A placebo-controlled, double-blind, randomized trial of an extract of Ginkgo biloba for dementia. North American EGb Study Group

Pl, Le Bars; Mm, Katz; Berman, Nancy; Tm, Itil; Am, Freedman; Af, Schatzberg

doi:10.1001/jama.278.16.1327

Cited by 406 publications

(174 citation statements)

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“…A 1997 report described a double-blind, placebo-controlled, randomized trial of antioxidant extracts of Ginkgo biloba leaf in patients with mild to severe AD or multi-infarct dementia [159]. The study enrolled 309 participants who received either Ginkgo extract (120 mg/day) or placebo.…”

Section: Clinical Trials Of Antioxidantsmentioning

confidence: 99%

Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models

Sonnen¹,

Breitner²,

Lovell³

et al. 2008

Free Radical Biology and Medicine

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Section: Clinical Trials Of Antioxidantsmentioning

confidence: 99%

Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models

Sonnen¹,

Breitner²,

Lovell³

et al. 2008

Free Radical Biology and Medicine

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“…This is being investigated in a large RCT currently in progress in North America. A weakly positive RCT of gingko biloba extract in AD 143 has also led to a large US study now in progress.…”

Section: Antioxidantsmentioning

confidence: 99%

Preventing Dementia

Black

Patterson

Feightner

2001

Can. J. Neurol. Sci.

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Suppl. 1 -S56The concept of primary prevention of dementia is relatively new but will assume increasing importance as dementia prevalence increases in our graying population 1 and as the etiological factors and molecular pathogenetic mechanisms of primary degenerative dementias become better understood. 2Current definitions of dementia require memory impairment and cognitive dysfunction in at least one other domain of sufficient degree to interfere with social functioning.3 In this review we emphasize prevention of dementia in individuals who are cognitively normal but may be at risk for dementia, or who are cognitively impaired but not yet demented. Potential preventative measures include avoidance or control of modifiable risk factors to prevent progression to clinically manifest dementia. Secondary prevention of the degenerative dementias is equivalent to treatment, which is discussed in a companion article in this series. Recent clinical trials have provided evidence for modest symptomatic stabilization with socalled cognitive enhancing agents. If effective retardive therapies or neuroregenerative strategies are developed, in the future it may be possible to delay progression or even partially reverse dementing illness.ABSTRACT: Primary prevention will become increasingly important as dementia prevalence increases and effective retardive therapies are developed. To date, only one randomized controlled trial (involving treatment of systolic hypertension) has demonstrated that the incidence of dementia can be reduced. Physicians should remain alert to possible secondary causes of dementia and correct these whenever possible. Primary and secondary prevention of stroke should reduce dementia related to cerebrovascular disease either directly or as a comorbid factor in Alzheimer's disease (AD). Epidemiological studies have revealed a number of risk factors for AD including genetic mutation, susceptibility genes, positive family history, Down's syndrome, age, sex, years of education, head trauma and neurotoxins. In casecontrol studies non-steroidal anti-inflammatory medication and estrogen replacement therapy appear to decrease the relative risk of developing AD. Further research to develop and test preventative therapies in AD and other dementias should be strongly encouraged.RÉSUMÉ: Prévention de la démence. La prévention primaire va devenir de plus en plus importante à mesure que la prévalence de la démence augmente et que des stratégies efficaces pour en retarder l'apparition sont développées. Pour l'instant, une seule étude randomisée contrôlée (traitement de l'hypertension systolique) a démontré que l'incidence de la démence peut être réduite. Les médecins devraient demeurer vigilants pour détecter la présence causes secondaires de démence et les corriger si possible. La prévention primaire et secondaire de l'accident vasculaire cérébral devrait diminuer l'incidence de la démence reliée à la maladie cérébrovasculaire, soit directement ou comme facteur de comorbidité dans la maladie d'Alzheimer (MA). Des étud...

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“…These drugs have included acetylcholine precursors, muscarinic agonists, nicotinic agonists, andacetylcholinesterase inhibitors [9] . Herbal drugs are alsopre-clinically as well as clinically tested and shown to be very effective as Galantamine [19,20] , Ginkgo biloba [21,22] , Bacopa monnieri (brahmi) [23,24] , Celastrus paniculatus [25,26] , Curcumin [27][28][29] , coffee [30][31][32] and Lavender essential oil [33] . Many naturally occurring compounds have been proposed as potential therapies to slow or prevent the progression of AD, mostly by acting as antioxidants [34] , but also with some direct anti-amyloid actions [35] .…”

Section: Polyphenol Ellagic Acid-targeting To Brain: a Hidden Treasurementioning

confidence: 99%

Polyphenol Ellagic Acid-Targeting To Brain: A Hidden Treasure

Mehan¹,

Kaur²,

Parveen³

et al. 2015

International Journal of Neurology Research

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Alzheimer's disease is a severe neurodegenerative disorder that gradually results in loss of memory and impairment of cognitive functions in the elderly.Thedeposition of amyloid plaques is the primary event that leads to an oxidative and inflammatory reactions, neurofibrillary tangle formation, and ultimately neuronal death. The most prominent losses occur with cholinergic neurons that plays an important role in the formation of memory and cognitive functions. Insulin receptor numbers also altered, thusglucosemetabolism is defected in AD. Polyphenol ellagic acid (EA) possesses antioxidant, anti-inflammatory, anti-carcinogenic, anti-diabetic and cardioprotection activities.Activities of EA that are linked with protection of neuronal abnormalities like anti-depressant, antianxiety, anti-nociception. Ellagic acid inhibits β-secretase enzymatic activities, thus prevents the main pathologic hallmark of AD. There are varieties of herbal extracts and phytochemicals formulations extensively used to provide symptomatic relief to AD patients. Together these results our hypothesis that EA may prevent the neuronal dysfunctions as well as further work is also required to examine the pharmacological properties of EA in the protection of specially neurodegenerative disorder like AD. Here, we discuss how we can use the knowledge to improve treatment strategies of EA in AD and to explore the various signaling pathways involved in the progression of neuronal death.

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A placebo-controlled, double-blind, randomized trial of an extract of Ginkgo biloba for dementia. North American EGb Study Group

Cited by 406 publications

References 0 publications

Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models

Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models

Preventing Dementia

Polyphenol Ellagic Acid-Targeting To Brain: A Hidden Treasure

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