Ginkgo biloba Extract in Cognitive Disorders
Hakima Amri
Mones Abu-Asab
Pierre Le Bars
Janet Kastelan
The work of Pierre Le Bars, author of the Ginkgo biloba chapter from the first edition of Natural Medications for Psychiatric Disorders is gratefully acknowledged.
Ginkgo biloba is a unique tree of gymnosperms and the only surviving species within the prehistoric family Ginkgoaceae. Cooling temperatures following the Mesozoic Era may have been responsible for the steady decline of the geographic distribution of this tree, which was abundant throughout the entire northern hemisphere some 230 million years ago. While essentially extinguished from the wild, G. biloba likely owes its survival to Chinese gardeners, who grew it for its impressive appearance, extreme resistance to pests and diseases, exceptional longevity, and valuable fruits and timber. Its leaves and fruits have long been used in traditional Chinese medicine and were introduced into Western phytomedicine during the 1950s. In the past 30 years, methodical procedures of extraction and standardization allowed the production of a highly concentrated and stable extract of G. biloba (EGb 761), which could be systematically studied in scientific programs. Research on this extract provided replicable outcomes and consequently led to its integration in modern pharmacopoeia.
Today, EGb 761 is one of the most highly recognized herbal supplements with well-proven efficacy; it is recommended for managing symptoms associated with a range of neurologic and vascular disorders including dementia, arterial occlusive disease, retinal deficit, and tinnitus. EGb 761 is approved for the treatment of Alzheimer disease (AD) in Belgium, the Czech Republic, and Germany, also suggested for memory complaints in France and Spain, and was classified by the World Health Organization (WHO) as one among the available antidementia drugs (1). The complexity of EGb 761’s composition is matched by its multivalent effect. Its ability to up-regulate and down-regulate signaling pathways, gene transcription, cellular metabolism, and other biofunctions distinguishes it from single-action synthetic pharmaceuticals. The wide spectrum of action of EGb 761 confers the capacity to regulate the general physiology of the cell and organism simultaneously in response to stressors (2).
The WHO and Germany’s Commission E list the use of EGb 761 for the treatment of a number of clinical indications (3,4). Their combined list of symptoms include acrocyanosis (bluish discoloration of the extremities), depressive emotional condition, disturbances in concentration, dizziness, headache, memory deficits, postphlebitis syndrome (painful swelling of veins), Raynaud’s disease, and tinnitus. In addition, Germany’s Commission E states that the main uses of EGb 761 are primary degenerative dementia (mental degeneration due to aging), vascular dementia, and a combination of both.
This chapter focuses on the relevant data that explain EGb 761’s molecular and physiologic effects in relation to its use in the treatment of cognitive disorders. Ginkgo’s proposed role as an attenuator of antidepressant-induced sexual dysfunction will be discussed in Chapter 17.
STANDARDIZATION OF GINKGO BILOBA EXTRACT
Standardization of herbal remedies is an essential process for their dose consistency, reducing variability in treatment outcomes, and scientific study. Due to its cultivation in controlled plantations, the standardization of G. biloba extract is easier than many other medicinal plants. Since the leaves offer the majority of the therapeutic agents, harvest of the green leaves at a precise period in their maturation further reduces variability of the raw material and improves the standardization of the final extraction.
The extract is prepared from the dried green leaves through a 15-step procedure achieving a final ratio of starting dried plant material to finished native extract in the range of 35 to 67:1 (5). The process produces a consistent ratio of certain constituents: flavonoid glycosides (22% to 26%, including the three flavonol glycosides quercetin, kaempferol, and isorhamnetin), proanthocyanidins (6% to 10%), and the terpenoid ginkgolides (2.8% to 3.4%) and bilobalide (2.6% to 3.2%). The standardization process also reduces the concentration of ginkgolic acids, considered allergenic, to less than 0.005% (6). Overall, about 70% of the total constituents of the extract are systematically verified to ensure a consistent chemical ratio, regardless of the origin of the starting raw material. Such rigorous standardization follows a patented method that uses the name: extract of G. biloba EGb 761. The identical formulation and composition of EGb 761 extract is also found in Germany’s Tebonin forte (Dr. Willmar Schwabe pharmaceuticals, Karlsruhe), and France’s Tanakan (Beaufour-Ipsen pharmaceuticals, Paris). Most of the studies cited in this chapter have used EGb 761 in their experiments, either as a whole extract or its constitutive fractions.
BIOAVAILABILITY OF THE EGb 761 INGREDIENTS
Full understanding of the bioavailability of the bioactive ingredients of EGb 761 is still lacking (7). EGb 761 flavonol glycosides undergo an extensive metabolism in the human intestine and liver via phase I and phase II metabolism in these organs (8).
After an oral administration of EGb 761, intestinal hydrolysis, secondary secretion, and reabsorption of flavonoids limit their immediate bioavailability (8), while the ginkgolides and bilobalide are rapidly and totally absorbed. These terpenoids reach a maximum concentration in the blood within 1 to 2 hours with an average half-life of 3 to 4 hours (9). The flavonol glycosides are absorbed directly in the small intestine or undergo an extensive transformation by the colonic microorganisms before absorption (10). Using radioisotope-labeled EGb 761 in rats, it was shown that, after oral administration, the EGb 761 components or their metabolites are broadly distributed in the whole body (e.g., blood, liver, spleen, lung, heart, skin, vitreous humor), and to a lesser degree in the nervous system (11).
A comparison between animal and human pharmacokinetic data estimates that an oral dose of 50 mg per kg for the rat roughly corresponds to a dose of 240 mg for a human. Since this human dose is commonly recommended as a total daily regimen, effects obtained with higher doses in animal studies may not be relevant to substantiate the clinical effects observed at a normal dose in humans. On the other hand, a number of effects described during in vitro experiments may not be observed in human pharmacology.
GENERAL MODES OF ACTION OF EGb 761
A large volume of data is currently available from experimental and clinical research on EGb 761, which has been the main focus of research. However, sorting out the relevant data to substantiate the clinical effects of EGb 761 on the human central nervous system (CNS) is a
tedious process. This is mainly due to the complex composition of the extract, which includes numerous interacting agents that generate additive, synergistic, or antagonistic effects depending on the doses, the status of the targeted tissue, and the condition of the experiment (in vitro, ex vivo, or in vivo). Furthermore, when EGb 761 is administered orally in humans, some of the extract constituents may not be absorbed, while others are transformed by intestinal microorganisms and metabolized by the liver. This transformation results in a complex in vivo processing where EGb 761 is converted in part to numerous metabolites. Several pharmacologic activities attributed to the total extract still could not be credited to any one specific ingredient or to a particular mode of action. Currently, what is known of the effects of the whole extract surpasses what is known of the pharmacology of its components.
tedious process. This is mainly due to the complex composition of the extract, which includes numerous interacting agents that generate additive, synergistic, or antagonistic effects depending on the doses, the status of the targeted tissue, and the condition of the experiment (in vitro, ex vivo, or in vivo). Furthermore, when EGb 761 is administered orally in humans, some of the extract constituents may not be absorbed, while others are transformed by intestinal microorganisms and metabolized by the liver. This transformation results in a complex in vivo processing where EGb 761 is converted in part to numerous metabolites. Several pharmacologic activities attributed to the total extract still could not be credited to any one specific ingredient or to a particular mode of action. Currently, what is known of the effects of the whole extract surpasses what is known of the pharmacology of its components.
 Figure 10.1 • Effects of EGb 761. Summary of the beneficial effects of EGb 761 and related clinical outcomes. |
The beneficial health effects attributed to EGb 761 may in part be explained by four main classes of actions: (a) antioxidant and free radical scavenger [radical nitric oxide (NO), hydroxyl radical, and superoxide anion] (10); (b) antagonist of platelet-activating factor (PAF) (a potent proinflammatory lipid mediator eliciting a variety of cellular functions) (12); (c) vasomodulator (13); and (d) energy enhancer (5). These modes of action of EGb 761 are mostly interrelated in vivo and some of them may be the end result of common underlying processes (Fig. 10.1).
EGb 761 Is a Free-Radical Scavenger and Antioxidant
The free-radical scavenging and antioxidant properties of EGb 761 are extensively documented in vitro and ex vivo (13). Independent of the concentrations tested, EGb 761 very efficiently scavenges hydroxyl free radicals mainly with its flavonoid fraction (10). Its action against superoxide anions seems to be concentration-dependent and mostly related to its terpenoid fraction. A synergistic effect at low doses of EGb 761 is as potent as vitamin E in reducing lipid peroxidation, as observed with rat brain synaptosomes as well as human lymphocytes, and is only slightly less potent against DNA-oxidative damage. Reduction of lipid peroxidation as a result of free radical scavenging is an important aspect of EGb 761’s direct action against membrane insults that occur during various oxidative stressors (10).
EGb 761’s scavenging activity is enhanced by its ability to balance the cellular redox state (reduction/oxidation reactions within the cell). It has been shown to increase the protein level and activity of antioxidant enzymes such as catalase (CAT) and superoxide dismutase (SOD) in rat hippocampus and ileum; glutathione reductase and its rate-limiting enzyme gammaglutamylcysteinyl synthetase in mouse liver (14). EGb 761 reduced oxidative stress in the mitochondria, the main target of free radicals. It may also affect the membrane fluidity and indirectly change the functions of amine receptors or transporters. Such direct and indirect actions may explain the beneficial effects of EGb 761 in reducing apoptosis, and regulating receptor density and amine availability.
EGb 761 Is an Antagonist of Platelet-Activating Factor
Ginkgolides are the antagonists of PAF, a proinflammatory phospholipid synthesized by platelets, certain leukocytes, and endothelial cells during anaphylaxis, tissue insults, and shock (12). Ginkgolides specifically inhibit the binding of PAF to platelets, thus reducing thrombus formation only in relation to PAF release (ginkgolides did not show activity against adenosine diphosphate or other aggregating agents). In relatively high doses, ginkgolides can blunt PAF-induced F-actin polymerization and chemotaxis of macrophages (15), aggregation and degranulation of leukocytes, PAF-increased vascular permeability, extravasation, and hemoconcentration, and PAF-induced contraction of gastrointestinal and pulmonary smooth muscles.
Of the A, B, C, J, and M forms of ginkgolides, ginkgolide B is the most potent PAF antagonist. Since the total extract contains less than 1% of the B form (A and C are the most abundant), parenteral administration or ultrahigh oral doses of EGb 761 are needed to reach clinically significant PAF inhibition. This may explain the moderate anti-PAF effect at the peripheral level reported for the total extract, and the substantial differences observed among individuals. At the CNS level, PAF release is a proinflammatory process that induces free radicals and lipid peroxidation. The ginkgolides’ inhibition of PAF complements the free radical scavenging action of bilobalide and the flavonol glycoside fraction, thus reducing the oxidative stress and inflammatory responses during brain insults (e.g., inhibition of beta-amyloid-induced cell death). Such an effect is observed during hypoxia in animals receiving moderate doses of EGb 761 (50 mg per kg orally) resulting in an increased survival time and decreased neuronal loss. Furthermore, it has been shown to enhance the protection of neurons during ischemia and postischemic reperfusion phases, particularly by reducing postischemic neuronal damage at the hippocampus level.
EGb 761 Relaxes the Vascular Wall
The circulatory effects of EGb 761 include relaxation of the vascular wall, hematopoiesis, aortic contraction, and local cerebral blood flow. All these vasoregulatory effects depend largely on the status of the vascular tone, as well as the dose and its mode of administration. The proanthocyanidins fraction of EGb 761, in moderate and high doses, activates the release of NO from endothelial cells (14).
NO, a highly reactive free radical, is a messenger molecule produced by NO synthase (NOS) from L-arginine. It is a critical mediator of vasorelaxation in blood vessels. It diffuses into smooth muscle cells of the blood vessel and interacts with soluble guanylate cyclase to produce cyclic guanine monophosphate (cGMP). Because EGb 761 can protect cGMP from phosphodiesterase and NOS from free radical attacks, it induces vasorelaxation. In synergy with this proanthocyanidin effect, ginkgolides might reduce arteriolar spasm by the direct inhibition of PAF or thromboxane A2. In lower doses, EGb 761 has been shown to enhance norepinephrine-induced aortic contraction, possibly related to an increase of catecholamine
release (tyramine-like action), an inhibition of catechol-O-methyl transferase, or a direct action on the α-adrenoreceptors. With regard to the CNS, EGb 761 has been shown to increase local cerebral blood flow, reduce brain edema in animal models, and improve parameters of cerebral blood dynamics in three open studies with patients suffering from cerebrovascular diseases (14).
release (tyramine-like action), an inhibition of catechol-O-methyl transferase, or a direct action on the α-adrenoreceptors. With regard to the CNS, EGb 761 has been shown to increase local cerebral blood flow, reduce brain edema in animal models, and improve parameters of cerebral blood dynamics in three open studies with patients suffering from cerebrovascular diseases (14).
EGb 761 Has Energy-Enhancing Properties
In line with its vasomodulation properties, EGb 761’s action on cerebral metabolism depends on the health state of the model tested. In normal animals, moderate and high doses of EGb 761 decrease glucose utilization in various brain areas. During hypoxia and ischemia, EGb 761 restores oxidative metabolism, ion homeostasis, and increases glucose consumption. During cerebral edema induced by triethyltrin, bilobalide was shown to be the EGb 761 fraction that protects the cell metabolism against the uncoupling of oxidative phosphorylation, thus improving mitochondrial respiration, restoring glucose utilization, and increasing adenosine triphosphate (ATP) levels. EGb 761’s effects on metabolism act synergistically with the free-radical scavenging, antioxidant action, the PAF inhibition, and the circulatory modulation to result in CNS protection against the cytotoxicity induced by insults, including those occurring during a number of degenerative diseases.
SPECIFIC EFFECTS OF EGb 761 ON THE CNS
Our current understanding of EGb 761’s modes of action goes beyond its antioxidant and scavenging roles. Recent data indicate that EGb 761 affects the apoptotic processes, oxidation of amino acids, and modulates signaling cascades of several pathways (Fig. 10.1). This section outlines the various roles that EGb 761 plays at the molecular level.
EGb 761 Ameliorates the Effect of Apolipoprotein E-ε4 (APOE-ε4)
The APOE protein is mainly synthesized in the liver and transports lipoproteins, fat-soluble vitamins, and cholesterol into the lymph system and then into the blood, and may be controlling vitamin E levels in specific brain regions (16). The APOE gene is polymorphic producing three isoforms of the protein: APOE-ε2, APOE-ε3, and APOE-ε4. Only APOE-ε3 is normal; the other two are dysfunctional. While the role of APOE-ε4 in the cognitive or functional decline of AD is questionable (17), APOE-ε4 has been implicated in an increased susceptibility to AD where 40% to 65% of AD patients carry at least one copy of the four alleles, and are at greater risk than noncarriers for developing psychotic symptoms when AD dementia progresses (18).
EGb 761 Decreases Neuronal Loss by Affecting Apoptosis
Neuronal death by apoptosis is among the causes of decline in mental capacities. Their death occurs through a process of programmed cell death called apoptosis. It is established that apoptosis takes place in a cell when its pro-apoptotic proteins (e.g., Bax) increase in relation to anti-apoptotics (e.g., Bcl-2). EGb 761 decreased the Bax to Bcl-2 expression ratio in the hippocampus of senescing mice, thus protecting the aging hippocampus from moving down the apoptotic pathway (20).
EGb 761 Increases Density of Neuroreceptors
There are additional indirect effects on the CNS that have been reported in animal models. However, most of these actions are secondary to membrane stabilization and neuroprotective properties of the EGb 761, e.g., EGb 761 increased the density of neuroreceptors. This is due neither to a direct interaction with the receptor sites nor to a particular neurotransmitter system. Increased density was reported for serotoninIA and muscarinic, as well as α-adrenergic receptors, depending on the brain regions studied. Furthermore, these effects are widely dependent on the model tested, and it is most exclusively observed as a preventative effect in treated aging animal groups compared to the placebo (21).
EGb 761’s Effect on Cholinergic System
This system’s functionality affects memory processes, and its degeneration contributes to the neuropathologic features of normal aging and sporadic AD (22). The parasympathetic nervous system is entirely cholinergic dependent on the neurotransmitter acetylcholine, which together with norepinephrine maintains normal cerebral microvessel diameter and their supply of oxygen and glucose. In a rat model, EGb 761 blocked the decline of acetylcholine receptor in the hippocampus of old animals, but not younger ones. A recent study shows that EGb 761 promotes the development of acetyl cholinesterase-positive neurons in the rat embryonic basal forebrain (23).
EGb 761’s Effect on Dopaminergic System
Although EGb 761 does not affect the density of dopamine receptors in animal models, it inhibits the degeneration of dopaminergic neurons in the striatum, suggesting that it has a neuroprotection action. Membrane fluidity as well as the dopamine uptake system of a mouse striatum synaptosomal preparation was preserved upon treatment with EGb 761 (10). Its dopaminergic effect is related to its action on NO, since the latter has been shown to influence dopaminergic transmission in the striatum.
EGb 761’s Effect on Glutamatergic and GABAergic System
Glutamate plays a role in synaptic plasticity where it is stored in vesicles, and released upon nerve impulses. Therefore, it is assumed that it affects cognitive functions like learning and memory. Glutamate is the precursor for the synthesis of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). The levels of GABA and its synthesis-limiting enzyme, glutamic acid decarboxylase, were increased in mice hippocampus by bilobalide treatment. Because this treatment did not change the levels of glutamate, it resulted in an increased inhibitory neurotransmission.
6-Hydroxykynurenic acid (6-HKA), a derivative of kynurenic acid (KYNA) present in EGb 761, has a selective affinity to the glutamate ionotropic receptors NMDA and AMPA but with different rate for each. As an antagonist, 6-HKA inhibits excitotoxicity—an overactivation of the glutamate receptors that results in neural damage and death (24).
EGb 761 Affects Glucocorticoid Hormones
Glucocorticoids are a class of steroid hormones synthesized by the adrenal cortex. These hormones, especially cortisol, are known for their involvement in the stress response. However, when stress becomes chronic, the hypothalamic-pituitary-adrenal system responds via an adaptation process that promotes an increased release of stress hormones which in turn could lead to several pathogenic outcomes such as cardiovascular problems, gastrointestinal dysfunction, and immune suppression (25). The broad pathogenic potential of excessive amounts of glucocorticoid hormones includes neurotoxicity and neuroendangerment (26,27). Excess
glucocorticoid synthesis has been described as inflicting irreversible damage on hippocampal neurons that are critical to cognitive functions such as learning and memory (26,27). Furthermore, glucocorticoid-induced neurotoxicity and neuroendangerment has been reported to negatively affect neural development and accelerate aging (28,29).
glucocorticoid synthesis has been described as inflicting irreversible damage on hippocampal neurons that are critical to cognitive functions such as learning and memory (26,27). Furthermore, glucocorticoid-induced neurotoxicity and neuroendangerment has been reported to negatively affect neural development and accelerate aging (28,29).
It has been reported that EGb 761’s antistress potential is due to its effect on the glucocorticoid hormones (30). Thus, daily administration for 8 days of EGb 761 maintained corticosterone levels within the physiologic range in adult male rats. Amri et al. (31) reported that this was due to EGb 761’s effect on the peripheral-type benzodiazepine receptor (PBR) as demonstrated in vivo, ex-vivo, and in vitro at the protein and gene expression levels. PBR is a key regulatory element in glucocorticoids synthesis and its decreased expression by EGb 761 reflects on the stress hormones production. EGb 761’s action was found to be specific to the adrenal gland, as no effect on the PBR was observed in other organs tested, such as kidney and testis (32). If such actions are confirmed in humans, they may shed some light on the stress-alleviating effects of EGb 761, which have been reported in some studies concomitant with the improvement of cognitive performance (5). Furthermore, EGb 761 suppresses prednisolone-induced down-regulation of hippocampal type II glucocorticoid receptors, a process possibly involved in stress-induced cognitive impairment (5).
EGb 761’s Effect on Insulin
Insulin plays an important role in maintaining a healthy CNS. In addition to its production in the pancreatic beta cells, insulin is partially synthesized in the brain’s hippocampus, prefrontal cortex, entorhinal cortex, and the olfactory bulb. It is responsible for supplying the system with acetyl-CoA and its derivative acetylcholine, and stimulating neuronal insulin receptors. Insulin receptors in the brain occur in a high density in the olfactory bulb, hypothalamus, cerebral cortex, and hippocampus (22). Insulin and its receptors regulate cytoskeleton-associated pathways that are directly responsible for synaptic activity and plasticity (22).
Ingestion of 120 mg per day of EGb 761 for 3 months increased pancreatic beta-cell insulin production in both healthy humans with normal glucose tolerance and patients with type 2 diabetes mellitus, and that the dose did not produce insulin resistance in the non-diabetic or prediabetic subjects or exacerbate the symptoms in type 2 diabetic subjects (33). However, in the latter group with pancreatic exhaustion, it is not yet clear whether the increased pancreatic function was due to resuscitation of previously nonviable “exhausted” beta cells or increased sensitivity to glucose by the remaining viable islets in the pancreas.
EGb 761’s Effect on Pituitary Hormones
The pituitary gland, or hypophysis, is an endocrine gland located at the base of the brain, and is functionally linked to the hypothalamus. EGb 761 regulates two of its hormones in mice: growth hormone and prolactin, by increasing their mRNA expression. Both hormones induce proliferation and differentiation of brain cells, and affect memory, alertness, and other metal and physical capacities (14).
EGb 761’s Effect on Serotoninergic System
This system plays an important role in adaptive stress response, as well as behavioral and cognitive processes. While reduction of serotonin and its receptor has been associated with senescence, treatment with EGb 761 restores some plasticity of the serotoninergic system and interacts with signaling pathways controlling its activity in older rodents, thus contributing to stress alleviation (34). In old rats, EGb 761 increased serotonin levels in all brain parts (except pons), and reversed the age-related decrease of serotonin receptor. Its effects on the serotoninergic system are attributed to its ability to reduce lipid peroxidation and membrane damage, as well as modulate receptor synthesis (34).
Effects of EGb 761 on Axonal Cytoskeletal Proteins
There are two proteins, amyloid beta (Aβ) and tau, involved in the formation of the extracellular plaques and intracellular tangles of AD deposits (35). Aβ polymerizes to form insoluble extracellular deposits. Hyperphosphorylation of the tau protein (tau inclusions) results in the self-assembly of tangles of paired helical filaments and straight filaments (36). EGb 761 induces the overexpression of the phosphatase mRNA implicated in the dephosphorylation of the microtubules’ tau protein, thus preventing tau’s intracellular aggregation and the development of AD. EGb 761 plays a role in protecting cells from Aβ by preventing its polymerization (10)
CLINICAL PHARMACOLOGY AND EFFICACY DATA
There is a large body of data to support the efficacy of EGb 761 as a neuroprotector and an enhancer of neural functioning (Tables 10.1, 10.2 and 10.3). Evidence from biomedical research supports EGb 761’s effects on memory impairment, lack of concentration, cerebral vascular insufficiency, as well as age-related and dementia-related cognitive weaknesses (5). However, some clinical studies have produced inconclusive and mixed findings. Analysis of published results revealed at least three factors that could have been a source of discrepancy among studies: (a) the characteristics of the population studied, (b) the type of outcome measurements selected, and (c) the EGb 761 regimen tested in the trial. Each of these factors may be an important element affecting the research design.
The following section will outline the clinical implications of EGb 761 effects on (a) memory and neuropsychology, (b) mental disorders, and (c) CNS changes as measured by electrophysiology (Fig. 10.1, Tables 10.1, 10.2 and 10.3).
Memory and Neuropsychology
The process of memory formation and retrieval is associated with a set of complex cellular and molecular pathways. However, memory and neuropsychology provide a favorable domain to assess EGb 761 efficacy on cognitive processes, and to delineate the influence of the population characteristics and the adequate selection of outcome measurements (Tables 10.1 and 10.2). This efficacy was systematically demonstrated when the study population consisted of the elderly or of individuals with cognitively impaired baseline, and was rarely observed when the subjects were a group of young healthy volunteers (37, 38, 39, 40, 41, 42, 43). Assessments measuring accuracy and speed, which are mostly related to working memory, better demonstrated the effect of EGb 761 than the assessments that measured long-term storage and retrieval abilities (delayed recall and recognition), regardless of the study population. EGb 761 seems to enhance complex attention, the speed of information processing, and the rate of working memory. Performance tests using response times as outcome measurements are particularly desirable and are sensitive enough to assess these cognitive domains. This may explain why the EGb 761 effect was observed mostly on scanning speed (40,44), word recognition time (37), the rate of information processing, the duration (42), and time for dual coding (41).
Warot et al. (39) reported a striking positive effect of EGb 761 on a memory test that assessed the immediate recall of 20 pictures. They found out that the difference in the amount of material recalled was not due to an increase of performance in the EGb 761 group (mean recall of 15.5 pictures at baseline versus 15.6 pictures after 1 hour of the administration of 600 mg EGb 761) but rather to a statistically significant decrease of performance in the placebo group (15.7 pictures at baseline versus 13 at the 1 hour session). The authors concluded that EGb 761 might have a preventative, rather than a memory-enhancing, effect. But support for short-term enhancing of cognitive skills in healthy individuals comes from a 6-week trial of intact older subjects (55 to 86 years) and with a daily dose of 180 mg where Mix and Crews (45) found a significant improvement in speed processing ability, but not in objective memory measures when compared to the placebo group.
TABLE 10.1 Clinical Trials Using Electrophysiology to Assess Ginkgo biloba Efficacy | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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