Mind)Xtra
A unique brain booster containing powerful nootropic compounds. Mind)Xtra delivers powerful effects on the central nervous system including: enhancing neuro-chemical transmissions, improving cognition and memory and protecting against neurodegenerative diseases such as Dementia.*
Supplement FactsServing Size:1 capsules Servings Per Container: 30 |
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Amount Per Serving |
% Daily Value |
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Ginkgo (Leaf) extract 24% standardised Bilobalide, Kaemferol, Ginkgolide A, Quercetin, Ginkgolide a and Ginkgolide b) (Yin Xing Ye) | 100mg | † |
Toothed Clubmoss (extract contains Huperzine A) Huperzia serrata (Jin Bu Huan) | 50mcg | † |
Lemon Balm (Melissa officinalis) (Xiang Feng Hua) | 75mg | † |
Rosemary officinalis (contains Rosmarinic Acid extract) | 25mg | † |
Chinese Salvia (root & rhizome) (Salvia miltiorrhiza) (Dan Shen) | 100mg | † |
Panaxea NotoGinseng (root) | 75mg | † |
Polygala (root) contains BT-11 extract (Yuan Zhi) | 25mg | † |
Ligusticum sinense | mg | † |
† Daily Value not established. |
Other Ingredients: Vegetable cellulose (hypromellose); Vegetable Stearic Acid; Microcrystalline Cellulose and Vegetable Magnesium Stearate.
Does Not Contain: Wheat, gluten, soy, milk, eggs, fish, crustacean shellfish, tree nuts, peanuts
Mind)Xtra
30 x 500 mg Capsules
Product Overview
Clouding of consciousness, also known as brain fog or mental fog, is a term used in conventional medicine denoting an abnormality in the "regulation" of mental processes. Brain fog includes symptoms of confusion, forgetfulness, and lack of focus and mental clarity. Losing mental clarity is often considered a “normal” side effect of aging, but that doesn’t mean it is an inevitable consequence of growing older. Modern life stressors and mental overload challenge cognitive function and mental focus. Mind)Xtra is a combination of herbs traditionally used to support memory and cognitive function.*
Actions
•Supports memory and cognitive function*
•Supports feeling of calm relaxation*
•Promotes mental acuity and focus*
•Encourages optimal neuronal health*
Suggested Use:
1 to 3 capsules daily
Warning:
Contraindicated in Epilepsy or seizures. Ginkgo is now thought to interact with omeprazole (Prilosec) and potentially many other drugs. New research shows that ginkgo induces cytochrome P450 2C19 enzymes and therefore decreases omeprazole (Prilosec) levels by up to 40%. Ginkgo might also decrease levels of other drugs metabolized by this enzyme nelfinavir (Viracept), amitriptyline (Elavil), citalopram (Celexa), propranolol (Inderal), lansoprazole (Prevacid), diazepam (Valium) and many others. Patients are advised not to take ginkgo if they are taking drugs that may interact.
*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.
Gingko biloba
Gingko biloba is the best-researched herb with over 400 published studies. Called Yin Xing in Chinese it is also the most frequently prescribed herb in Europe. Gingko increases blood circulation to the brain as well as the periphery. It protects the central nervous system and the cardio-vascular system from damage and the results of aging.*
Ginseng
Ginseng alleviates stress, fatigue and acts as an adaptogenic. Ginseng affects the HPA Axis (hypothalamus-pituitary-adrenal) to alter stress levels and acts as an anti-aging compound.*
MIND combines the best brain boosters to enhance thinking at the cellular level. By increasing blood circulation and by enhancing the neuro-chemical transmission between the neurons MIND has been shown to increase cognitive function up to 25% above base line tests. The anti-stress, anti-oxidant and anti-aging action of the formulation regulates stress levels and calms the body.*
A Systematic Review on Natural Medicines for the Prevention and Treatment of Alzheimer's Disease with Meta-Analyses of Intervention Effect of Ginkgo
Yang M, Xu DD, Zhang Y, Liu X, Hoeven R, Cho WC. The American Journal of Chinese Medicine. Volume 42, Issue 03, 2014
Yang et al., (2014) performed a systematic review to evaluate the efficacy of natural medicines for the treatment of Alzheimer's disease (AD) in randomized controlled trials (RCTs). Disease-specific and intervention terms were searched in MEDLINE, EMBASE, the Cochrane Library and PsycINFO to identify RCTs for the AD intervention of natural medicines, and searched for literatures in English language. The RCTs compared natural medicines and either placebo or orthodox medication in AD patients. The quality of literature was evaluated by Jadad's score and the Cochrane assessing tool to reduce the risk of bias. Meta-analysis and the heterogeneity of results across the trials were performed.*
Out of the literatures, 21 clinical reports were included in this review that satisfied the particular selection criteria. Apart from Ginkgo, other treatments we came across had minimal benefits and/or the methodological quality of the available trials was poor. The meta-analyses showed that Ginkgo had better outcomes than the placebo, with the standardized mean difference (SMD) between Ginkgo and the placebo on cognition being -1.62 (95% CI: -2.69 to -0.56) and on activities of daily living being -1.55 (95% CI: -2.55 to -0.55), with the existence of significant heterogeneity across studies. The meta-analysis for assessing the prevention effect of Ginkgo against AD suggested that risk ratio (RR) is 1.06 (95% CI: 0.92 to 1.22) between Gingko and the placebo, with no significant heterogeneity across studies (test for heterogeneity, p = 0.49).*
Our results suggest that Ginkgo may help established AD patients with cognitive symptoms but cannot prevent the neurodegenerative progression of the disease.*
Effect of Ginkgo Biloba extract on nos activity and nnos expression in cerebral cortex of dementia mice
WANG Peng, SHAN Yun-guan, ZHANG Jin-bo. Jie Fang Jun Yu Fang Yi Xue Za Zhi. 2008; 26(5): 328-330.
Objective: To observe the therapeutic effect of Ginkgo biloba extract (EGB) on mice experimental vascular dementia (VD). Methods: Model of vascular dementia in mice was made. NADPH-d histochemistry and ABC immunohistochemistry were used to investigate the changes of NOS and nNOS, and Y-maze test was used to observe the changes in learning and memory. Results: Y-maze test showed that the learning times in high and low dose of EGB group ( 60.2 ± 14.4, 87.6 ± 19.2 respectitvely) were less than that in VD control group(132.2 ± 40.8, P<0.05). The learning times in high EGB group was also significantly lower than that in low EGB group(P<0.05). NADPH histochemistry and ABC immunohistochemistry test showed that the number of NOS and nNOS positive neurons in VD control group (50.2 + 12.4, 62.4 ± 11.7 respectively) were more than in normal control group (47.4 ± 11.3, 41.0 ± 8.1), (P<0.05). And that in high and low dose of EGB group (44.3 ± 9.5, 43.6 ± 9.8 ; 42.7 ± 9.8, 44.9 ± 9.6 respectively) were less than in VD control group(P<0.05). Conclusion: Ginkgo biloba extract may have protective effect on the neurons of CNS in vascular dementia mice.*
Effects of Ginkgo Biloba Extract on Learning and Memory and Cytokines of Hippocampus in Senile Rats
XU Ying ZHANG Zhi-xiong LI Yun WANG Xing-yu. Shang Hai Zhong Yi Yao Da Xue Xue bao. 2008; 22(3): 51-54.
Objective: To observe the effects of Ginkgo biloba extract (GBE50) on learning and memory impairment induced by D-galactose and contents of IL-1b, IL-6 and TNF-et in hippocampus of senile rats, in an attempt to study its mechanisms in improving learning and memory. Methods: SD rats were randomly divided into 3 groups: control group, model group and treatment group. In modelling, D-galactose was injected into abdomen according to 100mg/ kg in the morning for 42 days. From the 21st day after modelling, GBE50 was given through gastric perfusion according to 150mg/kg in treatment group every day, and continuously for 21 days. Distilled water containing 1% CMC-Na was given in control and model groups. After treatment, Morris water maze tests were used to detect the change of rat behaviour and the contents of IL-1b, 1L-6 and TNF-et in hippocampus in all groups by radioimmunoassay. Results: The escape latency of the rats in model group was significantly longer than that in control group; the percentage of distance was lower (P<0.05, P<0.01); however, the escape latency of the rats in treatment group was significantly shorter than that in model group, and the percentage of distance was higher (P<0.05, P<0.01). The contents of IL-1b and TNF-et in hippocampus of model group were significantly higher than those of control group, but contents of IL-6 were lower (P<0.05, P<0.01). Compared with model group, the contents of IL-1b in treatment group were significantly decreased; and the contents of IL-6 were significantly increased (P<0.05, P<0.01). Conclusion: GBE50 can improve the impaired learning and memory of senile rats induced by D-galactose by regulating the contents of IL-1b and IL-6 in hippocampus, and inhibiting immune inflammatory reaction in central nerve system induced by D-galactose.*
Antagonism Effect of Ginkgolides on Vascular Dementia
GONG Xiao-Jian, RONG Zhi-Tao, ZHANG Le-Duo, JIANG Feng-Rong, LI Yun-Man, LIU Guo-Qing. Zhong Guo Tian Ran Yao Wu. 2008; 6(3): 227-231.
AIM: To study the effects of ginkgolides on vascular dementia (VD) in mice and rats model. METHODS: The model of mice and rats with VD were duplicated with the partial ligation of bilateral common carotid arteries and occlusion of the left middle cerebral artery. (MCAO) separately. Jumping stand test and Water or Y-labyrinth tests were measured to detect the leaning and memory capacities of mice or rats. The contents of AChE and ChAT in rat brain were assayed. And the gene expression of nNOS were detected with immunohistochemistry method. RESULTS: The learning and memory capacities of the model groups receded significantly, compared with the shame-operated group. Compared with the model group, ginkgolides increased memory capacity significantly. In the VD rats model, ginkgolide significantly decreased the activity of AChE and the gene expression of nNOS, increased the activity of ChAT in brain. CONCLUSION: Ginkgolides posses the role of promoting the capacities of learning and memory of VD mice and rats. The mechanism perhaps is related with reducing AChE and increasing ChAT levels in brain tissue. It also maybe inhibits the expression of nNOS, decreasing the production of NO.*
Effects of EGb761 on synaptophysin expression in hippocampus of vascular dementia rats
ZHANG Lan-ying, WANG Yu-liang. Zhong Guo Bing Li Sheng Li Za Zhi. 2008; 24(1): 40-43.
AIM: To investigate the effects of Ginkgo biloba extract 761 ( Egb761) on synaptophysin (SYN) expression in hippocampus of vascular dementia (VD) rats. METHODS: VD rat models, established by repeatedly cerebral ischemia/reperfusion, were randomly divided into two groups: model group and EGb761 treated group (both n = 30), and another 30 condition-matched rats were selected as the sham-operated controls. Spatial learning and memory abilities of rats were assessed by Morris water maze (MWM) task, and SYN expression in hippocampal formation of rats in different groups was detected by immunohistochemical technique and image analysis. RESULTS: The MWM escape latency (EL) in model group was highly longer than that in the sham-operated group (P<0.01), while the EL of EGb761-treated group was significantly shorter than that in model group, but still longer than that in the sham-operated group at 1 m, 2 m and 4 m after VD modelling operation (P<0.05 or P<0.01). Immunohistochemical analysis showed that the SYN immunoreactive expression in hippocampal formation in model group greatly decreased and mean optical density of SYN expression highly increased compared with both sham-operated group and EGb761-treated group at three time points (P<0.01). CONCLUSION: EGb761 can increase the expression of SYN in hippocampus, which may be one of important mechanisms of EGb761 in improving learning and memory dysfunction of VD rats.*
Effects of Ginkgolide B on the learning and memory ability of the model rats of Alzheimer’s disease
CHEN Ming-liang, GE Zhen-ying. He Nan Da Xue Xue Bao: Yi Xue Ban. 2007; 26(3): 23-24.
Objective: To test the effects of ginkgolide B(GB) on learning and memory ability of Alzheimer’s disease (AD) model rats. Methods: AD animal model was established by microinjecting IBO (5 mg) into bilateral NBM of rat to damage them. GB at different concentrations was injected intraperitioneally in the GB rats for 20 days. 20 days later, the learning and memory ability were tested using jumping table experiment and Y-maze experiment. Results: Compared with model group, the learning and memory abilities of GB groups were significantly improved. (P<0.01 or P<0.05). Conclusion: Ginkgolide B can improve the learning and memory ability of the model rats of Alzheimer’s disease.*
Effects of Extract from Ginkgo Biloba on Learning, Memory and Expression of Hippocampal Brain-derived Neurotrophic Factor in Senile Mice Induced by D-galactose
QIN Long, HUANG Jun-hong, XING Ze-gang, Hu Shibao, He Qinlan, Chen Lian, Zhao Weihai. Zhong Guo Lin Chuang Shen Jin Wai Ke Za Zhi. 2009; 14(10): 603-605.
Objective To explore the effect of the extract from ginkgo biloba (EGb) on learning, memory and the expression of hippocampal brain-derived neurotrophic factor(BDNF) in the senile mice induced by D-galactose. Methods Thirty-two mice were randomly divided into 4 groups of 8 mice each, i.e. blank control group, model group, low dose of EG (50 mg/kg) treatment group and high dose of EGb (100 mg/kg) treatment group. The senile mice model in the model and treatment groups induced by D-galactose. The activity of the mice was determined by the open field test in all the groups, where the ability of learning and memory of mice were examined by step down test. The expression of BDNF in the hippocampi was determined by western blotting in all the groups. Results The open field test showed that the activity of the mice in both the treatment groups significantly increased compared to that in the model group (P<0.05). The step down test showed that the latent period of step-down was significantly longer and the latent period of escape was significantly shorter in both the treatment groups than that in the model group (P<O.05). The expression of hippocampal BDNF was significantly enhanced in both the treatment group compared to that in the model group. Conclusions The learning, memory and open field activity in the senile mice induced by D-galactose may be improved by EGb. It is suggested that the improvement of learning, memory and open field activity may be related to the increase in the expression of hippocampal BDNF in the senile mice induced by D-galactose.*
Effects of Ginkgo Biloba extract on learning and memory ability of rats with Vascular Dementia
WU Yu, HU Chang-lin. Xian Dai Yu Fang Yi Xue. 2008; 35(13): 2585-2586.
Objective: To investigate effects of ginkgo biloba extract (GBE) on learning and memory ability of rats with vascular dementia. Methods: Rats’ model of vascular dementia was established. Sham-operation group and operation group were administered normal saline. GBE group was administered ginkgo biloba extract. The superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities and the malondialdehyde (MDA) content in the cerebral tissue were detected after 14 days. Meanwhile the neurons of the hippocampal CA1 was observed. Results: The SOD and GSH-Px activities in the GBE group increased, while the MDA content significantly decreased comparing with the those in operation group (P<0.05). The results indicated that the pathological changes in the GBE group were slighter than those in the operation group. Conclusion: Ginkgo biloba extract on rats with vascular dementia could enhance SOD and GSH-Px activities, decrease the MDA content, then protect nerve cells from apoptosis.*
Effect of extracts of Ginkgo biloba leaf on learning-memory ability and NMDA receptor 1 expression in the hippocampus in rats with kindling-induced epilepsy
DUAN Fang-Rong, YUAN Bao-Qiang. Zhong Guo Dang Dai Er Ke Za Zhi. 2008; 10(3): 367-370.
Objective: To study the effect of extracts of Ginkgo biloba leaf (EGb), a catalyzer of central nervous system, on learning-memory ability and possible mechanism in rats with kindling-induced epilepsy. Methods: Forty postnatal day 21 (P21) and 40 postnatal day 35 (P35) Sprague-Dawley (SD) rats were randomly respectively assigned to five groups: normal sodium (NS) control, kindling epilepsy model, high, middle and low dosage of EGb-treated kindling epilepsy. The kindling epilepsy model was established by an intraperitoneal injection of pentetrazole (FTZ). The learning-memory ability and NMDA receptor 1 (NMDAR1) expression in the hippocampus were measured by Y-maze test and immunohistochemistry assay respectively. Results: The stimulation times for reaching to academic standard in the Y-maze test in the two ages PTZ kindling groups was significantly more than that in the corresponding NS control groups (P<0.01). After EGb treatment the achievement of the Y-maze test in the three treatment groups was significantly improved in a dose-dependent manner, the higher the dosage, the better the achievement (P<0.01). Immunohistochemistry assay showed that the expression of NMDAR1 in the two ages FTZ kindling groups was significantly higher than that in the corresponding NS control groups (P<0.01). Compared with the corresponding untreated kindling model groups, the expression of NMDAR1 in the two ages EGb treatment groups was significantly reduced in a dose-dependent manner (P<0.01). Conclusions: EGb can improve learning-memory ability in epileptic rats at different developmental phases in a dose-dependent manner, possibly through a reduction of NMDAR1 expression in the hippocampus.*
Hyperzia serrata (contains Huperzine-A) (Shi Shan)
Huperzine A has been shown to improve memory, thinking, and behavioural function in people with Alzheimer's disease, multi-infarct dementia, and senile dementia. It is believed to work in a manner similar to some prescription drugs for treating symptoms of Alzheimer's disease, increasing the level of the neurotransmitter acetylcholine by blocking its breakdown. It may also protect neurons from cell death caused by toxic levels of glutamate and protect against some of the effects of chemical nerve agents used in warfare.*
Hyperzia serrata (Shi Shan) contains an alkaloid Huperzine A. It's effective in improving cognitive and memory abilities in humans, including those with Alzheimer's disease. In China , where HupA is used for treating Alzheimer's and myasthenia gravis, medical scientists have studied its effects on the mental functions of elderly Alzheimer's patients. Huperzine A has been shown to improve memory, thinking, and behavioural function in people with Alzheimer's disease, multi-infarct dementia, and senile dementia. It is believed to work in a manner similar to some prescription drugs for treating symptoms of Alzheimer's disease: increasing the level of the neurotransmitter acetylcholine by blocking its breakdown. It may also protect neurons from cell death caused by toxic levels of glutamate and protect against some of the effects of chemical nerve agents used in warfare.*
Research of the Patients with Vascular Cognitive Impairment no Dementia in Terms of Neuropsychology and the Clinical Study of Huperzine A in the Treatment
JIANG Bo, MENG Xiao-Luo, SHU Gang-Ming, YAO Cun-Shan, CHEN Yu-Mei, GUO Yue-Qi. Zhong Guo Lin Chuang Shen Jing Ke Xue. 2009(5): 510-514.
Aim: To investigate the characteristics of the patients with vascular cognitive impairment no dementia(VCIND) in terms of neuropsychology and to observe the efficacy of huperzine A in treating VCIND. Methods: 64 patients with VCIND and 42 normal controls were examined with the neuropsychological test, including mini-mental state examination (MMSE), clock-drawing test (CDT). 64 patients with VCIND were randomly divided into 2 groups: a huperzine A treated group and a control group. The whole course of treatment for each group lasted 8 weeks. MMSE and CDT were examined in the 4th week and 8th week. Results: (1) The scores of CDT and MMSE in the VCIND group were significantly lower than those in the control group(P<0.01). The scores of sub items of MMSE including time orientation, place orientation, account ability, short time memory, language repetition, reading comprehension, language expression, figure portrayal in patients with VCIND were lower than those in the normal subjects (all P<0.01). (2) After 8 weeks, the marks of MMSE and CDT of huperzine A treated group were more improved than before and the control group. Conclusion: (1) The combination of MMSE and CDT can be used for early finding of cognitive impairment in VCIND patients. (2) Huperzine A can improve the cognitive function of patients with VCIND.*
The Clinical Study of Huperzine A in the Treatment of Vascular Dementia
XU Zhi-Qiang, ZHANG Meng, LI Jing, ZHOU Hua-Dong. Zhong Guo Lin Chuang Shen Jing Ke Xue. 2009; 17(2): 163-165.
Aim: To observe the efficacy and safety of Huperzine A in treating the mild to moderate vascular dementia(VaD). Methods: Seventy-eight patients with the mild to moderate VaD were randomly divided into 2 groups: the Huperzine A treated group(n=39), M 24, F 15, [age(71.8 ± 7.2)years] and the control group(n=39), M 26, F 13, [age (72.3 ± 6.9)years]. The patients for Huperzine A treated group were treated with Huperzine A tablets 0.1 mg, po, bid. The patients for control group were treated with Vitamin C 100 mg, po, and bid. The whole course of treatment for each group was 12 weeks. Mini mental state examination (MMSE), clinical dementia rating (CDR) and activity of daily living scale (ADL) were taken as the main value targets. Results: After 12 weeks, the marks of MMSE, CDR, and ADL of the treatment group were more improved than those of the control group (P<0.01, respectively). Conclusion: Huperzine A can prominently improve the cognitive function of patients with the mild to moderate vascular dementia. Moreover, its security and tolerability is good.*
Puerarin and Huperzine A improve learning memory dysfunction induced by ischemia-reperfusion in mice
SHI Rui-li, SHEN Shu-ping, PANG Dong-wei, WANG Li-jun, ZHAO Li-juan, GAO Li-jun. Zhong Guo Yi Yao Dao Bao. 2009; 6(7): 25-27.
Objective: To observe the effects of Puerarin (Pur) and Huperzine A (Hup-A) on learning memory dysfunction induced by ischemia-reperfusion (I/R) in mice and explore its mechanism. Methods: I/R model in mice was performed by repetitious ligation of bilateral common carotid artery, and mice were randomly divided into five groups: Sham group, I/R group, Hup-A group, Pur group and Pur+Hup-A group. Learning memory ability was evaluated by step-down test. Monoamine nervous transmitter level and cortex neuron apoptosis were measured by HPLC and flow cytometry respectively. Results: Both Pur and Hup-A improved learning memory ability of I/R mice, the effect of Pur group was better and the effect of combination group was the most significant. Both Pur and Hup-A decreased neuron apoptosis and raised content of monoamine nervous transmitter of I/R mice. The cortex neuron apoptosis rate in combination group was lower than that in Hup-A group, the homovanillic acid (HVA) level of cerebral cortex in combination group was higher than that of Pur group. Conclusion: Learning memory dysfunction induced by I/R in mice could be improved by Put and Hup-A, the effect of Put was better than that of Hup-A with administered dose, the mechanisms of drugs might be related to reduction of neuron apoptosis and regulating of the monoamine nervous transmitter level in cerebral cortex, combination of Pur and Hup-A resulted in the most obvious effects.*
Study on Pharmacodynamics of Alzheimer’s Disease with Huperzine A
YONG Bin, LIU Jian-ting, ZHANG Xiao-yu, HUANG Chun-ping. Study on Pharmacodynamics of Alzheimer’s Disease with Huperzine A. Shi Pin Ke Xue. 2007; 28(5): 327-331.
In this paper, the effects of mice memory were studied merely by jumping platform experiment and avoiding darkness experiment with three doses respectively as 13.5, 41.0 and 61.0 mg/kg huperzine A. The results showed that huperzine A has the obvious effects on improving both the reappearance ability of passive avoidance and the avoiding darkness response. So huperzine can have the function to promote memory and improvement symptom of Alzheimer’s disease (Yong et al, 2007).*
Ginseng (Ren Shen)
Effects of panaxadiol saponins and lycopene on abilities of learning and memory of senile atlanto -axial joint instability
FAN Wenjing, ZHU Tongtong, GUO Yaxiong, Lin Guimiao, Zhao Lijuan. Zhong Guo Kang Fu Yi Xue Za Zhi. 2009(8): 731-733.
Objective: To compare the effects of panaxadiol saponins (PDS) with lycopene on the abilities of learning and memory in senile mice with learning and memory disorder by atlanto-axial joint instability. Method: The atlanto-axial joint instability model was established by injection with 30% lactic acid around the atlanto and axial vertebrae, 30ml once weekly, three times totally. The changes of abilities of learning and memory in mice were observed with water-maze test. The activities of acetylcholine esterase (AchE) and the content of acetylcholine (Ach) in brain tissue were tested. Immunohistochemical staining with b-amyloid protein in mice hippocampus was demonstrated. Result: The model mice had longer swimming time and more errors (P<0.05) in water maze test compared with control group. PDS mice had significant short latency period and less errors in water-maze test (P<0.01), but the difference between PDS and lycopene groups was not obvious. Compared with model group, the activities of AchE reduced(P<0.01), and the content of Ach increased in PDS and lycopene groups(P<0.01). And in the two therapy groups, expressions of b-amyloid protein in mice hippocampus were less than that in model group. Conclusion: This study indicate that PDS and lycopene can improve the learning and memory abilities of mice and the metabolism of senile mice brain, which may be the mechanism of its protective effect to cerebral damage.*
Effect of ginsenoside-Rg2 on learning and memory of vascular dementia rats
ZHANG Li, PAN Zhi-yuan, JIN Yi, LONG Chao-liang, WANG Hai. Zhong Guo Lin Chuang Yao LI Xue Yu Zhi Liao Xue. 2008; 13(3): 276-282.
AIM: To investigate the effect of ginsenoside-Rg2 on learning and memory of vascular dementia rats and it’s underlying mechanisms, especially the expression of NMDA/AMPA receptors. METHODS: Vascular dementia (VD) of rat was induced by permanent occlusion of bilateral common carotid arteries(2OV). The rats were given different doses of ginsenoside-Rg2 (2. 5, 5.0, 10.0 mg/kg) as while as operation. The spontaneous movement and the delayed non-matching-to-position task(DNMPT) in the water maze were used to examine the behaviour changes on learning and memory; the mRNA of four different subtypes of NMDA/AMPA receptors, including NR1, NR2A, NR2B and GluR2 in hippocampus were determined by the RT-PCR method. RESULTS: The spontaneous movement and spatial learning and memory of VD rats were all decreased. After ginsenoside-Rg2 administration, the spontaneous movement and the spatial learning and memory were improved; the latency of information swim (IS) and choice swim (CS) decreased, and choice accuration in choice swim increased. The expression of NR1 mRNA was enhanced while NR2A, NR2B and GluR2 were attenuated in hippocampus of VD rats. These pathological changes could be reversed by treatment with ginsenoside-Rg2. CONCLUSION: Ginsenoside-Rg2 can patently improve the spatial learning and memory of VD rats. The mechanism may be related to the regulation of ginsenoside-Rg2 on the expression of NMDA/AMPA receptors in hippocampus.*
Effect of ginsenoside Rbl on expression of b-secretase and presenilin-1 in the parietal lobe of Alzheimer disease-like rat
Fang Xin, Yang Jiping, Lai Hong. Jie Pou Xue Za Zhi. 2008; 31(6): 812-815.
Objective: To investigate the effect of ginsenoside Rb1 on the expression of b-secretase and presenilin-1 (PS-1) in the parietal lobe of Alzheimer disease-like rats. Methods: Thirty SD rats were randomly divided into a control group, a model group and a treatment group. The model rats were established with administration of I)-galactose 60 mg· kg-1· d-1 and aluminum chloride 200 mg·kg -1 · d-1 for 2 months, the control group were given the same dose of sodium chloride, and treatment group were given ginsenoside Rb1 10mg·kg-1·d -1 for 4 weeks after the model rats were established. The expressions of b-secretase and PS-1 in the parietal lobe were detected by immunohistochemistry with image analysis. Morris test was used to determine the ability of learning and memory. Results: Compared with the control group, the levels of b-secretase and PS-1 were significantly higher in the model group (P<0.05), and learning and recognition ability in this group was obviously worse (P<0.05); Compared with the moctel group, the levels of b-secretase and PS-1 were significantly lower in the treatment group (P<0.05), and learning and recognition ability in this group was better. The learning and recognition ability was obviously improved on the second and the third day (P<0.05). Conclusion: Ginsenoside Rbl has preventive and therapeutic effect on Alzheimer disease-like rats, via inhibiting the expression of b-secretase and PS-1.*
Effect of ginsenoside Rg1 on Alzheimer’s disease of model rats
LI Na, WANG Limin. Bin Zhou YI Xue Yuan Xue Bao. 2007; 30(5): 325-326.
Objective: To observe the effect of ginsenoside Rg1 on rat of Alzheimer’s disease (AD) model. Methods Bilateral NBM of elderly rats were damaged by quinolinic acid, and the AD model was established. The single passive avoidance step-down training and water-maze spatial localization test were used to study the effects of Ginsenoside Rg1 on learning and memory of AD rats. Results Treated with low and high dosages of ginsenoside Rg1, AD rat models decreased significantly in the number of errors in step-down (13 days) and the times training to reach the criterion in water maze task (16 days). Except for the fact that the times of training to reach the criterion with high dosage of ginsenoside Rg1 were those than that with 1, 2, 3, 4 tetrahydroacridine, there was no obvious difference in the effects of low, high dosage of GMC and THA. Conclusion Ginsenoside Rg1 can improve the ability of learning and memory of AD model rat.*
*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.
Supplement FactsServing Size:1 capsules Servings Per Container: 30 |
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Amount Per Serving |
% Daily Value |
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Ginkgo (Leaf) extract 24% standardised Bilobalide, Kaemferol, Ginkgolide A, Quercetin, Ginkgolide a and Ginkgolide b) (Yin Xing Ye) | 100mg | † |
Toothed Clubmoss (extract contains Huperzine A) Huperzia serrata (Jin Bu Huan) | 50mcg | † |
Lemon Balm (Melissa officinalis) (Xiang Feng Hua) | 75mg | † |
Rosemary officinalis (contains Rosmarinic Acid extract) | 25mg | † |
Chinese Salvia (root & rhizome) (Salvia miltiorrhiza) (Dan Shen) | 100mg | † |
Panaxea NotoGinseng (root) | 75mg | † |
Polygala (root) contains BT-11 extract (Yuan Zhi) | 25mg | † |
Ligusticum sinense | mg | † |
† Daily Value not established. |
Other Ingredients: Vegetable cellulose (hypromellose); Vegetable Stearic Acid; Microcrystalline Cellulose and Vegetable Magnesium Stearate.
Does Not Contain: Wheat, gluten, soy, milk, eggs, fish, crustacean shellfish, tree nuts, peanuts
Mind)Xtra
30 x 500 mg Capsules
Product Overview
Clouding of consciousness, also known as brain fog or mental fog, is a term used in conventional medicine denoting an abnormality in the "regulation" of mental processes. Brain fog includes symptoms of confusion, forgetfulness, and lack of focus and mental clarity. Losing mental clarity is often considered a “normal” side effect of aging, but that doesn’t mean it is an inevitable consequence of growing older. Modern life stressors and mental overload challenge cognitive function and mental focus. Mind)Xtra is a combination of herbs traditionally used to support memory and cognitive function.*
Actions
•Supports memory and cognitive function*
•Supports feeling of calm relaxation*
•Promotes mental acuity and focus*
•Encourages optimal neuronal health*
Suggested Use:
1 to 3 capsules daily
Warning:
Contraindicated in Epilepsy or seizures. Ginkgo is now thought to interact with omeprazole (Prilosec) and potentially many other drugs. New research shows that ginkgo induces cytochrome P450 2C19 enzymes and therefore decreases omeprazole (Prilosec) levels by up to 40%. Ginkgo might also decrease levels of other drugs metabolized by this enzyme nelfinavir (Viracept), amitriptyline (Elavil), citalopram (Celexa), propranolol (Inderal), lansoprazole (Prevacid), diazepam (Valium) and many others. Patients are advised not to take ginkgo if they are taking drugs that may interact.
*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.
Gingko biloba
Gingko biloba is the best-researched herb with over 400 published studies. Called Yin Xing in Chinese it is also the most frequently prescribed herb in Europe. Gingko increases blood circulation to the brain as well as the periphery. It protects the central nervous system and the cardio-vascular system from damage and the results of aging.*
Ginseng
Ginseng alleviates stress, fatigue and acts as an adaptogenic. Ginseng affects the HPA Axis (hypothalamus-pituitary-adrenal) to alter stress levels and acts as an anti-aging compound.*
MIND combines the best brain boosters to enhance thinking at the cellular level. By increasing blood circulation and by enhancing the neuro-chemical transmission between the neurons MIND has been shown to increase cognitive function up to 25% above base line tests. The anti-stress, anti-oxidant and anti-aging action of the formulation regulates stress levels and calms the body.*
A Systematic Review on Natural Medicines for the Prevention and Treatment of Alzheimer's Disease with Meta-Analyses of Intervention Effect of Ginkgo
Yang M, Xu DD, Zhang Y, Liu X, Hoeven R, Cho WC. The American Journal of Chinese Medicine. Volume 42, Issue 03, 2014
Yang et al., (2014) performed a systematic review to evaluate the efficacy of natural medicines for the treatment of Alzheimer's disease (AD) in randomized controlled trials (RCTs). Disease-specific and intervention terms were searched in MEDLINE, EMBASE, the Cochrane Library and PsycINFO to identify RCTs for the AD intervention of natural medicines, and searched for literatures in English language. The RCTs compared natural medicines and either placebo or orthodox medication in AD patients. The quality of literature was evaluated by Jadad's score and the Cochrane assessing tool to reduce the risk of bias. Meta-analysis and the heterogeneity of results across the trials were performed.*
Out of the literatures, 21 clinical reports were included in this review that satisfied the particular selection criteria. Apart from Ginkgo, other treatments we came across had minimal benefits and/or the methodological quality of the available trials was poor. The meta-analyses showed that Ginkgo had better outcomes than the placebo, with the standardized mean difference (SMD) between Ginkgo and the placebo on cognition being -1.62 (95% CI: -2.69 to -0.56) and on activities of daily living being -1.55 (95% CI: -2.55 to -0.55), with the existence of significant heterogeneity across studies. The meta-analysis for assessing the prevention effect of Ginkgo against AD suggested that risk ratio (RR) is 1.06 (95% CI: 0.92 to 1.22) between Gingko and the placebo, with no significant heterogeneity across studies (test for heterogeneity, p = 0.49).*
Our results suggest that Ginkgo may help established AD patients with cognitive symptoms but cannot prevent the neurodegenerative progression of the disease.*
Effect of Ginkgo Biloba extract on nos activity and nnos expression in cerebral cortex of dementia mice
WANG Peng, SHAN Yun-guan, ZHANG Jin-bo. Jie Fang Jun Yu Fang Yi Xue Za Zhi. 2008; 26(5): 328-330.
Objective: To observe the therapeutic effect of Ginkgo biloba extract (EGB) on mice experimental vascular dementia (VD). Methods: Model of vascular dementia in mice was made. NADPH-d histochemistry and ABC immunohistochemistry were used to investigate the changes of NOS and nNOS, and Y-maze test was used to observe the changes in learning and memory. Results: Y-maze test showed that the learning times in high and low dose of EGB group ( 60.2 ± 14.4, 87.6 ± 19.2 respectitvely) were less than that in VD control group(132.2 ± 40.8, P<0.05). The learning times in high EGB group was also significantly lower than that in low EGB group(P<0.05). NADPH histochemistry and ABC immunohistochemistry test showed that the number of NOS and nNOS positive neurons in VD control group (50.2 + 12.4, 62.4 ± 11.7 respectively) were more than in normal control group (47.4 ± 11.3, 41.0 ± 8.1), (P<0.05). And that in high and low dose of EGB group (44.3 ± 9.5, 43.6 ± 9.8 ; 42.7 ± 9.8, 44.9 ± 9.6 respectively) were less than in VD control group(P<0.05). Conclusion: Ginkgo biloba extract may have protective effect on the neurons of CNS in vascular dementia mice.*
Effects of Ginkgo Biloba Extract on Learning and Memory and Cytokines of Hippocampus in Senile Rats
XU Ying ZHANG Zhi-xiong LI Yun WANG Xing-yu. Shang Hai Zhong Yi Yao Da Xue Xue bao. 2008; 22(3): 51-54.
Objective: To observe the effects of Ginkgo biloba extract (GBE50) on learning and memory impairment induced by D-galactose and contents of IL-1b, IL-6 and TNF-et in hippocampus of senile rats, in an attempt to study its mechanisms in improving learning and memory. Methods: SD rats were randomly divided into 3 groups: control group, model group and treatment group. In modelling, D-galactose was injected into abdomen according to 100mg/ kg in the morning for 42 days. From the 21st day after modelling, GBE50 was given through gastric perfusion according to 150mg/kg in treatment group every day, and continuously for 21 days. Distilled water containing 1% CMC-Na was given in control and model groups. After treatment, Morris water maze tests were used to detect the change of rat behaviour and the contents of IL-1b, 1L-6 and TNF-et in hippocampus in all groups by radioimmunoassay. Results: The escape latency of the rats in model group was significantly longer than that in control group; the percentage of distance was lower (P<0.05, P<0.01); however, the escape latency of the rats in treatment group was significantly shorter than that in model group, and the percentage of distance was higher (P<0.05, P<0.01). The contents of IL-1b and TNF-et in hippocampus of model group were significantly higher than those of control group, but contents of IL-6 were lower (P<0.05, P<0.01). Compared with model group, the contents of IL-1b in treatment group were significantly decreased; and the contents of IL-6 were significantly increased (P<0.05, P<0.01). Conclusion: GBE50 can improve the impaired learning and memory of senile rats induced by D-galactose by regulating the contents of IL-1b and IL-6 in hippocampus, and inhibiting immune inflammatory reaction in central nerve system induced by D-galactose.*
Antagonism Effect of Ginkgolides on Vascular Dementia
GONG Xiao-Jian, RONG Zhi-Tao, ZHANG Le-Duo, JIANG Feng-Rong, LI Yun-Man, LIU Guo-Qing. Zhong Guo Tian Ran Yao Wu. 2008; 6(3): 227-231.
AIM: To study the effects of ginkgolides on vascular dementia (VD) in mice and rats model. METHODS: The model of mice and rats with VD were duplicated with the partial ligation of bilateral common carotid arteries and occlusion of the left middle cerebral artery. (MCAO) separately. Jumping stand test and Water or Y-labyrinth tests were measured to detect the leaning and memory capacities of mice or rats. The contents of AChE and ChAT in rat brain were assayed. And the gene expression of nNOS were detected with immunohistochemistry method. RESULTS: The learning and memory capacities of the model groups receded significantly, compared with the shame-operated group. Compared with the model group, ginkgolides increased memory capacity significantly. In the VD rats model, ginkgolide significantly decreased the activity of AChE and the gene expression of nNOS, increased the activity of ChAT in brain. CONCLUSION: Ginkgolides posses the role of promoting the capacities of learning and memory of VD mice and rats. The mechanism perhaps is related with reducing AChE and increasing ChAT levels in brain tissue. It also maybe inhibits the expression of nNOS, decreasing the production of NO.*
Effects of EGb761 on synaptophysin expression in hippocampus of vascular dementia rats
ZHANG Lan-ying, WANG Yu-liang. Zhong Guo Bing Li Sheng Li Za Zhi. 2008; 24(1): 40-43.
AIM: To investigate the effects of Ginkgo biloba extract 761 ( Egb761) on synaptophysin (SYN) expression in hippocampus of vascular dementia (VD) rats. METHODS: VD rat models, established by repeatedly cerebral ischemia/reperfusion, were randomly divided into two groups: model group and EGb761 treated group (both n = 30), and another 30 condition-matched rats were selected as the sham-operated controls. Spatial learning and memory abilities of rats were assessed by Morris water maze (MWM) task, and SYN expression in hippocampal formation of rats in different groups was detected by immunohistochemical technique and image analysis. RESULTS: The MWM escape latency (EL) in model group was highly longer than that in the sham-operated group (P<0.01), while the EL of EGb761-treated group was significantly shorter than that in model group, but still longer than that in the sham-operated group at 1 m, 2 m and 4 m after VD modelling operation (P<0.05 or P<0.01). Immunohistochemical analysis showed that the SYN immunoreactive expression in hippocampal formation in model group greatly decreased and mean optical density of SYN expression highly increased compared with both sham-operated group and EGb761-treated group at three time points (P<0.01). CONCLUSION: EGb761 can increase the expression of SYN in hippocampus, which may be one of important mechanisms of EGb761 in improving learning and memory dysfunction of VD rats.*
Effects of Ginkgolide B on the learning and memory ability of the model rats of Alzheimer’s disease
CHEN Ming-liang, GE Zhen-ying. He Nan Da Xue Xue Bao: Yi Xue Ban. 2007; 26(3): 23-24.
Objective: To test the effects of ginkgolide B(GB) on learning and memory ability of Alzheimer’s disease (AD) model rats. Methods: AD animal model was established by microinjecting IBO (5 mg) into bilateral NBM of rat to damage them. GB at different concentrations was injected intraperitioneally in the GB rats for 20 days. 20 days later, the learning and memory ability were tested using jumping table experiment and Y-maze experiment. Results: Compared with model group, the learning and memory abilities of GB groups were significantly improved. (P<0.01 or P<0.05). Conclusion: Ginkgolide B can improve the learning and memory ability of the model rats of Alzheimer’s disease.*
Effects of Extract from Ginkgo Biloba on Learning, Memory and Expression of Hippocampal Brain-derived Neurotrophic Factor in Senile Mice Induced by D-galactose
QIN Long, HUANG Jun-hong, XING Ze-gang, Hu Shibao, He Qinlan, Chen Lian, Zhao Weihai. Zhong Guo Lin Chuang Shen Jin Wai Ke Za Zhi. 2009; 14(10): 603-605.
Objective To explore the effect of the extract from ginkgo biloba (EGb) on learning, memory and the expression of hippocampal brain-derived neurotrophic factor(BDNF) in the senile mice induced by D-galactose. Methods Thirty-two mice were randomly divided into 4 groups of 8 mice each, i.e. blank control group, model group, low dose of EG (50 mg/kg) treatment group and high dose of EGb (100 mg/kg) treatment group. The senile mice model in the model and treatment groups induced by D-galactose. The activity of the mice was determined by the open field test in all the groups, where the ability of learning and memory of mice were examined by step down test. The expression of BDNF in the hippocampi was determined by western blotting in all the groups. Results The open field test showed that the activity of the mice in both the treatment groups significantly increased compared to that in the model group (P<0.05). The step down test showed that the latent period of step-down was significantly longer and the latent period of escape was significantly shorter in both the treatment groups than that in the model group (P<O.05). The expression of hippocampal BDNF was significantly enhanced in both the treatment group compared to that in the model group. Conclusions The learning, memory and open field activity in the senile mice induced by D-galactose may be improved by EGb. It is suggested that the improvement of learning, memory and open field activity may be related to the increase in the expression of hippocampal BDNF in the senile mice induced by D-galactose.*
Effects of Ginkgo Biloba extract on learning and memory ability of rats with Vascular Dementia
WU Yu, HU Chang-lin. Xian Dai Yu Fang Yi Xue. 2008; 35(13): 2585-2586.
Objective: To investigate effects of ginkgo biloba extract (GBE) on learning and memory ability of rats with vascular dementia. Methods: Rats’ model of vascular dementia was established. Sham-operation group and operation group were administered normal saline. GBE group was administered ginkgo biloba extract. The superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities and the malondialdehyde (MDA) content in the cerebral tissue were detected after 14 days. Meanwhile the neurons of the hippocampal CA1 was observed. Results: The SOD and GSH-Px activities in the GBE group increased, while the MDA content significantly decreased comparing with the those in operation group (P<0.05). The results indicated that the pathological changes in the GBE group were slighter than those in the operation group. Conclusion: Ginkgo biloba extract on rats with vascular dementia could enhance SOD and GSH-Px activities, decrease the MDA content, then protect nerve cells from apoptosis.*
Effect of extracts of Ginkgo biloba leaf on learning-memory ability and NMDA receptor 1 expression in the hippocampus in rats with kindling-induced epilepsy
DUAN Fang-Rong, YUAN Bao-Qiang. Zhong Guo Dang Dai Er Ke Za Zhi. 2008; 10(3): 367-370.
Objective: To study the effect of extracts of Ginkgo biloba leaf (EGb), a catalyzer of central nervous system, on learning-memory ability and possible mechanism in rats with kindling-induced epilepsy. Methods: Forty postnatal day 21 (P21) and 40 postnatal day 35 (P35) Sprague-Dawley (SD) rats were randomly respectively assigned to five groups: normal sodium (NS) control, kindling epilepsy model, high, middle and low dosage of EGb-treated kindling epilepsy. The kindling epilepsy model was established by an intraperitoneal injection of pentetrazole (FTZ). The learning-memory ability and NMDA receptor 1 (NMDAR1) expression in the hippocampus were measured by Y-maze test and immunohistochemistry assay respectively. Results: The stimulation times for reaching to academic standard in the Y-maze test in the two ages PTZ kindling groups was significantly more than that in the corresponding NS control groups (P<0.01). After EGb treatment the achievement of the Y-maze test in the three treatment groups was significantly improved in a dose-dependent manner, the higher the dosage, the better the achievement (P<0.01). Immunohistochemistry assay showed that the expression of NMDAR1 in the two ages FTZ kindling groups was significantly higher than that in the corresponding NS control groups (P<0.01). Compared with the corresponding untreated kindling model groups, the expression of NMDAR1 in the two ages EGb treatment groups was significantly reduced in a dose-dependent manner (P<0.01). Conclusions: EGb can improve learning-memory ability in epileptic rats at different developmental phases in a dose-dependent manner, possibly through a reduction of NMDAR1 expression in the hippocampus.*
Hyperzia serrata (contains Huperzine-A) (Shi Shan)
Huperzine A has been shown to improve memory, thinking, and behavioural function in people with Alzheimer's disease, multi-infarct dementia, and senile dementia. It is believed to work in a manner similar to some prescription drugs for treating symptoms of Alzheimer's disease, increasing the level of the neurotransmitter acetylcholine by blocking its breakdown. It may also protect neurons from cell death caused by toxic levels of glutamate and protect against some of the effects of chemical nerve agents used in warfare.*
Hyperzia serrata (Shi Shan) contains an alkaloid Huperzine A. It's effective in improving cognitive and memory abilities in humans, including those with Alzheimer's disease. In China , where HupA is used for treating Alzheimer's and myasthenia gravis, medical scientists have studied its effects on the mental functions of elderly Alzheimer's patients. Huperzine A has been shown to improve memory, thinking, and behavioural function in people with Alzheimer's disease, multi-infarct dementia, and senile dementia. It is believed to work in a manner similar to some prescription drugs for treating symptoms of Alzheimer's disease: increasing the level of the neurotransmitter acetylcholine by blocking its breakdown. It may also protect neurons from cell death caused by toxic levels of glutamate and protect against some of the effects of chemical nerve agents used in warfare.*
Research of the Patients with Vascular Cognitive Impairment no Dementia in Terms of Neuropsychology and the Clinical Study of Huperzine A in the Treatment
JIANG Bo, MENG Xiao-Luo, SHU Gang-Ming, YAO Cun-Shan, CHEN Yu-Mei, GUO Yue-Qi. Zhong Guo Lin Chuang Shen Jing Ke Xue. 2009(5): 510-514.
Aim: To investigate the characteristics of the patients with vascular cognitive impairment no dementia(VCIND) in terms of neuropsychology and to observe the efficacy of huperzine A in treating VCIND. Methods: 64 patients with VCIND and 42 normal controls were examined with the neuropsychological test, including mini-mental state examination (MMSE), clock-drawing test (CDT). 64 patients with VCIND were randomly divided into 2 groups: a huperzine A treated group and a control group. The whole course of treatment for each group lasted 8 weeks. MMSE and CDT were examined in the 4th week and 8th week. Results: (1) The scores of CDT and MMSE in the VCIND group were significantly lower than those in the control group(P<0.01). The scores of sub items of MMSE including time orientation, place orientation, account ability, short time memory, language repetition, reading comprehension, language expression, figure portrayal in patients with VCIND were lower than those in the normal subjects (all P<0.01). (2) After 8 weeks, the marks of MMSE and CDT of huperzine A treated group were more improved than before and the control group. Conclusion: (1) The combination of MMSE and CDT can be used for early finding of cognitive impairment in VCIND patients. (2) Huperzine A can improve the cognitive function of patients with VCIND.*
The Clinical Study of Huperzine A in the Treatment of Vascular Dementia
XU Zhi-Qiang, ZHANG Meng, LI Jing, ZHOU Hua-Dong. Zhong Guo Lin Chuang Shen Jing Ke Xue. 2009; 17(2): 163-165.
Aim: To observe the efficacy and safety of Huperzine A in treating the mild to moderate vascular dementia(VaD). Methods: Seventy-eight patients with the mild to moderate VaD were randomly divided into 2 groups: the Huperzine A treated group(n=39), M 24, F 15, [age(71.8 ± 7.2)years] and the control group(n=39), M 26, F 13, [age (72.3 ± 6.9)years]. The patients for Huperzine A treated group were treated with Huperzine A tablets 0.1 mg, po, bid. The patients for control group were treated with Vitamin C 100 mg, po, and bid. The whole course of treatment for each group was 12 weeks. Mini mental state examination (MMSE), clinical dementia rating (CDR) and activity of daily living scale (ADL) were taken as the main value targets. Results: After 12 weeks, the marks of MMSE, CDR, and ADL of the treatment group were more improved than those of the control group (P<0.01, respectively). Conclusion: Huperzine A can prominently improve the cognitive function of patients with the mild to moderate vascular dementia. Moreover, its security and tolerability is good.*
Puerarin and Huperzine A improve learning memory dysfunction induced by ischemia-reperfusion in mice
SHI Rui-li, SHEN Shu-ping, PANG Dong-wei, WANG Li-jun, ZHAO Li-juan, GAO Li-jun. Zhong Guo Yi Yao Dao Bao. 2009; 6(7): 25-27.
Objective: To observe the effects of Puerarin (Pur) and Huperzine A (Hup-A) on learning memory dysfunction induced by ischemia-reperfusion (I/R) in mice and explore its mechanism. Methods: I/R model in mice was performed by repetitious ligation of bilateral common carotid artery, and mice were randomly divided into five groups: Sham group, I/R group, Hup-A group, Pur group and Pur+Hup-A group. Learning memory ability was evaluated by step-down test. Monoamine nervous transmitter level and cortex neuron apoptosis were measured by HPLC and flow cytometry respectively. Results: Both Pur and Hup-A improved learning memory ability of I/R mice, the effect of Pur group was better and the effect of combination group was the most significant. Both Pur and Hup-A decreased neuron apoptosis and raised content of monoamine nervous transmitter of I/R mice. The cortex neuron apoptosis rate in combination group was lower than that in Hup-A group, the homovanillic acid (HVA) level of cerebral cortex in combination group was higher than that of Pur group. Conclusion: Learning memory dysfunction induced by I/R in mice could be improved by Put and Hup-A, the effect of Put was better than that of Hup-A with administered dose, the mechanisms of drugs might be related to reduction of neuron apoptosis and regulating of the monoamine nervous transmitter level in cerebral cortex, combination of Pur and Hup-A resulted in the most obvious effects.*
Study on Pharmacodynamics of Alzheimer’s Disease with Huperzine A
YONG Bin, LIU Jian-ting, ZHANG Xiao-yu, HUANG Chun-ping. Study on Pharmacodynamics of Alzheimer’s Disease with Huperzine A. Shi Pin Ke Xue. 2007; 28(5): 327-331.
In this paper, the effects of mice memory were studied merely by jumping platform experiment and avoiding darkness experiment with three doses respectively as 13.5, 41.0 and 61.0 mg/kg huperzine A. The results showed that huperzine A has the obvious effects on improving both the reappearance ability of passive avoidance and the avoiding darkness response. So huperzine can have the function to promote memory and improvement symptom of Alzheimer’s disease (Yong et al, 2007).*
Ginseng (Ren Shen)
Effects of panaxadiol saponins and lycopene on abilities of learning and memory of senile atlanto -axial joint instability
FAN Wenjing, ZHU Tongtong, GUO Yaxiong, Lin Guimiao, Zhao Lijuan. Zhong Guo Kang Fu Yi Xue Za Zhi. 2009(8): 731-733.
Objective: To compare the effects of panaxadiol saponins (PDS) with lycopene on the abilities of learning and memory in senile mice with learning and memory disorder by atlanto-axial joint instability. Method: The atlanto-axial joint instability model was established by injection with 30% lactic acid around the atlanto and axial vertebrae, 30ml once weekly, three times totally. The changes of abilities of learning and memory in mice were observed with water-maze test. The activities of acetylcholine esterase (AchE) and the content of acetylcholine (Ach) in brain tissue were tested. Immunohistochemical staining with b-amyloid protein in mice hippocampus was demonstrated. Result: The model mice had longer swimming time and more errors (P<0.05) in water maze test compared with control group. PDS mice had significant short latency period and less errors in water-maze test (P<0.01), but the difference between PDS and lycopene groups was not obvious. Compared with model group, the activities of AchE reduced(P<0.01), and the content of Ach increased in PDS and lycopene groups(P<0.01). And in the two therapy groups, expressions of b-amyloid protein in mice hippocampus were less than that in model group. Conclusion: This study indicate that PDS and lycopene can improve the learning and memory abilities of mice and the metabolism of senile mice brain, which may be the mechanism of its protective effect to cerebral damage.*
Effect of ginsenoside-Rg2 on learning and memory of vascular dementia rats
ZHANG Li, PAN Zhi-yuan, JIN Yi, LONG Chao-liang, WANG Hai. Zhong Guo Lin Chuang Yao LI Xue Yu Zhi Liao Xue. 2008; 13(3): 276-282.
AIM: To investigate the effect of ginsenoside-Rg2 on learning and memory of vascular dementia rats and it’s underlying mechanisms, especially the expression of NMDA/AMPA receptors. METHODS: Vascular dementia (VD) of rat was induced by permanent occlusion of bilateral common carotid arteries(2OV). The rats were given different doses of ginsenoside-Rg2 (2. 5, 5.0, 10.0 mg/kg) as while as operation. The spontaneous movement and the delayed non-matching-to-position task(DNMPT) in the water maze were used to examine the behaviour changes on learning and memory; the mRNA of four different subtypes of NMDA/AMPA receptors, including NR1, NR2A, NR2B and GluR2 in hippocampus were determined by the RT-PCR method. RESULTS: The spontaneous movement and spatial learning and memory of VD rats were all decreased. After ginsenoside-Rg2 administration, the spontaneous movement and the spatial learning and memory were improved; the latency of information swim (IS) and choice swim (CS) decreased, and choice accuration in choice swim increased. The expression of NR1 mRNA was enhanced while NR2A, NR2B and GluR2 were attenuated in hippocampus of VD rats. These pathological changes could be reversed by treatment with ginsenoside-Rg2. CONCLUSION: Ginsenoside-Rg2 can patently improve the spatial learning and memory of VD rats. The mechanism may be related to the regulation of ginsenoside-Rg2 on the expression of NMDA/AMPA receptors in hippocampus.*
Effect of ginsenoside Rbl on expression of b-secretase and presenilin-1 in the parietal lobe of Alzheimer disease-like rat
Fang Xin, Yang Jiping, Lai Hong. Jie Pou Xue Za Zhi. 2008; 31(6): 812-815.
Objective: To investigate the effect of ginsenoside Rb1 on the expression of b-secretase and presenilin-1 (PS-1) in the parietal lobe of Alzheimer disease-like rats. Methods: Thirty SD rats were randomly divided into a control group, a model group and a treatment group. The model rats were established with administration of I)-galactose 60 mg· kg-1· d-1 and aluminum chloride 200 mg·kg -1 · d-1 for 2 months, the control group were given the same dose of sodium chloride, and treatment group were given ginsenoside Rb1 10mg·kg-1·d -1 for 4 weeks after the model rats were established. The expressions of b-secretase and PS-1 in the parietal lobe were detected by immunohistochemistry with image analysis. Morris test was used to determine the ability of learning and memory. Results: Compared with the control group, the levels of b-secretase and PS-1 were significantly higher in the model group (P<0.05), and learning and recognition ability in this group was obviously worse (P<0.05); Compared with the moctel group, the levels of b-secretase and PS-1 were significantly lower in the treatment group (P<0.05), and learning and recognition ability in this group was better. The learning and recognition ability was obviously improved on the second and the third day (P<0.05). Conclusion: Ginsenoside Rbl has preventive and therapeutic effect on Alzheimer disease-like rats, via inhibiting the expression of b-secretase and PS-1.*
Effect of ginsenoside Rg1 on Alzheimer’s disease of model rats
LI Na, WANG Limin. Bin Zhou YI Xue Yuan Xue Bao. 2007; 30(5): 325-326.
Objective: To observe the effect of ginsenoside Rg1 on rat of Alzheimer’s disease (AD) model. Methods Bilateral NBM of elderly rats were damaged by quinolinic acid, and the AD model was established. The single passive avoidance step-down training and water-maze spatial localization test were used to study the effects of Ginsenoside Rg1 on learning and memory of AD rats. Results Treated with low and high dosages of ginsenoside Rg1, AD rat models decreased significantly in the number of errors in step-down (13 days) and the times training to reach the criterion in water maze task (16 days). Except for the fact that the times of training to reach the criterion with high dosage of ginsenoside Rg1 were those than that with 1, 2, 3, 4 tetrahydroacridine, there was no obvious difference in the effects of low, high dosage of GMC and THA. Conclusion Ginsenoside Rg1 can improve the ability of learning and memory of AD model rat.*
*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.