Ginkgo biloba
Selected from ~1500 articles
Napryeyenko O. Borzenko I. GINDEM-NP Study Group. Ginkgo biloba special extract in dementia with neuropsychiatric features. A randomised, placebo-controlled, double-blind clinical trial. Arzneimittel-Forschung. 57(1):4-11, 2007. BACKGROUND: In previous trials of the Ginkgo biloba special extract EGb 761 improvements in cognitive functioning and behavioural symptoms were found in patients with aging-associated cognitive impairment or dementia. This trial was undertaken to assess the efficacy of EGb 761 in mild to moderate dementia with neuropsychiatric features. METHODS: Double-blind trial including 400 patients aged 50 years or above with Alzheimer's disease (AD) or vascular dementia (VaD), randomized to receive EGb 761 or placebo for 22 weeks. Patients scored below 36 on the Test for the Early Detection of Dementia with Discrimination from Depression (TE4D), between 9 and 23 on the SKT test battery and at least 5 on the Neuropsychiatric Inventory (NPI). RESULTS: There was a mean -3.2-point improvement in the SKT upon EGb 761 treatment and an average deterioration by +1.3 points on placebo (p < 0.001, two-sided, ANOVA). EGb 761 was significantly superior to placebo on all secondary outcome measures, including the NPI and an activities-of-daily-living scale. Treatment results were essentially similar for AD and VaD subgroups. The drug was well tolerated; adverse events were no more frequent under drug than under placebo treatment. CONCLUSION: The data add further evidence on the safety and efficacy of EGb 761 in the treatment of cognitive and non-cognitive symptoms of dementia.
Rodriguez M. Ringstad L. Schafer P. Just S. Hofer HW. Malmsten M. Siegel G. Reduction of atherosclerotic nanoplaque formation and size by Ginkgo biloba (EGb 761) in cardiovascular high-risk patients. Atherosclerosis. 192(2):438-44, 2007. Coating a silica surface with the isolated lipoprotein receptor proteoheparan sulfate (HS-PG) from arterial endothelium and vascular matrices and adding both the atherogenic VLDL/IDL/LDL lipid fraction in its native composition and Ca(2+) ions, we could observe in vitro the earliest stages of atherosclerotic plaque development by ellipsometric techniques (patent EP 0 946 876). This so-called nanoplaque formation is represented by the ternary aggregational complex of the HS-PG receptor, lipoprotein particles and calcium ions. The model was validated in several clinical studies on statins in cardiovascular high-risk patients. In eight patients who had undergone an aortocoronary bypass operation, the reduction of atherosclerotic nanoplaque formation amounted to 11.9+/-2.5% (p<0.0078) and of nanoplaque size to 24.4+/-8.1% (p<0.0234), respectively, after a 2-month therapy with Ginkgo biloba extract (2x 120 mg daily, EGb 761). Additionally, superoxide dismutase (SOD) activity was upregulated by 15.7+/-7.0% (p<0.0391), the quotient oxLDL/LDL lowered by 17.0+/-5.5% (p<0.0234) and lipoprotein(a) concentration decreased by 23.4+/-7.9% (p<0.0234) in the patients' blood. The concentration of the vasodilating substances cAMP and cGMP was augmented by 37.5+/-9.1% (p<0.0078) and 27.7+/-8.3% (p<0.0156), respectively. A multiple regression analysis between the patients' VLDL/IDL/LDL lipoprotein fraction applied in the ellipsometry measurements as well as the further risk factors oxLDL/LDL and Lp(a) on the one hand and changes in nanoplaque formation on the other hand reveals a basis for a mechanistic explanation of nanoplaque reduction under ginkgo treatment. The atherosclerosis inhibiting effect is possibly due to an upregulation in the body's own radical scavenging enzymes and an attenuation of the risk factors oxLDL/LDL and Lp(a).
Trumbeckaite S. Bernatoniene J. Majiene D. Jakstas V. Savickas A. Toleikis A. Effect of Ginkgo biloba extract on the rat heart mitochondrial function. Journal of Ethnopharmacology. 111(3):512-6, 2007. Ginkgo biloba L. (Ginkgoaceae) originated from China, first introduced to Europe in the 18th century, it is now distributed all over the world. The leaves of Ginkgo biloba include a rich complex of active compounds responsible for various pharmacological properties. Ginkgo biloba extract improves blood circulation, protects against oxidative cell damage, blocks platelet aggregation that could be important for prevention of cardiovascular diseases. Therefore the fluid extract from Ginkgo biloba leaves was prepared and tested for it is effect on rat mitochondrial function. Our data showed that 0.5 microl/ml of GE (containing 0.57 ng/ml of rutin, 0.23 ng/ml of quercitrin, 0.105 ng/ml of hyperosid and 0.02 ng/ml of quercetin) had no effect on the State 2 respiration rate of mitochondria with all used substrates: pyruvate+malate, succinate and palmitoyl-L-carnitine. Further increase in GE concentration (2 and 4 microl/ml), increased the State 2 respiration rate with all respiratory substrates in a dose-dependent manner (by 35-116%). The State 3 respiration rate was not affected by GE. In order to identify which compounds of GE could be responsible for the observed effects, we measured the effect of pure flavonoids: rutin, quercetin, hyperosid and quercitrin on mitochondrial respiration. All flavonoids (except of hyperosid) at maximal used concentration, comparable/identical to that in GE, stimulated the State 2 respiration rate only by 8-20%, i.e. less effectively as compared to GE. Therefore, for the explanation of the GE-induced uncoupling of oxidative phosphorylation, other biologically active compounds of GE have to be taken into account in future studies.
Ye B. Aponte M. Dai Y. Li L. Ho MC. Vitonis A. Edwards D. Huang TN. Cramer DW. Ginkgo biloba and ovarian cancer prevention: epidemiological and biological evidence. Cancer Letters. 251(1):43-52, 2007. There is considerable interest in herbal therapies for cancer prevention but often with little scientific evidence to support their use. In this study, we examined epidemiological data regarding effects of commonly used herbal supplements on risk for ovarian cancer and sought supporting biological evidence. 4.2% of 721 controls compared to 1.6% of 668 cases regularly used Ginkgo biloba for an estimated relative risk (and 95% confidence interval) of 0.41 (0.20,0.84) (p=0.01); and the effect was most apparent in women with non-mucinous types of ovarian cancer, RR=0.33 (0.15,0.74) (p=0.007). In vitro experiments with normal and ovarian cancer cells showed that Ginkgo extract and its components, quercetin and ginkgolide A and B, have significant anti-proliferative effects ( approximately 40%) in serous ovarian cancer cells, but little effect in mucinous (RMUG-L) cells. For the ginkgolides, the inhibitory effect appeared to be cell cycle blockage at G0/G1 to S phase. This combined epidemiological and biological data provide supportive evidence for further studies of the chemopreventive or therapeutic effects of Ginkgo and ginkgolides on ovarian cancer.
Lovera J. Bagert B. Smoot K. Morris CD. Frank R. Bogardus K. Wild K. Oken B. Whitham R. Bourdette D. Ginkgo biloba for the improvement of cognitive performance in multiple sclerosis: a randomized, placebo-controlled trial. Multiple Sclerosis. 13(3):376-85, 2007. OBJECTIVES: To determine if Ginkgo biloba (GB) improves the cognitive performance of subjects with multiple sclerosis (MS). METHODS: Randomized, double-blind, placebo-controlled trial of GB, 120 mg twice a day or placebo for 12 weeks. The primary outcomes were: the long delay free recall from the California Verbal Learning Test-II; the Paced Auditory Serial Addition Test; the Controlled Oral Word Association Test; the Symbol Digit Modalities Test; Useful Field of View Test; and the color-word interference condition from the Stroop Color and Word Test. RESULTS: On completion, the GB group (n=20) was 4.5 seconds (95% confidence interval (CI) (7.6, 0.9), P=0.015) faster than the placebo group (n=18) on the color-word interference condition of the Stroop test. Subjects who were more impaired at baseline experienced more improvement with GB (treatment*baseline interaction, F=8.10, P=0.008). We found no differences on the other neuropsychological tests. Subjects on GB reported fewer cognitive difficulties in the Retrospective Memory Scale of the Perceived Deficits Questionnaire than subjects on placebo (1.5 points, 95% CI (2.6, 0.3), P=0.016). No serious drug related side-effects occurred and GB did not alter platelet function assays. CONCLUSION: Overall, GB did not show a statistically significant improvement in cognitive function. A treatment effect trend, limited to the Stroop test, suggests that GB may have an effect on cognitive domains assessed by this test, such as susceptibility to interference and mental flexibility.
Yuan G. Gong Z. Li J. Li X. Ginkgo biloba extract protects against alcohol-induced liver injury in rats. Phytotherapy Research. 21(3):234-8, 2007. Ginkgo biloba extract has been shown to be hepatoprotective. However, its benefits when used in alcoholic liver injury have not been demonstrated. This study investigated the effects of Ginkgo biloba extract on alcohol-induced liver injury in a chronic alcohol plus fish oil gavage model in rats. Liver injury was evaluated histologically and by serum alanine aminotransferase (ALT). Liver tumor necrosis factor-alpha (TNF-alpha) protein levels, malondialdehyde (MDA) and glutathione (GSH) contents were determined. TNF-alpha mRNA expression in the liver was analysed by reverse transcriptase-polymerase chain reaction (RT-PCR). Rats given fish oil plus alcohol developed macrovesicular and microvesicular steatosis, spotty necrosis and mild inflammation in the liver and elevated serum ALT levels, which were accompanied by increased MDA contents, reduced GSH contents and elevated TNF-alpha protein and mRNA expressions in the liver. Supplementation with Ginkgo biloba extract (200 mg/kg, orally) improved the liver injury, blunted the rises of MDA contents and TNF-alpha expression, and restored the GSH content in the liver. Ginkgo biloba extract protects against alcohol-induced liver injury, and the mechanism may involve a reduction of lipid peroxidation, prevention of GSH depletion and inhibition of TNF-alpha expression in the liver.
Dong XX. Hui ZJ. Xiang WX. Rong ZF. Jian S. Zhu CJ. Ginkgo biloba extract reduces endothelial progenitor-cell senescence through augmentation of telomerase activity. Journal of Cardiovascular Pharmacology. 49(2):111-5, 2007. Our previous studies have shown that Ginkgo biloba extract increased endothelial progenitor-cell (EPC) numbers and functional activity. However, the mechanisms remain to be determined. Recent studies have demonstrated that increased EPC numbers and activity were associated with the inhibition of EPC senescence, which involved activation of telomerase. Therefore, we investigated whether Ginkgo biloba extract inhibited the onset of EPC senescence through telomerase activation, leading to potentiation of cellular activity. After ex vivo cultivation, EPCs became senescent as determined by acidic ss-galactosidase staining. Ginkgo biloba extract dose-dependently prevented the onset of EPC senescence in culture. Moreover, Ginkgo biloba extract increased proliferation of EPCs as assessed by MTT assay and colony-forming capacity. To get further insights into the underlying mechanisms of these effects, we measured telomerase activity and determined the phosphorylation of Akt by Western blotting. Ginkgo biloba extract significantly increased telomerase activity and phosphorylation of the serine/threonine protein kinase Akt, a downstream effector of phosphoinositide 3-kinase (PI3K). Moreover, pretreatment with PI3K inhibitor, LY294002, significantly attenuated the Ginkgo biloba extract-induced telomerase activity. Taken together, the results indicated that Ginkgo biloba extract delayed the onset of EPC senescence, which may be related to activation of telomerase through the PI3k/Akt signaling pathway. The inhibition of EPC senescence by Ginkgo biloba extract in vitro may improve the functional activity of EPCs in a way that is important for potential cell therapy.
Welt K. Weiss J. Martin R. Hermsdorf T. Drews S. Fitzl G. Ginkgo biloba extract protects rat kidney from diabetic and hypoxic damage. Phytomedicine. 14(2-3):196-203, 2007. Ginkgo biloba extract EGb 761 was studied for its nephroprotective effects in experimentally diabetic and hypoxic rats. Duration of streptozotocin-induced diabetes was 4 months, that of respiratoric hypoxia of the diabetic group 20 min. The daily dose of 100 mg EGb/kg bodyweight started 1 month after induction of the diabetes. EGb reduced diabetes-induced morphological alterations of the kidney such as increase in volume of glomeruli, capillary tufts, urinary space, and thickening of Bowman's capsule basement membrane. Diabetically increased immunostaining of interstitial collagenes of types I, III, and VI was diminished by the EGb extract. EGb reduced the relative total SOD activity from 163% in diabetic kidney to 46%. Additional hypoxia-induced ultrastructural damage was also diminished.
Liu KX. Wu WK. He W. Liu CL. Ginkgo biloba extract (EGb 761) attenuates lung injury induced by intestinal ischemia/reperfusion in rats: roles of oxidative stress and nitric oxide. World Journal of Gastroenterology. 13(2):299-305, 2007. AIM: To investigate the effect of ginkgo biloba extract (EGb 761) on lung injury induced by intestinal ischemia/reperfusion (II/R). METHODS: The rat model of II/R injury was produced by clamping the superior mesenteric artery for 60 min followed by reperfusion for 180 min. The rats were randomly allocated into sham, II/R, and EGb + II/R groups. In EGb + II/R group, EGb 761 (100 mg/kg per day) was given via a gastric tube for 7 consecutive days prior to surgery. Rats in II/R and sham groups were treated with equal volumes of the vehicle of EGb 761. Lung injury was assessed by light microscopy, wet-to-dry lung weight ratio (W/D) and pulmonary permeability index (PPI). The levels of malondialdehyde (MDA) and nitrite/nitrate (NO2(-)/NO3(-)), as well as the activities of superoxide dismutase (SOD) and myeloperoxidase (MPO) were examined. Western blot was used to determine the expression of inducible nitric oxide synthase (iNOS). RESULTS: EGb 761 markedly improved mean arterial pressure and attenuated lung injury, manifested by the improvement of histological changes and significant decreases of pulmonary W/D and PPI (P < 0.05 or 0.01). Moreover, EGb 761 markedly increased SOD activity, reduced MDA levels and MPO activity, and suppressed NO generation accompanied by down-regulation of iNOS expression (P < 0.05 or 0.01). CONCLUSION: The results indicate that EGb 761 has a protective effect on lung injury induced by II/R, which may be related to its antioxidant property and suppressions of neutrophil accumulation and iNOS-induced NO generation. EGb 761 seems to be an effective therapeutic agent for critically ill patients with respiratory failure related to II/R.
Yamamoto Y. Adachi Y. Fujii Y. Kamei C. Ginkgo biloba extract improves spatial memory in rats mainly but not exclusively via a histaminergic mechanism. Brain Research. 1129(1):161-5, 2007. In order to clarify the mechanism of Ginkgo biloba extract (GBE) on learning and memory, we studied the effect of GBE on spatial memory deficits induced by diphenhydramine, pyrilamine and scopolamine using the eight-arm radial maze performance of rats, in comparison with donepezil. Total error (TE), reference memory error (RME) and working memory error (WME) were used as indices of spatial memory deficits. Both GBE and donepezil caused a potent antagonistic effect on the increase in TE, RME and WME induced by diphenhydramine. GBE and donepezil also antagonized scopolamine-induced spatial memory deficits. Although the antagonistic effect of GBE on pyrilamine-induced spatial memory deficits was weak, a significant difference was observed with TE and WME. However, donepezil caused no antagonistic effect on pyrilamine-induced memory deficits. From these findings, we concluded that the effects of GBE are mainly contributable to cholinergic activity and perhaps partly due to a histaminergic mechanism.
Tunali-Akbay T. Sener G. Salvarli H. Sehirli O. Yarat A. Protective effects of Ginkgo biloba extract against mercury(II)-induced cardiovascular oxidative damage in rats. Phytotherapy Research. 21(1):26-31, 2007. This study was designed to determine the possible protective effect of Ginkgo biloba extract (EGb) against Hg II-induced oxidative damage and also thromboplastic activity in the aorta and heart tissues. Wistar albino rats of either sex (200-250 g) were divided into four groups. Rats were injected intraperitoneally with (1) control (C) group: 0.9% NaCl; (2) EGb group: Ginkgo biloba extract (Abdi Ibrahim Pharmaceutical Company, Istanbul, Turkey) at a dose of 50 mg/kg/day; (3) Hg group: a single dose of 5 mg/kg mercuric chloride (HgCl(2)); and (4) Hg + EGb group: First day EGb at a dose of 50 mg/kg/day, i.p., 1 hour after HgCl(2) (5 mg/kg) injection; following four days EGb at a dose 50 mg/kg/day, i.p. After decapitation of the rats, trunk blood was obtained and serum tumor necrosis factor-alpha (TNF-alpha), lactate dehydrogenase (LDH) activity, and malondialdehyde (MDA) and glutathione (GSH) levels were analysed. In the aorta and heart tissues total protein, MDA, GSH levels and thromboplastic activity were determined. The results revealed that HgCl(2) induced oxidative tissue damage, as evidenced by increases in MDA levels and decreased GSH levels both in serum and tissue samples. Thromboplastic activity was increased significantly following Hg administration, which verifies the cardiotoxic effects of HgCl(2). Serum LDH and TNF-alpha were elevated in the Hg group compared with the control group. Since EGb treatment reversed these responses, it seems likely that Ginkgo biloba extract can protect the cardiovascular tissues against HgCl(2)-induced oxidative damage.
Fitzpatrick AL. Buchanan CK. Nahin RL. Dekosky ST. Atkinson HH. Carlson MC. Williamson JD. Ginkgo Evaluation of Memory (GEM) Study Investigators. Associations of gait speed and other measures of physical function with cognition in a healthy cohort of elderly persons. Journals of Gerontology Series A-Biological Sciences & Medical Sciences. 62(11):1244-51, 2007. BACKGROUND: Recent evidence suggests that physical decline and slower gait may be associated with early signs of dementia, but more information on healthy older adults is needed. METHODS: We determined associations between cognitive function, gait speed, and self-reported measures of physical function in 3035 healthy mobile participants of the Ginkgo Evaluation of Memory Study evaluated in 2000-2001. Gait speed was measured over a 15-foot course with participants walking at both their usual and rapid pace. Self-reported difficulties with Activities of Daily Living (ADLs) and other physical function tasks were also collected. Results of the Modified Mini-Mental State Examination (3MSE) determined cognitive function. RESULTS: The average age of the cohort was 78.6 years (standard deviation [SD] 3.3), and 53.9% of participants were men. Mean gait speed was 0.95 (SD 0.23) m/s at a usual pace and 1.35 (SD 0.58) m/s at a rapid pace. More than three-fourths of participants had 3MSE scores > 90. In multiple logistic models adjusted for demographics and comorbidities, risk of low cognition (defined as 3MSE score of 80-85) was almost twice as great for participants in the slowest quartile of the rapid-paced walking task than for the fastest walkers (odds ratio: 1.96, 95% confidence interval, 1.25-3.08). Associations between cognition and usual-paced walking were borderline, and no relationships were found with self-reported measures of physical function, including ADLs. CONCLUSIONS: In very healthy older adults, performance-based measures better predict early cognitive decline than do subjective measures, and tasks requiring greater functional reserve, such as fast-paced walking, appear to be the most sensitive in assessing these relationships.
Akiba S. Yamaguchi H. Kumazawa S. Oka M. Sato T. Suppression of oxidized LDL-induced PDGF receptor beta activation by ginkgo biloba extract reduces MMP-1 production in coronary smooth muscle cells. Journal of Atherosclerosis & Thrombosis. 14(5):219-25, 2007. AIM: An extract of Ginkgo Biloba L. was shown to have preventive effects on cardiovascular disorders, but the molecular mechanisms of its actions remain to be elucidated. Since matrix metalloproteinases (MMPs) are implicated in the rupture of atherosclerotic plaques and the subsequent occurrence of acute coronary syndrome, we examined the effects of a leaf extract (Ginkgolon-24) on the production of MMP-1 in human coronary smooth muscle cells stimulated with oxidized low-density lipoprotein (oxLDL) and 4-hydroxynonenal, which are factors proposed to play a pivotal role in atherogenesis. METHODS: The production of MMP-1 and phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 were estimated by immunoblotting. The tyrosine-phosphorylated form of platelet-derived growth factor receptor beta (PDGFR-beta) was analyzed by immunoprecipitation of the receptor followed by immunoblotting. RESULTS: oxLDL and 4-hydroxynonenal accelerated the production of MMP-1 with the preceding phosphorylation of ERK1/2 and PDGFR-beta;. Pretreatment with Ginkgolon-24 inhibited the production of MMP-1 and phosphorylation of ERK1/2 induced by oxLDL and 4-hydroxynonenal, but did not affect the production and phosphorylation induced by phorbol ester. Furthermore, Ginkgolon-24 prevented tyrosine phosphorylation of the receptor induced by oxLDL and 4-hydroxynonenal. CONCLUSION: These results suggest that Ginkgo Biloba extract suppresses the oxLDL- and 4-hydroxynonenal-induced production of MMP-1, probably through the inhibition of PDGFR-beta activation in human coronary smooth muscle cells.
Takuma K. Hoshina Y. Arai S. Himeno Y. Matsuo A. Funatsu Y. Kitahara Y. Ibi D. Hayase M. Kamei H. Mizoguchi H. Nagai T. Koike K. Inoue M. Yamada K. Ginkgo biloba extract EGb 761 attenuates hippocampal neuronal loss and cognitive dysfunction resulting from chronic restraint stress in ovariectomized rats. Neuroscience. 149(2):256-62, 2007. We have recently found that a combination of ovariectomy (OVX) and chronic restraint stress causes cognitive dysfunction and reduces hippocampal CA3 neurons in female rats and that estrogen replacement suppresses the OVX/stress-induced behavioral and morphological changes. In this study, we examined the effect of Ginkgo biloba extract (EGb 761), a popular herbal supplement, on the cognitive dysfunction and neuromorphological change in OVX/stress-subjected rats. Female Fisher 344 rats were randomly divided into three groups: vehicle-treated OVX, EGb 761 (50 mg/kg) -treated OVX and vehicle-treated sham-operated control groups. Two months after ovariectomy, all animals received restraint stress for 21 days (6 h/day), and were then subjected to a novel object recognition test followed by morphological examination by Nissl staining. EGb 761 was orally administered once daily until the behavioral analysis was done. Treatment with EGb 761 improved memory impairment and neuronal loss of hippocampus in the OVX/stress-subjected group in the same ways as 17beta-estradiol. On the other hand, EGb 761 did not affect the loss of bone mineral density and increase in body weight after OVX, although 17beta-estradiol attenuated them. These results have important implications for neuroprotective and cognition enhancing effects of EGb 761 in postmenopausal women and suggest that the effects are mediated by a different mechanism from estrogen.
Canter PH. Ernst E. Ginkgo biloba is not a smart drug: an updated systematic review of randomised clinical trials testing the nootropic effects of G. biloba extracts in healthy people. [Review] [27 refs] Human Psychopharmacology. 22(5):265-78, 2007. Here, we update our earlier systematic review of 2001, which critically evaluated the data from clinical trials to determine whether Ginkgo biloba enhances cognitive function in healthy subjects. Literatures searches of six computerised databases, updated to January 2007, were made for randomised, placebo-controlled, double-blind clinical trials of the effects of standardised Ginkgo biloba (G. biloba) extracts on cognitive function in healthy subjects under the age of 60 years. Trials published in any language were included, and data were extracted independently by the two authors following a standardised protocol. We include 15 randomised clinical trials of which 7 are single-dose studies and 8 are longer term studies with treatment periods ranging from 2 days to 13 weeks. Three single dose studies and 4 longer term studies are newly included. Several of the studies have methodological flaws. A number of the acute studies used multiple outcomes and report positive effects on one or more of these at particular time points with particular doses but these findings are either not replicated, or are directly contradicted by other studies. The evidence from longer term studies is largely negative. Of those studies which measured subjective effects, only one of five acute studies and one of six longer term studies reported any significant positive results. Overall, and in line with our previous conclusions, we have found no convincing evidence from randomised clinical trials for a robust positive effect of G. biloba ingestion upon any aspect of cognitive function in healthy young people, after either acute or longer term administration.
Huang X. Whitworth CA. Rybak LP. Ginkgo biloba extract (EGb 761) protects against cisplatin-induced ototoxicity in rats. Otology & Neurotology. 28(6):828-33, 2007. HYPOTHESIS: A standardized Ginkgo biloba extract, EGb 761, may have protective effect against cisplatin-induced ototoxicity in rats. BACKGROUND: Cisplatin-induced ototoxicity is a major dose-limiting side effect in anticancer chemotherapy. Cisplatin-induced ototoxicity has been correlated to depletion of the cochlear antioxidant system and increased lipid peroxidation. EGb 761 contains potent antioxidants capable of scavenging free radicals, inhibiting nitric oxide synthesis, reducing lipid peroxidation, and protecting against apoptosis. The purpose of this study was to investigate the effect of EGb 761 on cisplatin-induced ototoxicity in rats. METHODS: Male Wistar rats were divided into four groups and were treated as follows: 1) vehicle control; 2) cisplatin (13 mg/kg, intraperitoneally) plus vehicle; 3) EGb 761 (200 mg/kg, intraperitoneally); and 4) EGb 761 plus cisplatin. Auditory brainstem responses (ABRs) were measured pretreatment and 72 hours posttreatment, and threshold shifts were analyzed. Endocochlear potentials (EPs) were also obtained at 72 hours posttreatment. Cochleae were harvested and processed for scanning electron microscopy after completion of auditory testing. RESULTS: Cisplatin-treated rats showed significant ABR threshold shifts across all frequencies (click, and 2-, 4-, 8-, 16-, and 32-kHz tones) compared with each of the other groups (p < 0.001). Rats treated with EGb 761 plus cisplatin did not show significant ABR threshold shifts (p > 0.05). Similarly, the EPs of cisplatin-treated rats were decreased significantly approximately 50% in comparison with the other groups (p < 0.001). The EPs of EGb 761 plus cisplatin-treated rats were decreased less than 20% compared with vehicle control group or the EGb 761 only group (p < 0.01). The scanning electron microscopy observation indicated severe outer hair cell loss in the basal turn of cochleae of cisplatin-treated rats, whereas outer hair cells remained intact in the rats treated with EGb 761 plus cisplatin. CONCLUSION: These results demonstrate that EGb 761 protects against cisplatin-induced ototoxicity.
Scripnikov A. Khomenko A. Napryeyenko O. GINDEM-NP Study Group. Effects of Ginkgo biloba extract EGb 761 on neuropsychiatric symptoms of dementia: findings from a randomised controlled trial. Wiener Medizinische Wochenschrift. 157(13-14):295-300, 2007. In a randomised, double-blind, 22-week trial 400 patients with dementia associated with neuropsychiatric features were treated with Ginkgo biloba extract EGb 761 (240 mg/day) or placebo. Patients with probable Alzheimer's disease, possible Alzheimer's disease with cerebrovascular disease or vascular dementia were eligible if they scored 9 to 23 on the SKT cognitive test battery and at least 5 on the Neuropsychiatric Inventory (NPI). EGb 761 was significantly superior to placebo with respect to the primary (SKT test battery) and all secondary outcome variables. The mean composite score (frequency x severity) and the mean caregiver distress score of the NPI dropped from 21.3 to 14.7 and 13.5 to 8.7, respectively, in the EGb 761-treated patients, but increased from 21.6 to 24.1 and 13.4 to 13.9, respectively, under placebo (p < 0.001). The largest drug-placebo differences in favour of EGb 761 were found for apathy/indifference, anxiety, irritability/lability, depression/dysphoria and sleep/nighttime behaviour.
Wang J. Zhou S. Bronks R. Graham J. Myers S. Supervised exercise training combined with ginkgo biloba treatment for patients with peripheral arterial disease. Clinical Rehabilitation. 21(7):579-86, 2007. OBJECTIVES: To evaluate whether a combination of supervised exercise training and ginkgo biloba treatment is a better treatment than exercise training alone for patients with peripheral arterial disease. DESIGN: A 24-week double-blind, placebo-controlled ginkgo biloba trial with the first 12-week period as a non-exercise control stage and the second 12-week period as an exercise training stage. SETTING: Exercise physiology laboratory. SUBJECTS: Twenty-two subjects with peripheral arterial disease. INTERVENTIONS: The subjects were randomly allocated into a ginkgo or a placebo group. During the first stage, the ginkgo group ingested standardized ginkgo biloba tablets with a daily dosage of 240 mg, while the placebo group received placebo tablets. During the second stage, all subjects engaged in a supervised treadmill-walking programme while continuing to take the same dosage of ginkgo biloba or placebo tablets. MAIN MEASURES: Walking capacity on treadmill, oxygen consumption during exercise, peripheral haemodynamics and blood viscosity were measured at baseline, and after the first and the second stages of treatment. RESULTS: The ginkgo group did not show significant changes in most of the measured variables after each stage of treatment, except that the maximal walking time was significantly increased after the combined treatment (from 236 +/- 112 seconds to 557 +/- 130 seconds, P < 0.001). However, similar response was also found in the placebo group after exercise training (from 384 +/- 125 seconds to 820 +/- 146 seconds, P < 0.001). CONCLUSION: Supervised exercise training combined with ginkgo biloba treatment did not produce greater beneficial effects than exercise training alone in patients with peripheral arterial disease.
Tchantchou F. Xu Y. Wu Y. Christen Y. Luo Y. EGb 761 enhances adult hippocampal neurogenesis and phosphorylation of CREB in transgenic mouse model of Alzheimer's disease. FASEB Journal. 21(10):2400-8, 2007. Standardized Ginkgo biloba extract EGb 761 exhibits beneficial effects to patients with Alzheimer's disease (AD). It was previously demonstrated that EGb 761 inhibits amyloid beta (Abeta) oligomerization in vitro, protects neuronal cells against Abeta toxicity, and improves cognitive defects in a mouse model of AD (Tg 2576). In this study, the neurogenic potential of EGb 761 and its effect on cAMP response element binding protein (CREB) were examined in a double transgenic mouse model (TgAPP/PS1). EGb 761 significantly increases cell proliferation in the hippocampus of both young (6 months) and old (22 months) TgAPP/PS1 mice, and the total number of neuronal precursor cells in vitro in a dose-dependent manner. Furthermore, Abeta oligomers inhibit phosphorylation of CREB and cell proliferation in the hippocampus of TgAPP/PS1 mice. Administration of EGb 761 reduces Abeta oligomers and restores CREB phosphorylation in the hippocampus of these mice. The present findings suggest that 1) enhanced neurogenesis by EGb 761 may be mediated by activation of CREB, 2) stimulation of neurogenesis by EGb 761 may contribute to its beneficial effects in AD patients and improved cognitive functions in the mouse model of AD, and 3) EGb 761 has therapeutic potential for the prevention and improved treatment of AD.
Yao P. Li K. Song F. Zhou S. Sun X. Zhang X. Nussler AK. Liu L. Heme oxygenase-1 upregulated by Ginkgo biloba extract: potential protection against ethanol-induced oxidative liver damage. Food & Chemical Toxicology. 45(8):1333-42, 2007. Oxidative stress plays a pivotal role in the pathogenesis and progression of alcoholic liver disease (ALD) and HO-1 induction is suggested to protect hepatocytes from ethanol hepatotoxicity. Here, we present the data to explore the hepatoprotective effect and underlying mechanism(s) of Ginkgo biloba extract (EGB), a naturally occurring HO-1 inducer, against ethanol-induced oxidative damage. Ethanol-fed (2.4 g/kg) male rats were pretreated by EGB (48 or 96 mg/kg) for 90 days. Liver damage was evaluated by histopathology and serum aminotransferase assay. Hepatic redox parameters were measured by spectrophotometry. Heme oxygenase-1 (HO-1) expression was determined by RT-PCR and flow cytometry on mRNA and protein level, respectively. Our results showed that EGB, especially at high dose, ameliorated ethanol-induced macrovesicular steatosis and parenchymatous degeneration in hepatocytes, and decreased serum aminotransferases level. Furthermore, EGB reduced ethanol-derived glutathione depletion and lipid peroxidation, and inhibited the inactivation of superoxide dismutase, glutathione peroxidase and catalase, although EGB itself had no influence on such parameters. Importantly, EGB induced hepatic microsomal HO-1 on mRNA, protein expression and enzymatic activity, which is paralleled to the EGB-derived hepatoprotective effect. Hence, HO-1 upregulation by EGB may enhance the antioxidative capacity against the ethanol-induced oxidative stress and maintain the cellular redox balance.
Ramassamy C. Longpre F. Christen Y. Ginkgo biloba extract (EGb 761) in Alzheimer's disease: is there any evidence?. [Review] [126 refs] Current Alzheimer Research. 4(3):253-62, 2007. For centuries, extracts from the leaves of the Ginkgo biloba tree have been used as Chinese herbal medicine to treat a variety of health disorders. The standardized Ginkgo biloba extract EGb 761 was marketed in France and Germany 30 years ago for various vascular and cerebral deficits and is now classified as a food supplement in the United States. EGb 761 is currently the focus of phase-III clinical trials, GEM and GuidAge studies, to evaluate its efficacy on the prevention of Alzheimer's disease (AD) in subjects over 70 years old. This review summarizes recent advancements in our understanding of the potential role of EGb 761 in the prevention of AD. Besides its well-known free radical scavenging properties, the ability of EGb 761 to protect neurons probably also involves other intracellular pathways. We will point out potential targets of EGb 761 in the amyloid cascade such as its antiamyloidogenic properties or the regulation of gene expression. Moreover we will discuss the complexity of the cellular and molecular mechanisms of EGb 761 and the significance of the synergic effect of different constituents of EGb 761.
Wu Y. Li S. Cui W. Zu X. Wang F. Du J. Ginkgo biloba extract improves coronary blood flow in patients with coronary artery disease: role of endothelium-dependent vasodilation. Planta Medica. 73(7):624-8, 2007. Ginkgo biloba extract (GBE) has well-documented cardioprotective effects on coronary flow and positive effects on vasodilation through endothelium-derived nitric oxide in experimental animals, but these impacts in patients with coronary artery disease (CAD) have not yet been investigated. We designed this study to test the effects of GBE on distal left anterior descending coronary artery (LAD) blood flow and endothelium-dependent brachial artery flow-mediated dilation (FMD) in patients with CAD. Eighty CAD patients were randomly assigned to either GBE or saline (control) groups. LAD blood flow and brachial artery FMD were measured non-invasively using high-resolution ultrasound before and after intravenous administration of GBE or saline. GBE significantly increased LAD blood flow in maximal diastolic peak velocity (MDPV), maximal systolic peak velocity (MSPV) and diastolic time velocity integral (DTVI) compared with the control group (16.14 +/- 10.93 % vs. 0.28 +/- 2.14 %, 9.14 +/- 8.23 % vs. 0.79 +/- 2.56 %, and 15.23 +/- 7.28 % vs. 0.42 +/- 2.43 %, respectively, p < 0.01). Brachial artery FMD was also increased by 69.75 % (from 3.95 +/- 1.49 % to 6.55 +/- 2.51 %, p < 0.01). A linear correlation was found between the percentage changes in MDPV, MSPV, or DTVI of LAD blood flow and the percentage change in brachial artery FMD following treatment with GBE (r = 0.612, 0.486, or 0.521, respectively, p < 0.01). In summary, our data demonstrate that GBE treatment in CAD patients leads to an increase of LAD blood flow in MDPV, MSPV and DTVI, and the increase response might relate to the improved endothelium-dependent vasodilatory capacity. CAD: coronary artery disease DTVI: diastolic time velocity integral FMD: flow-mediated dilation GBE: GINKGO BILOBA extract LAD: distal left anterior descending coronary artery MDPV: maximal diastolic peak velocity MSPV: maximal systolic peak velocity NO: nitric oxide TTDE: transthoracic Doppler echocardiography.
Carlson JJ. Farquhar JW. DiNucci E. Ausserer L. Zehnder J. Miller D. Berra K. Hagerty L. Haskell WL. Safety and efficacy of a ginkgo biloba-containing dietary supplement on cognitive function, quality of life, and platelet function in healthy, cognitively intact older adults.[see comment]. Journal of the American Dietetic Association. 107(3):422-32, 2007. OBJECTIVE: To determine if a ginkgo biloba-containing supplement improves cognitive function and quality of life, alters primary hemostasis, and is safe in healthy, cognitively intact older adults. DESIGN: Four-month, randomized, double-blind, placebo-controlled parallel design. SUBJECTS/SETTING: Ninety men and women (age range 65 to 84 years) were recruited to a university clinic. Eligibility included those without dementia or depression, not taking psychoactive medications or medications or supplements that alter hemostasis. INTERVENTION: Ninety subjects were randomly assigned to placebo or a ginkgo biloba-based supplement containing 160 mg ginkgo biloba, 68 mg gotu kola, and 180 mg decosahexaenoic acid per day for 4 months. MAIN OUTCOME MEASURES: Assessments included: six standardized cognitive function tests, the SF-36 Quality of Life questionnaire, the Platelet Function Analyzer-100 (Dade Behring, Eschbom, Germany), and the monitoring of adverse events. STATISTICAL ANALYSES: Baseline characteristics and study hypotheses were tested using analysis of covariance. Tests were two-tailed with a 0.05 significance level. RESULTS: Seventy-eight subjects (87%) completed both baseline and 4-month testing (n=36 in placebo group, n=42 in ginkgo biloba group). At baseline, the participants' cognitive function was above average. One of six cognitive tests indicated significant protocol differences at 4 months (P=0.03), favoring the placebo. There were no significant differences in quality of life, platelet function, or adverse events. CONCLUSIONS: These finding do not support the use of a ginkgo biloba-containing supplement for improving cognitive function or quality of life in cognitively intact, older, healthy adults. However, high baseline scores may have contributed to the null findings. The ginkgo biloba product seems safe and did not alter platelet function, though additional studies are needed to evaluate the interaction of varying doses of ginkgo biloba and ginkgo biloba-containing supplements with medications and supplements that alter hemostasis.
Zhou YH. Yu JP. Liu YF. Teng XJ. Ming M. Lv P. An P. Liu SQ. Yu HG. Effects of Ginkgo biloba extract on inflammatory mediators (SOD, MDA, TNF-alpha, NF-kappaBp65, IL-6) in TNBS-induced colitis in rats. Mediators of Inflammation. 2006(5):92642. Inflammatory mediators play a critical role in ulcerative colitis immune and inflammatory processes. The aim of the study was to investigate the effects of Ginkgo biloba extract on inflammatory mediators (SOD, MDA, TNF-alpha, NF-kappaBp65, IL-6) in TNBS-induced colitis in rats. Colitis in rats was induced by colonic administration with 2,4,6-trinitrobenzene sulfonic acid (TNBS, 150 mg/kg). EGB in doses of (50, 100, 200 mg/kg) was administered for 4 weeks to protect colitis. The results showed that EGB could significantly ameliorate macroscopic and histological damage, evidently elevate the activities of SOD and reduce the contents of MDA, inhibit the protein and mRNA expressions of TNF-alpha, NF-kappaBp65, and IL-6 in the colon tissues of experimental colitis in a dose-dependent manner compared with the model group. We concluded that the probable mechanisms of EGB ameliorated inflammatory injury in TNBS-induced colitis in rats by its modulation of inflammatory mediators and antioxidation.
Domorakova I. Burda J. Mechirova E. Ferikova M. Mapping of rat hippocampal neurons with NeuN after ischemia/reperfusion and Ginkgo biloba extract (EGb 761) pretreatment. Cellular & Molecular Neurobiology. 26(7-8):1193-204, 2006. The neuroprotective effect of Ginkgo biloba extract (EGb 761) against transient forebrain ischemia following 7 days of reperfusion was studied in male Wistar rats after four-vessel occlusion for 20 min. 2. NeuN, a neuronal specific nuclear protein was used for immunohistochemical detection of surviving pyramidal neurons in the hippocampus, as well as counterstaining with hematoxylin in the same sections for detection of neurons that underwent delayed neuronal death and for glial nuclei staining. GFAP immunohistochemistry was used for detection of astrocytes in the studied area of CA1 region. 3. In the group of rats pretreated 7 days with Ginkgo biloba extract (EGb 761), following 20 min of ischemia and 7 days of reperfusion without EGb 761, increased number of NeuN immunoreactive cells were counted in the most vulnerable CA1 pyramidal layer of hippocampus. On the other hand, the group of rats with 7 days of EGb 761 pretreatment following 20 min of ischemia and 7 days of reperfusion with EGb 761 showed decreased number of surviving NeuN immunoreactive CA1 pyramidal cells in comparison with the first above-mentioned experimental group. 4. Increased number of reactive astrocytes immunolabeled for GFAP (Glial fibrilary acidic protein) was observed in both experimental groups in the stratum oriens and stratum lacunosum and moleculare. 5. Twenty minutes of ischemia is lethal for most population of CA1 pyramidal cell layer. Our results showed that prophylactic oral administration of Ginkgo biloba extract (EGb 761) in the dose 40 mg/kg/day during the 7 days protects the most vulnerable CA1 pyramidal cells against 20 min of ischemia.
Urikova A. Babusikova E. Dobrota D. Drgova A. Kaplan P. Tatarkova Z. Lehotsky J. Impact of Ginkgo Biloba Extract EGb 761 on ischemia/reperfusion - induced oxidative stress products formation in rat forebrain. Cellular & Molecular Neurobiology. 26(7-8):1343-53, 2006. Dysbalance in reactive oxygen/nitrogen species is involved in the pathogenesis of cerebral ischemia/reperfusion injury (IRI). Ginkgo biloba extract (Egb 761) pre-treatment was used to observe potential antioxidant/neuroprotective effect after global ischemia/reperfusion. Egb 761 significantly decreased the level of lipoperoxidation (LPO) in rat forebrain total membrane fraction (homogenate) induced by in vitro oxidative stress (Fe(2+)+H(2)O(2)). In animals subjected to four-vessel global ischemia for 15 min and 2-24 h reperfusion the EGb pretreatment slightly decreased LPO in forebrain homogenate. However, as detected in EGb treated group, the LPO-induced lysine conjugates are attenuated in comparison to non-treated IRI animals. EGb significantly improved parameters which indicate forebrain protein oxidative damage after IRI. The intensity of tryptophane fluorescence was increased by the 18.2% comparing to non-treated IRI group and bityrosine fluorescence was significantly decreased in ischemic (21%) and 24 h reperfused (15.9%) group in comparison non-treated IRI group. In addition, the level of total free SH- groups in pre-treated animals was significantly higher comparing to non-treated animals. Our results indicate that extract of EGb 761 has potent antioxidant activity and could play a role to attenuate the IRI-induced oxidative protein modification and lipoperoxidation in the neuroprotective process.
Ao Q. Sun XH. Wang AJ. Fu PF. Gong K. Zuo HC. Gong YD. Zhang XF. Protective effects of extract of Ginkgo biloba (EGb 761) on nerve cells after spinal cord injury in rats.[erratum appears in Spinal Cord. 2006 Nov;44(11):697 Note: Zuo, H-Z [corrected to Zuo, H-C]]. Spinal Cord. 44(11):662-7, 2006STUDY DESIGN: An experimental animal model was used to assess spinal cord injury following lateral hemitransection at thoracic spinal cord level. OBJECTIVE: To determine whether extract of Ginkgo biloba (EGb) could have a neuroprotective effect in spinal cord injury (SCI) in rats. SETTING: Department of Biological Sciences and Biotechnology, Tsinghua University, China. METHODS: A total of 72 adult rats were divided randomly into three groups: the EGb group, normal saline (NS) group, and sham operation group (sham group). After thoracic spinal cord hemitransection was performed at the level of the 9th thoracic vertebra (T9), rats in the EGb group were given 100 mg/kg EGb 761 daily, while rats in the NS group received NS. The rats in the sham group only underwent laminectomy without spinal cord hemitransection. At various time points after surgery, thoracic spinal cords were sampled and sliced for histochemistry, immunohistochemistry of inducible nitric oxide synthase (iNOS), and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) of apoptotic cells. RESULTS: Myelin staining showed that the area of cavities was small and the demyelinated zones were limited at and around the injury site of the spinal cord in the EGb group, while the area of cavities was large and the demyelinated zones were serious in the NS group. Nissl staining showed that the ratio of bilateral ventral horn neurons (transection side/uninjured side) in the EGb group was higher than that in the NS group (P<0.05). The apoptotic index and the percentage of iNOS-positive cells were lower in the EGb group than in the NS group. Furthermore, the percentage of iNOS-positive cells positively correlated with the apoptotic index (r( 2)=0.729, P<0.01) after SCI. CONCLUSION: This study demonstrated that EGb 761 could inhibit iNOS expression and have neuroprotective effect by preventing nerve cells from apoptosis after SCI in rats.
Al-Yahya AA. Al-Majed AA. Al-Bekairi AM. Al-Shabanah OA. Qureshi S. Studies on the reproductive, cytological and biochemical toxicity of Ginkgo Biloba in Swiss albino mice. Journal of Ethnopharmacology. 107(2):222-8, 2006. Ginkgo biloba (an herbal product), used as a folkloric medicine in the treatment of dementia, was evaluated for its effects on reproductive, cytological and biochemical toxicity in male Swiss albino mice. The mice were treated with different doses (25, 50 and 100mg/kg/day) of the aqueous suspension of Ginkgo biloba for 90 days by oral gavage. The following parameters were evaluated: (1) reproductive organ weight; (2) motility and content of sperms; (3) spermatozoa morphology; (4) cytology of the testes chromosomes; (5) study on reproduction; (6) biochemical study on proteins, nucleic acids, malondialdehyde (MDA) and nonprotein sulfhydryl (NP-SH). The treatment caused significant changes in the weight of caudae epididymis, prostate, chromosomal aberrations, rate of pregnancy and pre-implantation loss. However, the percent motility, sperm count and morphology of spermatozoa were not affected. Our study on biochemical parameters showed depletion of nucleic acids, NP-SH and increase of MDA, which elucidated the role of free radical species in the induced changes in testis chromosomes and the reproductive function. The exact mechanism is not known, however, the activation of GABA, glycine and glutamate under the influence of Ginkgo biloba and its constituents might have generated free radicals and depleted cellular glutathione by calcium influx and membrane depolarization. The observed toxicity is attributed to the toxic constituents (ginkgolic acids, biflavones, cardanols, cardols, bilobalides and quercetin) of Ginkgo biloba. Our results warrant careful use of Ginkgo biloba as a remedy for impotence and/or erectile dysfunction.
Schneider LS. DeKosky ST. Farlow MR. Tariot PN. Hoerr R. Kieser M. A randomized, double-blind, placebo-controlled trial of two doses of Ginkgo biloba extract in dementia of the Alzheimer's type.[see comment]. Current Alzheimer Research. 2(5):541-51, 2005. CONTEXT: Previous studies of Ginkgo biloba extract (GbE) in patients with various forms of cognitive impairment or dementia have shown promising results. OBJECTIVE: To determine the clinical efficacy of GbE in mild to moderate dementia of the Alzheimer type. DESIGN: Randomized, placebo-controlled, double-blind, parallel-group, multicenter trial. SETTING: Outpatient clinics of universities and private research centers specialized in dementia. PATIENTS: 513 outpatients with uncomplicated dementia of the Alzheimer's type scoring 10 to 24 on the Mini-Mental State Examination and less than 4 on the modified Hachinski Ischemic Score, free of other serious illnesses and not requiring continuous treatment with any psychoactive drug. INTERVENTION: 26-week treatment with GbE at daily doses of 120 mg or 240 mg or placebo. MAIN OUTCOMES: Cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-cog), Alzheimer's Disease Cooperative Study Clinical Global Impression of Change (ADCS-CGIC). RESULTS: There were no significant between-group differences for the whole sample. There was little cognitive and functional decline of the placebo-treated patients, however. For a subgroup of patients with neuropsychiatric symptoms there was a greater decline of placebo-treated patients and significantly better cognitive performance and global assessment scores for the patients on GbE. CONCLUSION: The trial did not show efficacy of GbE, however, the lack of decline of the placebo patients may have compromised the sensitivity of the trial to detect a treatment effect. Thus, the study remains inconclusive with respect to the efficacy of GbE.
Halil M. Cankurtaran M. Yavuz BB. Ozkayar N. Ulger Z. Dede DS. Shorbagi A. Buyukasik Y. Haznedaroglu IC. Arogul S. No alteration in the PFA-100 in vitro bleeding time induced by the Ginkgo biloba special extract, EGb 761, in elderly patients with mild cognitive impairment. Blood Coagulation & Fibrinolysis. 16(5):349-53, 2005. EGb 761 is widely used in the management of mild cognitive impairment in the elderly population. Elucidation of the effects of EGb 761 on primary haemostasis via PFA-100 could represent an important step for better understanding of the haemostatic safety of EGb 761. The purpose of this prospective study is to assess the effects of Ginkgo biloba special extract, EGb 761, on PFA-100 in vitro bleeding time in elderly patients with mild cognitive impairment. A total of 40 elderly patients aged 65-79 years who were referred for geriatric assessment and who were diagnosed as having mild cognitive impairment were included. Patients were started on 80 mg EGb-761 three times daily. The complete set of PFA-100 in vitro bleeding time and coagulation parameters including prothrombin time, activated partial thromboplastin time and International Normalized Ratio were assessed before and on the seventh day of treatment with EGb 761. There was no statistically significant prolongation in PFA-100 in vitro bleeding time or coagulation parameters in patients receiving EGb 761 after 7 days. The data about the safety of EGb 761 from the point of primary haemostasis in our elderly patient population with mild cognitive impairment casts hope for the future management of this 'difficult-to-treat' population with the promising Ginkgo extracts.