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Ginko (Ginkgo biloba) and Cognitive function: evidence and sources
inferred from neuroprotective action
For educational purposes only, not medical advice. Always consult a qualified practitioner before using medicinal plants, especially alongside prescribed medication, during pregnancy, or for a serious condition.
Context Ginkgo biloba is widely used for its potential effects on memory and cognition. To date, adequately powered clinical trials testing the effect of G. biloba on dementia incidence are lacking. Objective To determine effectiveness of G. biloba vs placebo in reducing the incidence of all-cause dementia and Alzheimer disease (AD) in elderly individuals with normal cognition and those with mild cognitive impairment (MCI). Design, setting, and participants Randomized, double-blind, placebo-controlled clinical trial conducted in 5 academic medical centers in the United States between 2000 and 2008 with a median follow-up of 6.1 years. Three thousand sixty-nine community volunteers aged 75 years or older with normal cognition (n = 2587) or MCI (n = 482) at study entry were assessed every 6 months for incident dementia. Intervention Twice-daily dose of 120-mg extract of G. biloba (n = 1545) or placebo (n = 1524). Main outcome measures Incident dementia and AD determined by expert panel consensus. Results Five hundred twenty-three individuals developed dementia (246 receiving placebo and 277 receiving G. biloba) with 92% of the dementia cases classified as possible or probable AD, or AD with evidence of vascular disease of the brain. Rates of dropout and loss to follow-up were low (6.3%), and the adverse effect profiles were similar for both groups. The overall dementia rate was 3.3 per 100 person-years in participants assigned to G. biloba and 2.9 per 100 person-years in the placebo group. The hazard ratio (HR) for G. biloba compared with placebo for all-cause dementia was 1.12 (95% confidence interval [CI], 0.94-1.33; P = .21) and for AD, 1.16 (95% CI, 0.97-1.39; P = .11). G. biloba also had no effect on the rate of progression to dementia in participants with MCI (HR, 1.13; 95% CI, 0.85-1.50; P = .39). Conclusions In this study, G. biloba at 120 mg twice a day was not effective in reducing either the overall incidence rate of dementia or AD incidence in elderly individuals with normal cognition or those with MCI. Trial Registration clinicaltrials.gov Identifier: NCT00010803.
The efficacy of the Ginkgo biloba special extract EGb 761 in outpatients with presenile and senile primary degenerative dementia of the Alzheimer type (DAT) and multi-infarct dementia (MID) according to DSM-III-R was investigated in a prospective, randomized, double-blind, placebo-controlled, multi-center study. After a 4-week run-in period, 216 patients were included in the randomized 24-week treatment period. These received either a daily oral dose of 240 mg EGb 761 or placebo. In accordance with the recommended multi-dimensional evaluation approach, three primary variables were chosen: the Clinical Global Impressions (CGI Item 2) for psychopathological assessment, the Syndrom-Kurztest (SKT)(1) for the assessment of the patient's attention and memory, and the Nürnberger Alters-Beobachtungsskala (NAB)(2) for behavioral assessment of activities of daily life. Clinical efficacy was assessed by means of a responder analysis, with therapy response being defined as response in at least two of the three primary variables. The data from the 156 patients who completed the study in accordance with the study protocol were taken into account in the confirmatory analysis of valid cases. The frequency of therapy responded in the two treatment groups differed significantly in favor of EGb 761, with p<0.005 in Fisher's Exact Test. The intent-to-treat analysis of 205 patients led to similar efficacy results. Thus, the clinical efficacy of the ginkgo biloba special extract EGb 761 in dementia of the Alzheimer type and multi-infarct dementia was confirmed. The investigational drug was found to be well tolerated.
3 sources supporting Ginko for Cognitive function. Includes scientific publications, books, monographs and traditional-use references.
Mechanistic basis
This use is associated with the plant's neuroprotective / cognition support action. Further evidence for that pharmacology:
Alzheimer's disease (AD) is the most common progressive human neurodegenerative disorder affecting elderly population worldwide. Hence, prevention of AD has been a priority of AD research worldwide. Based on understanding of disease mechanism, different therapeutic strategies involving synthetic and herbal approaches are being used against AD. Among the herbal extract, Ginkgo biloba extract (GBE) is one of the most investigated herbal remedy for cognitive disorders and Alzheimer's disease (AD). Standardized extract of Ginkgo biloba is a popular dietary supplement taken by the elderly population to improve memory and age-related loss of cognitive function. Nevertheless, its efficacy in the prevention and treatment of dementia remains controversial. Specifically, the added effects of GBE in subjects already receiving "conventional" anti-dementia treatments have been to date very scarcely investigated. This review summarizes recent advancements in our understanding of the potential use of Ginkgo biloba extract in the prevention of AD including its antioxidant property. A better understanding of the mechanisms of action of GBE against AD will be important for designing therapeutic strategies, for basic understanding of the underlying neurodegenerative processes, and for a better understanding of the effectiveness and complexity of this herbal medicine.
Ginkgo biloba special extract (EGb761) is used in most randomized control trials. Indications include cognition and memory in Alzheimer disease, age-associated dementia, cerebral insufficiency, intermittent claudication, schizophrenia, and multi-infarct dementia. Dosages range from 80 to 720 mg/d for durations of 2 weeks to 2 years. Mechanisms of action include increasing cerebral blood flow, antioxidant and antiinflammatory effects, with antiplatelet effects attributed to flavone and terpene lactones. Possible interactions with monoamine oxidase inhibitors, alprazolam, haloperidol, warfarin, and nifedipine have been reported. Optimal dosage/duration, dose-response characteristics, drug interactions, bioavailability, long-term effects, and optimal intervention timing should be the focus of future work.
Aims Alzheimer's disease (AD) is a neurodegenerative disorder with limited treatment options. This study aimed to investigate the therapeutic effects of Ginkgo biloba leaf extract (GBE) on AD and explore its potential mechanisms of action. Methods Key chemical components of GBE, including quercetin, luteolin, and kaempferol, were identified using network pharmacology methods. Bioinformatics analysis revealed their potential roles in AD through modulation of the PI3K/AKT/NF-κB signaling pathway. Results Mouse experiments demonstrated that GBE improved cognitive function, enhanced neuronal morphology, and reduced serum inflammatory factors. Additionally, GBE modulated the expression of relevant proteins and mRNA. Conclusion GBE shows promise as a potential treatment for AD. Its beneficial effects on cognitive function, neuronal morphology, and inflammation may be attributed to its modulation of the PI3K/AKT/NF-κB signaling pathway. These findings provide experimental evidence for the application of Ginkgo biloba leaf in AD treatment and highlight its potential mechanisms of action.
Objective Ginkgo biloba may have a role in treating impairments in memory, cognitive speed, activities of daily living (ADL), edema, inflammation, and free-radical toxicity associated with traumatic brain injury (TBI), Alzheimer's dementia, stroke, vasoocclusive disorders, and aging. The purpose of this review is to provide a synthesis of the mechanisms of action, clinical indications, and safety of Ginkgo biloba extract. Data sources Empirical studies, reviews, chapters, and conference proceedings were identified in the following databases: Medline, the Research Council for Complementary Medicine based on the British Library database, and Psychlnfo. Ginkgo biloba, EGb 761, Tanakan, Tebonin, Rokan, and LI 1370 were the principal index terms. Study selection and data extraction Controlled clinical studies with both positive and negative findings are included, in addition to animals studies illustrating mechanisms of activity. Data synthesis Ginkgo has shown activity centrally and peripherally, affecting electrochemical, physiologic, neurologic, and vascular systems in animals and humans with few adverse side effects or drug interactions. Ginkgo shows promise in patients with dementia, normal aging, and cerebrovascular-related disorders. Clinical indications include memory, information processing, and ADL. Conclusions Ginkgo shows promise in treating some of the neurologic sequelae associated with Alzheimer's disease, TBI, stroke, normal aging, edema, tinnitus, and macular degeneration. Mechanisms of action may include antioxidant, neurotransmitter/receptor modulatory, and antiplatelet activating factor properties. While safe, caution is advised when recommending ginkgo to patients taking anticoagulants. Future studies should examine dose effects, component activity, mechanisms, and clinical applications.
The Gingko biloba extract EGb 761 has been the subject of many studies which confirm its usefulness for the prevention and treatment of neurodegenerative pathologies. These studies have focused on: a) the probable mechanisms of action that are involved in these disorders (including non-specific mechanisms implicated in diverse neurodegenerative disorders, particularly oxidative stress, or specific mechanisms such as those associated with beta-amyloid in Alzheimer's disease) and the processes of neuronal death; b) available animal models, and c) healthy individuals or those suffering from mild cognitive impairment or Alzheimer's disease. This data must be completed, particularly with regard to new knowledge about the pathogenesis of these disorders. Ambitious interventional studies are underway and may provide new evidence regarding the effect of EGb 761 in preventing Alzheimer's disease in humans. Positive findings would be particularly interesting since this drug is very safe to use.
The effects of EGb 761 on the CNS underlie one of its major therapeutic indications; i.e., individuals suffering from deteriorating cerebral mechanisms related to age-associated impairments of memory, attention and other cognitive functions. EGb 761 is currently used as symptomatic treatment for cerebral insufficiency that occurs during normal ageing or which may be due to degenerative dementia, vascular dementia or mixed forms of both, and for neurosensory disturbances. Depressive symptoms of patients with Alzheimer's disease (AD) and aged non-Alzheimer patients may also respond to treatment with EGb 761 since this extract has an "anti-stress" effect. Basic and clinical studies, conducted both in vitro and in vivo, support these beneficial neuroprotective effects of EGb 761. EGb 761 has several major actions; it enhances cognition, improves blood rheology and tissue metabolism, and opposes the detrimental effects of ischaemia. Several mechanisms of action are useful in explaining how EGb 761 benefits patients with AD and other age-related, neurodegenerative disorders. In animals, EGb 761 possesses antioxidant and free radical-scavenging activities, it reverses age-related losses in brain alpha 1-adrenergic, 5-HT1A and muscarinic receptors, protects against ischaemic neuronal death, preserves the function of the hippocampal mossy fiber system, increases hippocampal high-affinity choline uptake, inhibits the down-regulation of hippocampal glucocorticoid receptors, enhances neuronal plasticity, and counteracts the cognitive deficits that follow stress or traumatic brain injury. Identified chemical constituents of EGb 761 have been associated with certain actions. Both flavonoid and ginkgolide constituents are involved in the free radical-scavenging and antioxidant effects of EGb 761 which decrease tissue levels of reactive oxygen species (ROS) and inhibit membrane lipid peroxidation. Regarding EGb 761-induced regulation of cerebral glucose utilization, bilobalide increases the respiratory control ratio of mitochondria by protecting against uncoupling of oxidative phosphorylation, thereby increasing ATP levels, a result that is supported by the finding that bilobalide increases the expression of the mitochondrial DNA-encoded COX III subunit of cytochrome oxidase. With regard to its "anti-stress" effect, EGb 761 acts via its ginkgolide constituents to decrease the expression of the peripheral benzodiazepine receptor (PBR) of the adrenal cortex.
(1) Background: Ginkgo biloba extract (GBE) has been widely used to treat central nervous system and cardiovascular diseases. Accumulating evidence has revealed the therapeutic potential of GBE against Alzheimer's disease (AD); however, no systematic evaluation has been performed; (2) Methods: a total of 17 preclinical studies and 20 clinical trials assessing the therapeutic effects of GBE against AD were identified from electronic databases. The data in the reports were extracted to conduct a meta-analysis of the AD-related pathological features or symptoms; (3) Results: For the preclinical reports, 45 animals treated with GBE, in six studies, were subjected to cognitive function assessments by the Morris water maze. GBE was shown to reduce the escape latencies in several studies, in both rats and mice (I 2 > 70%, p < 0.005). For the clinical trials, eight trials, including 2100 individuals, were conducted. The results show that GBE improved the SKT and ADAS-Cog scores in early-stage AD patients after high doses and long-term administration; (4) Conclusions: GBE displayed generally consistent anti-AD effects in animal experiments, and it might improve AD symptoms in early-stage AD patients after high doses and long-term administration. A lack of sample size calculations and the poor quality of the methods are two obvious limitations of the studies. Nevertheless, the preclinical and clinical data suggest that further large-scale clinical trials may be needed in order to examine the effects of long-term GEB administration on early-stage AD.
Objectives To review current evidence of efficacy of Ginkgo biloba extract EGb 761 ® in dementia with behavioural and psychological symptoms (BPSD). Methods Randomized, placebo-controlled trials assessing the effects of EGb 761 ® in dementia patients with BPSD were included if the diagnosis was made in accordance with internationally accepted criteria, the treatment period was at least 22 weeks, outcome measures covered BPSD and at least two of the following domains of assessment, i.e. cognition, activities of daily living and clinical global assessment, and methodological quality was adequate. An analysis of covariance (ANCOVA) model was used to calculate the pooled effect estimates and to compare effects of EGb 761 ® and placebo; furthermore, combined risk differences of response rates were calculated. Results Four published trials were identified, involving altogether 1,628 outpatients with mild to moderate dementia. Least-square mean differences for change from baseline in cognition, BPSD (including caregiver distress rating), activities of daily living, clinical global impression, and quality of life favoured EGb 761 ® (P Conclusions The pooled analyses provide evidence of efficacy of EGb 761 ® at a daily dose of 240 mg in the treatment of out-patients suffering from Alzheimer's, vascular or mixed dementia with BPSD.