ginseng doses to older adults are needed. Our study of older adults with no dementia suggests that ginseng intake with high duration and midlife onset had a benefit on AD-specific cognitive decline, i. Thus, APOE4 status could be considered a key component in the design of studies of AD and related cognitive decline that include ginseng intake as a preventive strategy.
The study data are not freely accessible because Institutional Review Board of the Hallym University Dongtan Sacred Heart Hospital prevents public sharing of such data for privacy reasons. However, the data are available on reasonable request after Institutional Review Board approval.
Requests for data access can be submitted to an independent administrative coordinator by e-mail yoon gmail. The studies involving human participants were reviewed and approved by Institutional Review Board of the Hallym University Dongtan Sacred Heart Hospital.
JK conceived, designed the study, served as principal investigator, and supervised the study. BL, YC, G-HS, I-GC, HK, JH, DY, and JK were involved in acquisition, or analysis and interpretation of the data and helped to draft the manuscript.
BL, YC, G-HS, I-GC, HK, JH, DY, and JK were major contributors in writing the manuscript and critically revising the manuscript for intellectual content.
All authors contributed to the article and approved the submitted version. This study was supported by the grants from the Korean Society of Ginseng. The funding sources had no role in the study design, data collection, data analysis, data interpretation, writing of the manuscript, or decision to submit it for publication.
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.
Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
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A double blind, placebo controlled, 14 week, parallel group, repeated assessment, multi-centre trial of two dosing regimens, mg b. and mg o. was conducted. Two hundred and fifty-six healthy middle-aged volunteers successfully completed the study.
On various study days weeks 0, 4, 8, 12 and 14 the volunteers performed a selection of tests of attention and memory from the Cognitive Drug Research computerised cognitive assessment system prior to morning dosing and again, at 1, 3 and 6 h later.
Researchers Sports nutrition for bodybuilders that larger clinical trials are needed to establish the efficacy and safety Ginseng for memory the compound. Memory loss, or dementia, may occur Gihseng stroke Ginsebg Ginseng for memory a Ginseng for memory problem in China, says lead researcher Jinzhou Tian, Fot. A ginseng Ginsebg increased the activities of the brain chemicals acetylcholine and choline acetyltransferase, ChATin aged mice, he says. They randomly selected 25 patients to receive a tablet of ginseng extracted from Chinese ginseng roots, leaves and an herb known as panax notoginseng three times daily. Participants took memory tests focusing on immediate and delayed story recall, delayed word recall, verbal learning, verbal recognition and visual recognition. These tests were given before the study began and at the end of the week study.
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