The Efficacy of Ginkgo for Elderly People with Dementia and Age‐Associated Memory Impairment: New Results of a Randomized Clinical Trial

Dongen, M.C.J.M. van; Rossum, Erik van; Kessels, Alfons G.H.; Sielhorst, Hilde; Knipschild, Paul

doi:10.1111/j.1532-5415.2000.tb02589.x

Cited by 177 publications

(102 citation statements)

References 29 publications

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“…51,52 In addition, Curcumin was able to reverse the amyloid-induced neuropathology, along with its capacity to block amyloid polymerization. 53 Ginkgo biloba another natural product is largely used as a positive memory modulator 54 and it has been reported that shows prevention of age-related spatial memory deficits in a transgenic mouse model of AD. 55 Also, certain ingredients of green tea modulate APP cleavage sufficiently to reduce the Ab levels and amyloid plaques in AD mouse models.…”

Section: Discussionmentioning

confidence: 99%

Hyperforin prevents β-amyloid neurotoxicity and spatial memory impairments by disaggregation of Alzheimer's amyloid-β-deposits

Dinamarca¹,

Cerpa²,

Garrido

et al. 2006

Mol Psychiatry

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The major protein constituent of amyloid deposits in Alzheimer's disease (AD) is the amyloid b-peptide (Ab). In the present work, we have determined the effect of hyperforin an acylphloroglucinol compound isolated from Hypericum perforatum (St John's Wort), on Ab-induced spatial memory impairments and on Ab neurotoxicity. We report here that hyperforin: (1) decreases amyloid deposit formation in rats injected with amyloid fibrils in the hippocampus; (2) decreases the neuropathological changes and behavioral impairments in a rat model of amyloidosis; (3) prevents Ab-induced neurotoxicity in hippocampal neurons both from amyloid fibrils and Ab oligomers, avoiding the increase in reactive oxidative species associated with amyloid toxicity. Both effects could be explained by the capacity of hyperforin to disaggregate amyloid deposits in a dose and time-dependent manner and to decrease Ab aggregation and amyloid formation. Altogether these evidences suggest that hyperforin may be useful to decrease amyloid burden and toxicity in AD patients, and may be a putative therapeutic agent to fight the disease.

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Section: Discussionmentioning

confidence: 99%

Hyperforin prevents β-amyloid neurotoxicity and spatial memory impairments by disaggregation of Alzheimer's amyloid-β-deposits

Dinamarca¹,

Cerpa²,

Garrido

et al. 2006

Mol Psychiatry

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“…Recent epidemiological and dietary intervention studies in humans and animals suggest that flavonoids may play a useful role in preventing neurodegeneration, especially age-related cognitive, motoric, and mood decline and protect against oxidative stress as well as cerebral ischemia/ reperfusion injuries. Studies in humans using flavonoidcontaining plant extracts, such as Ginkgo biloba, or pure flavonoid preparations demonstrate positive effects on cognitive function and memory performance in healthy volunteers from all age groups [42,97,213] as well as in patients with age-or Alzheimer' disease-associated dementia [128,146,208]. Watanabe et al [211] reported that G. biloba supplementation in mice had neuromodulatory effects as indicated by a more than three-fold increase of mRNA expression for neuronal tyrosine/threonine phosphatases-1, microtubule-associated tau, prolactin, different calcium, and chloride channels as well as transthyretin.…”

Section: Flavonoids: Neuroprotective Agents In Vivo and In Vitro?mentioning

confidence: 99%

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

Schroeter

Boyd

Spencer

et al. 2002

Neurobiology of Aging

310

178

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Oxidative and nitrosative stress is increasingly associated with the pathology of neurodegeneration and aging. The molecular mechanisms underlying oxidative/nitrosative stress-induced neuronal damage are emerging and appear to involve a mode of death in which mitogen-activated protein kinase (MAPK) signaling pathways are strongly implicated. Thus, attention is turning towards the modulation of intracellular signaling as a therapeutic approach against neurodegeneration. Both endogenous and dietary agents have been suggested as potent modulators of intracellular signal transduction, e.g. nitric oxide and flavonoids, respectively. This review addresses recent findings on the biological effects of flavonoids and nitric oxide in neurodegeneration and aims to elucidate the rationale for their prospective use as modulators of cellular signal transduction. © 2002 Elsevier Science Inc. All rights reserved.Keywords: Apoptosis; Oxidative stress; Neuron; Flavonoids; MAP kinase; JNK; ERK; Epicatechin; Nitric oxide; Mitochondria; Redox status; Polyphenols Abbreviations: AKT, serine/threonine kinase (also known as protein kinase B); AP-1, activator protein-1; Apaf-1, apoptosis protease activating factor-1; ASK1, apoptosis signal-regulating kinase-1; Bad, Bcl-2/BclX Lassociated death promoting protein; Bax, pro-apoptotic protein of the Bcl-2 family; Bcl-2, B-cell lymphoma 2: protein with anti-apoptotic properties; BclX L , long form of Bclx: anti-apoptotic protein of the Bcl-2 family; Caspase, cysteinyl aspartic acid-protease; c-Jun, mammalian equivalent of Jun: part of the AP-1 transcription complex; CREB, cAMP response element binding protein; DIABLO/smac, mitochondria-related pro-apoptotic protein: inhibits XIAP; ERK1/2, extracellular signal-related kinase; Fas, CD95: member of the TNF receptor family; GSHST, glutathione Stransferase; JNK, c-Jun amino-terminal kinase; MAPK, mitogen-activated protein kinase; MAPKK, MAPK kinase; MAPKKK, MAPKK kinase; MEK1/2, ERK1/2-specific MAPKK; MKK4/7, JNK-specific MAPKK; MSK1, mitogen-and stress-activated kinase-1; NF-B, nuclear factor of immunoglobulin k locus in B-cells; ONOO − , peroxynitrite anion; p53, pro-apoptotic tumor suppressor gene product; PI3-kinase, phosphoinositol 3-kinase; Ras, small G-protein; RNS, reactive nitrogen species; ROS, reactive oxygen species; RSK, pp90 ribosomal S6 kinase; SAPK, stressactivated protein kinase; XIAP, X-linked inhibitor of apoptosis: inhibits the activation of caspase-9

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“…Even though the EGb761 is widely used in prescription drugs, the efficacy of EGb761 as a nootropic agent is somewhat controversial. Some clinical trials failed to find any improvement in older people with dementia or age-associated memory impairment (Van Dongen et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Extract of Ginkgo biloba EGb761 Facilitates Extinction of Conditioned Fear Measured by Fear-Potentiated Startle

Yang

et al. 2006

Neuropsychopharmacol

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A standard extract of Ginkgo biloba (EGb761) has been used in the treatment of various common geriatric complaints including vertigo, short-term memory loss, hearing loss, lack of attention, or vigilance. We demonstrated that acute systemic administration of EGb761 facilitated the acquisition of conditioned fear. Many studies suggest the neural mechanism underlies extinction is similar to the acquisition. This raises a possibility that EGb761 may modulate and accelerate the fear extinction process. We tested this possibility by using fearpotentiated startle (FPS) on laboratory rats. Acute systemic injection of EGb761 (10, 20, or 50 mg/kg) 30 min before extinction training facilitated extinction in a dose-dependent manner. Intra-amygdaloid infusion of EGb761 (28 ng/side, bilaterally) 10 min before extinction training also facilitated extinction. Control experiments showed that facilitation effect of EGb761 was not the result of impaired expression of conditioned fear or accelerated forgetting. Rats previously injected with EGb761 showed significant FPS after retraining. Extinction of conditioned fear appeared to result from acute drug effects rather than from toxic action. Systemic administration of EGb761 immediately after extinction training did not facilitate extinction, suggested the EGb761 facilitation effect is contributed to the acquisition phase of extinction learning. Western blot results showed that extinction induced amygdaloid extracellular signal-regulated kinase (ERK1/2) phosphorylation was significantly elevated by EGb761 treatment. Intra-amygdala injection of ERK1/2 inhibitor PD98059 completely blocked the EGb761 effect. Therefore, acute EGb761 administration modulated extinction of conditioned fear by activating ERK1/2.

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The Efficacy of Ginkgo for Elderly People with Dementia and Age‐Associated Memory Impairment: New Results of a Randomized Clinical Trial

Abstract: OBJECTIVES: To evaluate the efficacy, the dose-dependence , and the durability of the effect of the ginkgo biloba special extract EGb 761 (ginkgo) in older people with dementia or age-associated memory impairment.

Cited by 177 publications

References 29 publications

Hyperforin prevents β-amyloid neurotoxicity and spatial memory impairments by disaggregation of Alzheimer's amyloid-β-deposits

Hyperforin prevents β-amyloid neurotoxicity and spatial memory impairments by disaggregation of Alzheimer's amyloid-β-deposits

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

Extract of Ginkgo biloba EGb761 Facilitates Extinction of Conditioned Fear Measured by Fear-Potentiated Startle

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