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A Review on Evidence Based Practice of Ginkgo biloba in Brain Health

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The brain is the platform for our mental health. But there is a growing body of evidence, and a number of significant voices are championing the role of diet in the care and treatment of people with mental health problems. Ginkgo biloba leaf extract has shown beneficial effect 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, vaso-occlusive disorders, and aging. The purpose of this chapter is to provide the mechanisms of action, clinical indications, and safety of Ginkgo biloba extract (GBE).
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International Journal of Chemical and Pharmaceutical Analysis
Volume 1, Issue 1, 2013, PP.24-30
www.ijcpa.in
24
Review Article
A Review on Evidence Based Practice of Ginkgo biloba in Brain Health
AR. Mullaicharam
Professor, Department of Pharmacy, Oman Medical College, Muscat, Sultanate of Oman
ABSTRACT
The brain is the platform for our mental health. But there is a growing body of evidence, and a number of significant voices are
championing the role of diet in the care and treatment of people with mental health problems. Ginkgo biloba leaf extract has
shown beneficial effect 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, vaso-occlusive disorders, and
aging. The purpose of this chapter is to provide the mechanisms of action, clinical indications, and safety of Ginkgo biloba extract
(GBE).
Key words: Ginkgo biloba, Pharmacology, Memory impairment, Safety issues, Dosage forms.
1. INTRODUCTION
The ginkgo tree (Fig.1) is having apricot shaped mature,
yellow color fruits1 the name ginkgo comes from the
Chinese words sankyo or yin-kuo, which means a hill apricot
or silver fruit. So the name ginkgo comes from the Chinese
words sankyo or yin-kuo.The family name of ginkgo tree is
Ginkgoaceae, which is in the class of Ginkgoatae. Englbert
Kaempfer, a German surgeon, first used the term “Ginkgo”
in 1712, but it was Linnaeus who termed it Ginkgo biloba in
1771.2
1.1 Botanical Information
Ginkgo biloba L. (Mantissa Plantarum Altera, 1771,
Ginkgoceae) belongs to the botanical family of Ginkgoceae.
The common names are Ginkgo,Kew tree,Ginkyo,Yinhsing
(Silver Apricot-Japanese) ,Maidenhair tree ,Fossil Tree
,Ginkgo Folium, Salisburia Adiantifolia3
The synonyms are Salisburia adiantifolia, Salisburia
macrophylla, and Pterophylla
salisburiensis. Today, nearly 500 scientific papers now
documenting Ginkgo's effects make it the well-researched
botanical medicine available. With 10 million prescriptions
written worldwide for Ginkgo biloba extract (GBE) in 1989
alone, and a 140% growth in the use of Ginkgo from 1997
to 1998, it is likely a plant medicine your patients are using
or considering.4,5
While firmly rooted in antiquity, GB is today the most
frequently prescribed herbal preparation in Germany and
one of the most commonly used over-the-counter (OTC)
herbal preparations in the United States6.The German
Commission Es (equivalent to the US Food and Drug
Administration for botanicals) has approved GB for
symptomatic treatment of deficits in memory,
concentration, and depression from organic brain disease7.
2. ACTIVE INGREDIENTS OF GINKGO BILOBA
EXTRACT
Ginkgo biloba, like most plant medicines contains many
active constituents, believed to have synergistic effects.
Flavonoids including quercetin, kaempferol, and
isorhamnetins; trilactonic diterpenes: Ginkgolide A,
Ginkgolide B, Ginkgolide C; a trilactonic sesquiterpene:
bilobalide; and proanthocyanidins are thought to afford
Ginkgo it's medicinal effects.5,8 Other constituents such as
Fig.1:
Ginkgo biloba
25
glucose, rhamnose, hydroxykinurenic, kynurenic,
protocatechic, vanillic, and shikimic acids, D-glucaric acid,
ginkgolic acid, and related alkyphenols have also been
isolated.8
The main active ingredients of ginkgo biloba
extract (GbE) are :
Flavonol and Flavone glycosides
Ginkgolides
Catechin
Diterpene lactones
Ascorbic acid
Iron-based superoxide dismutase
Sesquiterpenes
P-hydroxybenzoic acid
The dried green leaves from the ginkgo tree are used to
obtain the crude drug formulation of ginkgo.9
Flavonoids (including meletin, kaempferol and
isorhamnetin) and laetones (including ginkgolides and
bilobalide). GbE can remove free radicals, protect the
endothelial cells of blood vessels, block platelet activating
factors, and improve brain circulation10, 11. GbE has been
widely used in the treatment of dementia, cognitive
impairment, peripheral nerve problems, and vascular
tinnitus14. However, clinical studies about the efficacy of
GbE in the treatment of dementia have been inconclusive:
some studies report beneficial effects on cognition and
functioning.15, 16 while others do not.12, 15, 16.
There are two main pharmacologically active groups of
compounds present in the Ginkgo leaf extract.They are are
the flavonoids and the terpenoids17.
Flavonoids, also called phenylbenzopyrones or
phenylchromones, are a group of low molecular weight
substances that are widely spread in the plant kingdom.
Flavonoids present in the Ginkgo leaf extract are flavones,
flavonols, tannins, biflavones (amentoflavone, bilobetol, 5-
methoxybilobetol, ginkgetin, isoginkgetin and
sciadopitysin), and associated glycosides of quercitin and
kaempferol attached to 3-rhamnosides, 3-rutinosides, or p-
coumaric esters1. These compounds are known to
actmainly as antioxidants/free radical scavengers, enzyme
inhibitors, and cation chelators18.
In general, the bioavailability of flavonoids is relatively low
due to limited absorption and rapid elimination19.
Flavonoids in the glycosidic form are poorly absorbed in the
intestine; only in the aglycone form can they be absorbed
directly19. Once absorbed, flavonoids reach the liver where
they are metabolized to conjugated derivatives21 .It is
known that the biological activities of flavonoid metabolites
are not always the same as those of the parent
compound.20. There are no adequate studies determining
the dose of Ginkgo extract needed to achieve beneficial
effects, although the recommended dose of standardized
extract, EGb 761, is 40 to 60 mg, 3 to 4 times daily based on
clinical trials 24.
3. PHARMACOLOGICAL EFFECTS OF GINKGO BILOBA
Ginkgo leaf extract is having multifaceted
pharmacological activities. The Ginkgo leaf extract may
work through various mechanisms of action. Following
are the suggested mechanisms of the Ginkgo leaf extract
proved by various studies22.
Antioxidant effect, anti-platelet activating factor
(Anti-PAF) activity for cardio and cerebral
vascular diseases,
Inhibition of beta amyloid peptide (Aβ)
aggregation to reduce Alzheimer’s progression,
Decreased expression of peripheral
benzodiazepine receptor (PBR) for stress
Alleviation,
Stimulation of endothelium derived relaxing factor
to improve blood circulation23, 24, 18, 17.
A.
Ginkgolides A, B, and C, and bilobalide have been shown
to increase circulatory perfusion, antagonize platelet
activating factor (PAF), have neuroprotective effects, and
serve as cognitive activators. The flavone glycosides
possess antioxidant and mild platelet aggregation
inhibiting activities25,26,33.
GBE stimulates choline uptake in the hippocampus,
improves hypoxic tolerance, and glucose utilization28. It
also has membrane stabilizing and blood viscosity
lowering effects29.
Absorption of Ginkgo biloba in animal studies using
radiolabeled extract showed a 60% absorptive efficiency
following oral administration with peak serum levels at
1.5 hours supporting an upper GI absorption site31. The
flavonoids were found to accumulate in the aorta, eyes,
skin, and lungs; the heart muscle retained twice the
activity of a comparative volume of skeletal muscle, and
adrenal glands were also a site of accumulation31. Seventy
two hours post administration, the hippocampus and
26
striated bodies showed 5 times greater uptake than the
blood,27,30 while T1/2 for Ginkgolide A, B, and bilobalide
were 4.50, 10.57, and 3.21 hours respectively, supporting
the need for TID dosage31.
3.1 Mechanism of Actions
Ginkgo exhibits anti-inflammatory effects by interfering
with the release of inflammatory compounds by
competitively inhibiting the platelet-activating factor
(PAF). Ginkgo comprises ginkgolides A and B antagonists
that competitively inhibit the binding of PAF to the
membrane receptor that may exert neuroprotective and
antithrombotic effects. In addition, flavonoid glycosides
and ginkgolide B may inhibit the oxidization of lipoprotein
formation, platelet aggregation, and platelet adherence
that may reduce the events of atherosclerosis and
vascular injury. Furthermore, PAF antagonism may
prevent cyclosporin-induced nephrotoxicity, and decrease
coronary blood flow and myocardial contractility.
Additionally, this mechanism may provide beneficial
effects in circulatory diseases, hypersensitivity reaction,
and bronchospasm9,32,33.
Flavonoid glycosides may exert antioxidant effects that
may reduce endothelial cell injury due to free radical
oxidation thus decrease the development of
atherosclerosis. In addition, the ginkgo extract may offer
intestinal mucosa protection against ischemic injury by
decreasing neutrophil infiltration and lipid peroxidation,
stimulate choline uptake and prevent declination of age-
related muscarinic receptors, and decrease blood
viscosity9,32,33. Further, there is a potential inhibitory
effect of ginkgo on monoamine oxidase activity; however,
the mechanism of action is unclear.
3.2 Clinical Applications
3.2.1 Cerebrovascular Insufficiency
Quite a lot of studies have tested the efficacy of GBE for
improving status in those with cerebrovascular
insufficiency. In a double blind trial of 90 patients
conducted by Vesper and Hansgen over a twelve-week
course28.
Ginkgo was found to improve several clinical parameters of
measure including:
1) Patient attention in tasks requiring quick orientation and
readaptation, 2) for cerebral insufficiency, 3) Changes in the
patient's subjective performance, and 4) Changes in the
patient's objective behavior as observed by others.
The results of previous studies proved that GBE has
significantly superior effect than placebo in all parameters
measured.
The multicenter study carried out by Taillandier et al with
longitudinal design, performed under strict methodological
conditions, found GBE was effective against cerebral
disorders associated with aging in166 patients. Results
became statistically significant at 3 months, increased
during the following months, and were congruent with the
overall clinical assessment by the specialist in charge34.
Another study carried out by Grassel for 24-week duration
with 72 patients with cerebral insufficiency.The results
showed statistically significant improvements in short term
memory after 6 weeks, and learning rate (as measured by
psychometric testing) after 24 weeks35.
GBE produced improvement in parameters including: single
symptoms, total score of clinical symptoms, and global
effectiveness36.
3.2.2 Memory Impairment
While in a crossover study of 18 elderly men and women
(mean age 69.3 years), orally administered GBE was found
to significantly improve the speed of information
processing in dual-coding tests, a study of eight healthy
females found differences between GBE and placebo in
only one of three methods of evaluation.37,38
3.2.3. Alzheimer's disease and Multi-infarct Dementia
Several studies suggest that GBE may be helpful in treating
Alzheimer's disease and multiinfarct dementia, with few if
any side effects31.
A 1996 multicenter double-blind, placebo controlled
prospective study by Kanowski et al. evaluated 156 patients
with presenile and senile primary degenerative dementia of
the Alzheimer's type (DAT), and multi-infarct dementia
(MID) who used either GBE 120mg bid or placebo for 24
weeks. A multidimensional evaluation approach using
objective variables of Clinical Global Impressions (CGI) for
psychopathological assessment, Syndrome-Kurztest(SKT)
for assessment of attention and memory, and Nurnberger
Alters-Beobachtungsskala (NAB) for assessment of activities
of daily life were used. Efficacy was defined as response in
at least two of the three variables. Within a conservatively
defined response criterion, 28% of the GBE group
responded vs. 10% in the placebo group. Similar effects
were noted with GBE in both types of dementia with a
slightly better response for those with DAT. Five patients
reported minor side effects of skin reactions,
gastrointestinal complaints, and headache.40
GBE also ranked superior in self-rated activities of daily
living, improvement of the most prominent symptom, and
decrease in depression, demonstrating GBE efficacy on
behavioral, psychopathologic, and psychometric planes41.
3.2.4. Prevention of Neurodegenerative Diseases
Alzheimer’s disease is a form of dementia that
progressively deteriorates intellectual
capacity of various domains of the brain, particularly with
aging42 . Alzheimer’s disease affects about 4% of the
population over 65 and 20% of those over 80.43 Research
27
has now found links between Alzheimer’s disease and
deposition of amyloid beta peptide (Aβ)44, 4 5, 46. Aβ is a
polypeptide with 39 to 43 amino acid residues and a major
component of senile plaques and vascular amyloid deposits
of the brains of patients suffering from Alzheimer’s disease.
Ginkgo leaf extract is known to inhibit the formation of
from β-amyloid precursor protein (APP), a crucial process in
the pathogenesis of Alzheimer’s disease46. Formation of
amyloid precursor protein has been indirectly linked to high
cholesterol levels 47,48,49. It has been postulated that the
inhibition of is through the Ginkgo leaf extract’s ability
to compete with free cholesterol for interaction with Aβ
and thereby decrease their aggregation46. Alternatively, the
Ginkgo leaf extract inhibits ROS accumulation induced by
Aβ (particularly flavonol quercitin) and also reduces neuron
apoptosis, where apoptosis is considered to be one of the
main causes for neurodegenerative diseases44, 45, 50, 51 and
thus help to relieve Alzheimer’s disease. Ginkgolide B and
bilobalide are reported to inhibit apoptosis induced by
staurosporine (alkaloid anticancer drug) and serum
deprivation50. Bilobalide also prevented DNA fragmentation
due to hydroxyl radical β-amyloid and hydrogen peroxide50.
3.2.5. Resistant Depression
In the GBE group, the median Hamilton Depression Scale
scores dropped from 14 to a remarkable 7 in four weeks,
then to 4.5 by week eight. Only a one-point drop occurred
in the placebo group. Overall cognitive function was
improved, and no side effects were reported showing
potential therapeutic benefit of GBE in resistant
depression28.
Table 1 shows overview of various clinical studies carried
out by using Ginkgo extract7.
Table 1: Overview of Clinical Studies
Authors Symptoms Outcome Measures Dose/Duration
Allain et al
Memory impairment
Dual
-
coding task (information processing)
320 or 600 mg. 1 h prior to testing
Arrigo and Cattaneo Cerebrovascular insufficiency
Wechsler Adult Intelligence Scale (WAIS), block design,
word recognition; Rey’s complex figure, memory;
Spielberg State-Trait Anxiety Inventory
120 mg/d for 45 days
Bruchen et al
Aging, cerebral insufficiency
Figure connection test
50 mg TID for 12
weeks
Deberdt Cognitive impairment Memory 160mg/d one time
Eckmann Cerebral insufficiency Concentration, fatigue, cerebral function 160mg/d for 6 weeks
Eckmann et aI Cerebrovascular insufficiency Dizziness, motor activity, speech comprehensi on /
pro duc
tion, depression
Tebonin forte drops, 60/d for 30
days
Hamann Vestibular disorder
Vertigo, body sway amplitude 4 drops mice/d
Hartmann and Frick Vascular dementia Psychometric tests 20mL TID solution 3month
Hofferberth
Senile dementia
Memory, attention
, psychomotor, physiology
80mg TID
Kanowski et al Alzheimer’s and multi-infarct
dementia Syndrome short test, attention and memory EGb761 and placebo: 24Omg / d
BID
Le Bars et aI Alzheimer ’s disease, multi-infarct
dementia
Alzheimer ’s disease Assessment Scale-Cognitive
subscale (ADAS-Cog), Geriatric Evaluation by Relative
Rating Instrument (GERRI) 120 mg/d for 52 weeks
Maier-Hauff Subarachnoid hemorrhage,
cerebral insufficiency Reaction time, attention, short term memor y,
accuracy 150mg / d LI 1370 for 12 weeks.
Mancini et al Psychoorganic senile
dementia SCAG scale. Toulouse-Pieron cancellation 80 mg ID for 6weeks
Rai et al Memory impairment
Kendrick Digit Copying and Learning (KDC and KDL) task;
digit recall task, P300 latency 40 mg TID for 12 - 24weeks
Wesnes et al Idiopathic cognitive
impairment
Recall, reaction time, recognition. Crichton geriatric
rating scale
Tanakan: 120 mg /d
for 12 weeks
Abbreviations: R, randomized; DB, double-blind; SB, single-blind; RPC, randomized placebo-controlled; PC, placebo-controlled; TID, three
times a day; BID, twice a day.
Table 2 shows Dosage of Ginkgo extract and duration of administration required by Etiology/ Symptom and Adverse events7.
28
Table 2 : Dosage and duration classified by Etiology/ Symptom and Adverse events.
Indications/Symptoms Dosage Duration
Cerebral 400 mg / d; 3.5mg / mL 3 weeks to 13 month
Cerebrovascular 101- 200 mg/d; O-60 drops/d 3weeks to 3month
Information processing 600 mg / d 3 months to 6 months
Dementia 200 mg / d 5 weeks to 3 months
Hypoxia 1-10 ml / d 2 weeks
lschemia 100 mg / d: 0 -150g/m l/d 7-9 weeks
Vestibular 101-200 mg / d 3 weeks to 9 weeks
Subarachnoid Hemorrhage
101
-
200 mg / d
3 months
Memory 150 mg/d to 320 mg/ d 24 hours to 24 weeks
Memory impairment 50 mg three times daily 6 months
Table 3: Investigator, Isolated Component, and Activity7
Investigator
Isolated Component
Function
Barth et al (1991) Flavone Inhibits lipid peroxidation
Ramassamy et al (1992) Flavone Mediates 5-HT uptake
Gryglewski et al (1987) Flavone Inhibits platelet aggr e gation
Coeffler (1998) Ginkgolide B Anti-platelet activating factor properties
Janssens et al (1995) Bilobalide Delays onset of hypox ic glycolysis
Amri et al (1996) Bilobalide, Ginkgolide A, Ginkgolide B Induces PBR downregulation; increases ACTH
concentration.
Abbreviations: 5-HT. serotonin; PBR, peripheral benzodiazepere-type receptor; ACTH, adrenocorticotropic hormone.
4. SAFETY ISSUES
Based on previous studies33, it was proved that Ginkgo
Biloba is relatively safe. There have been very few reported
cases of adverse effects, which included stomach
complaints, dyspepsia, and nausea. It is likely to be unsafe
to use gingko intravenously due to severe adverse effects
and has been withdrawn from the market. Due to inhibiting
effects of ginkgo on platelet activating factors it raises great
concerns during perioperative stage. Further, safety in
pregnancy and lactation is unclear due to lack of reliable
information; thus, it may be better to avoid using this
product completely. The use of ginkgo is relatively safe
however it is not commonly prescribed by providers due to
unregulated sales of herbal products that may have been
exposed to adulterants, variable dosing, and heavy metal
toxicity.
5. CONCLUSION
Ginkgo biloba extract (GBE) is used for effective brain
function. Various research studied were carried out to find
its phytomedicines and its efficacy under many conditions.
Many research reports regarding the use of GBE in
cerebrovascular insufficiency, memory impairment in the
elderly, Alzheimer’s disease, multi-infarct dementia,
resistant depression, peripheral artery insufficiency, venous
insufficiency, and asthma is well supported by multiple
studies. GBE for tinnitus, schizophrenia, psychotic organic
brain syndrome, vertigo of undetermined origin, and PMS,
although less supported, still deserves serious
consideration because of GBE’s high tolerability, and the
limited or complete lack of efficacy with conventional
treatments for these conditions.28 Specifically, further
research is needed in the following areas: (1) dose-
response characteristics;(2) quantification of bioavailability,
washout periods, and long-term effects; (3) determination
of optimal timing for treatment interventions; (4)
examination of ways that GB can be used most effectively
as an adjunctive therapy, so that treatment effects are
optimized 20; (5) clearer delineation of the conditions for
which GB is most (and least) useful; and (6) examination of
possible drug interactions7. Before making informed clinical
decisions, physicians should be clear about the
mechanisms, indications, dose/duration ranges, and safety
history of GB in conjunction with the patient’s medical
history and current medications, which will provide very
effective beneficial effects.
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... Ginkgolides A, B, and C, and bilobalide have been shown to increase circulatory perfusion, antagonize platelet activating factor (PAF), have neuroprotective effects, and serve as cognitive activators. The flavone glycosides possess antioxidant and mild platelet aggregation inhibiting activities [15][16]. ...
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In the present review, we are highlighted various pharmacognostic and pharmacological aspects of the different parts of plant Ginkgo biloba. Leaves are mainly potential source of phytochemical constituents. The plant encompasses variety of pharmacological activities namely antioxidant, hypolipidemic, antibacterial, etc. The pharmacological profile of plant is mainly attributed to the presence of chemicals such as Ginkgolide A, Ginkgolide B, Ginkgolide C, Bilobalide, Ginkgotoxin, ginkgolides and bilobalide are the major constituents. The pills with the highest concentration of plant extract (100 mg) allow the intake of the highest antioxidants concentration. It is also used along with 5-flurouracil in cancer treatment. There is need to explore more activities of the plant.
... Kaemferol. [64] Ginkgo biloba extract shows neuroprotective property against 6-hydroxydopamine (6-OHDA) induced neurotoxicity in the nigrostriatal dopaminergic system i.e. Parkinson's disease in experimental animals. ...
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... Nutraceutical products based on bioflavonoids of Citrus are available for prevention as well as amelioration of cardiovascular problems. Ginkgo biloba has been traditionally used for treatment of memory impairment (Mullaicharam 2013). Several nutraceutical products based on this plant are available for treatment of dementia and improvement of memory (Chauhan et al. 2013). ...
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... Nutraceutical products based on bioflavonoids of Citrus are available for prevention as well as amelioration of cardiovascular problems. Ginkgo biloba has been traditionally used for treatment of memory impairment (Mullaicharam 2013). Several nutraceutical products based on this plant are available for treatment of dementia and improvement of memory (Chauhan et al. 2013). ...
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... However, as they are essential for reaching the full lifespan, they have been termed "lifespan essential" [6]. Standardized Ginkgo biloba extract (EGb) includes over 60 bioactive components, the most important being flavonoids and terpene lactones [7,8]. Due to their potent antioxidant properties, flavonoids, such as quercetin and kaempferol, can directly quench free radicals; however, through induction of cytochrome P450 enzyme system activity, they can also indirectly reduce free radical formation [4,9,10]. ...
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Extracts of Ginkgo biloba leaves, a natural source of flavonoids and polyphenolic compounds, are commonly used as therapeutic agents for the improvement of both cognitive and physiological performance. The present study was aimed to test the effects of a six-week supplementation with 160 mg/day of a standardized extract of Ginkgo biloba or a matching placebo on aerobic performance, blood antioxidant capacity, and brain-derived neurotrophic factor (BDNF) level in healthy, physically active young men, randomly allocated to two groups (n = 9 each). At baseline, as well as on the day following the treatment, the participants performed an incremental cycling test for the assessment of maximal oxygen uptake. Venous blood samples taken at rest, then immediately post-test and following 1 h of recovery, were analyzed for activities of antioxidant enzymes and plasma concentrations of non-enzymatic antioxidants, total phenolics, uric acid, lipid peroxidation products, ferric reducing ability of plasma (FRAP), and serum brain-derived neurotrophic factor (BDNF). Our results show that six weeks’ supplementation with Ginkgo biloba extract in physically active young men may provide some marginal improvements in their endurance performance expressed as VO2max and blood antioxidant capacity, as evidenced by specific biomarkers, and elicit somewhat better neuroprotection through increased exercise-induced production of BDNF.
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Ginkgo biloba also known as 'maidenhair tree' is a therapeutic herbal medicine consumed by people around the globe and is commonly used to treat neurological and cardiovascular disorders as well as neurological illnesses such as Alzheimer's disease, dementia, and cognitive impairment. As it is rich in vitamins and has a number of bioactive compounds which are helpful in treating many health-related issues. This review aims to cover the benecial side of Ginkgo biloba like its pharmacological effects, antidiabetic effects, anti-inammatory effects, and its role in treating diseases.
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Ginkgo biloba also known as ‘maidenhair tree’ is a therapeutic herbal medicine consumed by people around the globe and is commonly used to treat neurological and cardiovascular disorders as well as neurological illnesses such as Alzheimer’s disease, dementia, and cognitive impairment. As it is rich in vitamins and has a number of bioactive compounds which are helpful in treating many health-related issues. This review aims to cover the beneficial side of Ginkgo biloba like its pharmacological effects, antidiabetic effects, anti-inflammatory effects, and its role in treating diseases
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Aim: The study was conducted to evaluate the effect of Ginkgo biloba on serum uric acid level when used as add-on therapy to valsartan in hypertensive patients. Patients and Methods: The study was conducted in Private Clinics in Mosul City-Iraq, during a period of sixth months from 15 October 2017 to15 April 2018. The total number of patients enrolled in the study was 50 hypertensive patients using Valsartan mono-therapy of both sexes. The patients were administered Ginkgo biloba 80 mg twice daily and followed for 2 months duration. Their serum uric acid level was determined at baseline level and after 2 months from administration of Ginkgo biloba. Results: There was a significant reduction on serum uric acid level after two months from addition of Ginkgo biloba. Conclusions: This study revealed that Ginkgo biloba could be regarded as natural and relatively safe drug in reducing serum uric acid level.
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Background: Scopolamine can induce amyloid β accumulation, oxidative stress, synaptic loss, and learning/memory deficit as seen in Alzheimer’s disease. Ginkgo biloba extract increases neurogenesis and suppresses the happening of pathological processes and cognitive decline. Objectives: Herein, we explored the effect of Ginkgo biloba extract on scopolamine-induced congophilic amyloid plaque accumulation and neurons density in the rats’ brain. Methods: Ginkgo biloba extract (40 and 80 mg/kg/day) was injected daily intraperitoneally for seven days before and after the scopolamine injection (3 mg/kg) in protective and treatment group rats. At the end of the experiments, the rats’ brains were removed and fixed in 4% paraformaldehyde. After histological processing, Congo red staining was used to assess amyloid plaques while cresyl violet staining was employed to determine the neuron density. Results: The administration of scopolamine led to increased congophilic amyloid plaque density in the hippocampus and cingulate cortex of the rats. Pretreatment with Ginkgo biloba extract significantly decreased congophilic amyloid plaque numbers in the hippocampus and cingulate cortex. In addition, scopolamine could reduce the hippocampal and cingulate cortex neuron numbers compared to the control group rats. However, Ginkgo biloba extract increased the hippocampal and cingulate cortex neuron numbers before and after the injection of scopolamine. Conclusions: Our results showed that Ginkgo biloba extract could play protective roles against some scopolamine-induced Alzheimer’s disease-like pathologic dysfunctions, including amyloid β accumulation and neuronal loss, suggesting that treatment with Ginkgo biloba extract might be a promising prophylactic target for Alzheimer’s disease. Copyright © 2018, Jundishapur Journal of Natural Pharmaceutical Products.
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Ginkgo biloba L. has been used as a herbal medicine in the traditional treatment of insufficient blood flow, memory deficits, and cerebral insufficiency. The terpene trilactone components, the bioactive agents of Ginkgo biloba L., have also been reported to exhibit useful functionality such as anti-inflammatory and neuroprotective effects. Therefore, in the present research, we attempted to analyze quantitatively the terpene trilactone components in Ginkgo biloba leaf extract, with quantitative 1H NMR (qNMR) and obtained almost identical results to data reported using HPLC. Application of the qNMR method for the analysis of the terpene trilactone contents in commercial Ginkgo extract products, such as soft gel capsules and tablets, produced the same levels noted in package labels. Thus, qNMR is an alternative method for quantification of the terpene trilactone components in commercial Ginkgo extract products.
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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. 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). 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. Twice-daily dose of 120-mg extract of G. biloba (n = 1545) or placebo (n = 1524). Incident dementia and AD determined by expert panel consensus. 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). 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.
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Glucocorticoid excess has broad pathogenic potential including neurotoxicity, neuroendangerment, and immunosuppression. Glucocorticoid synthesis is regulated by ACTH, which acts by accelerating the transport of the precursor cholesterol to the mitochondria where steroidogenesis begins. Ginkgo biloba is one of the most ancient trees, and extracts from its leaves have been used in traditional medicine. A standardized extract of Ginkgo biloba leaves, termed EGb 761 (EGb), has been shown to have neuroprotective and antistress effects. In vivo treatment of rats with EGb, and its bioactive components ginkgolide A and B, specifically reduces the ligand binding capacity, protein, and messenger RNA expression of the adrenocortical mitochondrial peripheral-type benzodiazepine receptor (PBR), a key element in the regulation of cholesterol transport, resulting in decreased corticosteroid synthesis. As expected, the ginkgolide-induced decrease in glucocorticoid levels resulted in increased ACTH release, which in turn induced the expression of the steroidogenic acute regulatory protein. Because ginkgolides reduced the adrenal PBR expression and corticosterone synthesis despite the presence of high levels of steroidogenic acute regulatory protein, these data demonstrate that PBR is indispensable for normal adrenal function. In addition, these results suggest that manipulation of PBR expression could control circulating glucocorticoid levels, and that the antistress and neuroprotective effects of EGb are caused by to its effect on glucocorticoid biosynthesis.
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Eight healthy female volunteers were included in a double-blind, cross-over trial comparing Ginkgo biloba extract in acute and ascending doses (120, 240, 600 mg) with a placebo. One hour after treatment they were subjected to a battery of tests, including: critical flicker fusion, choice reaction time, subjective rating scale and Sternberg memory scanning test. No statistically significant differences with the placebo were observed in the first three tests. In contrast, short-term memory, as assessed by the Sternberg technique, was very significantly improved following 600 mg of Ginkgo biloba extract, as compared with the placebo. These results differentiate Ginkgo biloba extract from sedative and stimulant drugs and suggest a specific effect on memory processes.
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More than 10 years ago it has been demonstrated, that an extract of the leaves of Ginkgo biloba (EGb 761) clearly increased the local cerebral blood flow and the tolerance against hypoxia in rats and mice. Using various models of cerebral ischemia and cultured neurons in vitro ginkgolides A and B as well as bilobalide were shown to be neuroprotective. The ginkgolides are known to be antagonists of the platelet activating factor (PAF) and this activity could be responsible for their neuroprotective potency. Bilobalide reduced the infarct size after focal cerebral ischemiia of mice and rats more efficaciously than the ginkgolides A and B and was capable of protecting neurons and astrocytes against damage, however, its mechanism of action however is still unknown.
Article
Background: Dementia is a prevalent and disabling condition which still presents a therapeutic conundrum. There is increasing evidence to suggest that Ginkgo biloba might be a valuable therapeutic option. Aim: To update a systematic review, published in 1999, which assessed the clinical evidence of Ginkgo biloba extract as a symptomatic treatment for vascular dementia and Alzheimer's disease. Method: Computerised literature searches were performed to identify all randomized, double-blind, placebo-controlled trials of Ginkgo biloba for dementia. Databases were Medline, Embase, Biosis and the Cochrane Library. There were no restrictions regarding the language of publication. The screening of studies, selection, validation, data extraction and the assessment of methodological quality were performed independently by both authors. Results: One additional trial and five re-analyses of previously published data were located. The majority of the studies suggest that Ginkgo biloba is more effective than placebo in delaying the clinical deterioration of vascular dementia and Alzheimer's disease. Few, generally mild and transient adverse events were reported. Conclusion: Ginkgo biloba is a promising herbal medicine for the symptomatic treatment of vascular dementia and Alzheimer's disease.
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Absorption from the diet is normally a prerequisite for the potential in vivo beneficial role of flavonoids. Antioxidant activity of flavonoids in vitro has been the subject of several studies, and important structure–activity relationships of the antioxidant activity have been established. However, there is still debate about the stability and absorption of polyphenols under gastrointestinal conditions. Ginkgo biloba, a product well known for its flavonoid content, was chosen for this study. Ginkgo biloba leaves, standardised leaf extract EGb 761 and commercial tablets (containing EGb761) were incubated in simulated gastrointestinal fluids to determine the stability of their flavonoid profiles. The experiment was designed to mimic the human gut condition. HPLC analysis was then conducted to determine the resulting breakdown compounds and intact flavonoids after the incubation, thus indicating those compounds likely to be available for absorption. The different samples seem to react differently to the simulated digestion process. The results indicate a trend of conversion from the glycosides to the aglycones for some samples and subsequent degradation of the aglycones. This may indicate a need to further investigate the reported benefits of Ginkgo flavonoids as in vivo antioxidants and/or to consider the antioxidant activity of the resulting digestion-derived compounds.
Article
Background: Extracts of the leaves of the maidenhair tree, Ginkgo biloba, have long been used in China as a traditional medicine for various disorders of health. A standardized extract is widely prescribed for the treatment of a range of conditions including memory and concentration problems, confusion, depression, anxiety, dizziness, tinnitus and headache. The mechanisms of action are thought to reflect the action of several components of the extract and include increasing blood supply by dilating blood vessels, reducing blood viscosity, modification of neurotransmitter systems, and reducing the density of oxygen free radicals. Objectives: To assess the efficacy and safety of Ginkgo biloba for dementia or cognitive decline. Search strategy: The Specialized Register of the Cochrane Dementia and Cognitive Improvement Group (CDCIG), The Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL and LILACS were searched on 20 September 2007 using the terms: ginkgo*, tanakan, EGB-761, EGB761, "EGB 761" and gingko*. The CDCIG Specialized Register contains records from all major health care databases (The Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL, LILACS) as well as from many trials databases and grey literature sources. Selection criteria: Randomized, double-blind studies, in which extracts of Ginkgo biloba at any strength and over any period were compared with placebo for their effects on people with acquired cognitive impairment, including dementia, of any degree of severity. Data collection and analysis: Data were extracted from the published reports of the included studies, pooled where appropriate and the treatment effects or the risks and benefits estimated. Main results: 36 trials were included but most were small and of duration less than three months. Nine trials were of six months duration (2016 patients). These longer trials were the more recent trials and generally were of adequate size, and conducted to a reasonable standard. Most trials tested the same standardised preparation of Ginkgo biloba, EGb 761, at different doses, which are classified as high or low. The results from the more recent trials showed inconsistent results for cognition, activities of daily living, mood, depression and carer burden. Of the four most recent trials to report results three found no difference between Ginkgo biloba and placebo, and one found very large treatment effects in favour of Ginkgo biloba.There are no significant differences between Ginkgo biloba and placebo in the proportion of participants experiencing adverse events.A subgroup analysis including only patients diagnosed with Alzheimer's disease (925 patients from nine trials) also showed no consistent pattern of any benefit associated with Ginkgo biloba. Authors' conclusions: Ginkgo biloba appears to be safe in use with no excess side effects compared with placebo. Many of the early trials used unsatisfactory methods, were small, and publication bias cannot be excluded. The evidence that Ginkgo biloba has predictable and clinically significant benefit for people with dementia or cognitive impairment is inconsistent and unreliable.
Article
Several clinical trials have reported beneficial effects of the Ginkgo biloba extract EGb761 in the prevention and therapy of cognitive disorders including Alzheimer's disease (AD). The aim of the present long-term feeding trial was to study the impact of dietary EGb761 on Amyloid precursor protein (APP) metabolism in mice transgenic for human APP (Tg2576). Tg2576 mice were fed diets with and without EGb761 (300 mg/kg diet) for 1 and 16 months, respectively. Long-term treatment (16 months) with EGb761 significantly lowered human APP protein levels by approximately 50% as compared to controls in the cortex but not in the hippocampus. However, APP levels were not affected by EGb761 in young mice. Current data indicate that APP seems to be an important molecular target of EGb761 in relation to the duration of the Ginkgo biloba treatment and/or the age of the animals. Potential neuroprotective properties of EGb761 may be, at least partly, related to its APP lowering activity.