[Is an animal a person? And are scientists always rational animals?].

An accumulation of scientific observations now challenges the idea that there is a huge difference between human beings and other animal species. There is no longer any need to assume that man possesses something special. Yet many scientists refuse to admit that this is so.

The extract of Ginkgo biloba EGb 761 reactivates a juvenile profile in the skeletal muscle of sarcopenic rats by transcriptional reprogramming.

Background: Sarcopenia is a major public health problem in industrialized nations, placing an increasing burden on public healthcare systems because the loss of skeletal muscle mass and strength that characterizes this affection increases the dependence and the risk of injury caused by sudden falls in elderly people. Albeit exercise and caloric restriction improve sarcopenia-associated decline of the muscular performances, a more suitable and focused pharmacological treatment is still lacking.

Methodology/principal Findings: In order to evaluate such a possible treatment, we investigated the effects of EGb 761, a Ginkgo biloba extract used in chronic age-dependent neurological disorders, on the function of the soleus muscle in aged rats.

Ginkgo biloba extract neuroprotective action is dependent on heme oxygenase 1 in ischemic reperfusion brain injury.

Background And Purpose: Ginkgo biloba extracts are now prescribed in several countries for their reported health benefits, particularly for medicinal properties in the brain. The standardized Ginkgo extract, EGb761, has been reported to protect neurons against oxidative stress, but the underlying mechanisms are not fully understood.

Methods: To characterize the oral consumption of EGb761 in transient ischemia, we performed the middle cerebral artery occlusion (MCAO) filament model in wild-type and heme oxygenase 1 (HO-1) knockouts.

Ginkgo biloba extract EGb 761 and Wisconsin Ginseng delay sarcopenia in Caenorhabditis elegans.

Previously we reported that the standardized Ginkgo biloba extract EGb 761 extended life span and increased stress resistance in Caenorhabditis elegans. In this study, pharmacological modulation of age-dependent muscle degeneration, or sarcopenia, was determined. Transgenic C.

Restoration of impaired phosphorylation of cyclic AMP response element-binding protein (CREB) by EGb 761 and its constituents in Abeta-expressing neuroblastoma cells.

Cyclic AMP response element-binding protein (CREB) plays important roles in neuronal plasticity and amyloid beta-peptide (Abeta)-induced cognitive impairment in Alzheimer's disease (AD). Here we demonstrated that Ginkgo biloba extract, EGb 761, displayed the neuron protective effect by activating the CREB signaling pathway. Wild-type neuroblastoma cells cultured in a conditioned medium containing cell-secreted Alphabeta exhibited reduced levels of phosphorylated CREB (pCREB).

Ginkgo biloba extract (EGb 761) in Alzheimer's disease: is there any evidence?

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.

Is antioxidant therapy a viable alternative for mild cognitive impairment? Examination of the evidence.

Therapeutic interventions for the prodromal stages of dementia are currently being sought with a view to delaying if not preventing disease onset. Uncertainty as to whether cognitive disorder in a given individual will progress towards dementia and adverse drug side effects has led to hesitancy on the part of drug regulators to instigate preventive pharmacotherapies. In this context, antioxidant therapies may provide a low-risk alternative, targeting very early biological changes.

EGb 761 enhances adult hippocampal neurogenesis and phosphorylation of CREB in transgenic mouse model of Alzheimer's disease.

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).

Amyloid-beta-induced pathological behaviors are suppressed by Ginkgo biloba extract EGb 761 and ginkgolides in transgenic Caenorhabditis elegans.

Amyloid-beta (Abeta) toxicity has been postulated to initiate synaptic loss and subsequent neuronal degeneration seen in Alzheimer's disease (AD). We previously demonstrated that the standardized Ginkgo biloba extract EGb 761, commonly used to enhance memory and by AD patients for dementia, inhibits Abeta-induced apoptosis in neuroblastoma cells. In this study, we use EGb 761 and its single constituents to associate Abeta species with Abeta-induced pathological behaviors in a model organism, Caenorhabditis elegans.

Protection by EGb 761 against beta-amyloid-induced neurotoxicity: involvement of NF-kappaB, SIRT1, and MAPKs pathways and inhibition of amyloid fibril formation.

Abeta peptide-induced toxicity is mediated through oxidative stress and is associated with an activation of intracellular signaling such as the redox-sensitive transcription factor NF-kappaB and MAPK pathways. We demonstrate on neuroblastoma cell line N2a that EGb 761 could prevent the activation of NF-kappaB, ERK1/2, and JNK pathways induced by Abeta. Furthermore, our results show that EGb 761 can also activate SIRT1.

Ginkgo biloba and neurodegenerative disorders.

The Gingko biloba extract EGb 761 has been the subject of many studies which confirm its usefulness for the prevention and treatment of neurodegenerative pathologies. These studies have focused on: a) the probable mechanisms of action that are involved in these disorders (including non-specific mechanisms implicated in diverse neurodegenerative disorders, particularly oxidative stress, or specific mechanisms such as those associated with beta-amyloid in Alzheimer's disease) and the processes of neuronal death; b) available animal models, and c) healthy individuals or those suffering from mild cognitive impairment or Alzheimer's disease. This data must be completed, particularly with regard to new knowledge about the pathogenesis of these disorders.

Amyloid precursor protein metabolism is regulated toward alpha-secretase pathway by Ginkgo biloba extracts.

Clinical trials report that Ginkgo biloba extracts (e.g., EGb761) reduce cognitive symptoms in age-associated memory impairment and dementia, including Alzheimer disease (AD).

Effect of Ginkgo biloba (EGb 761) on staurosporine-induced neuronal death and caspase activity in cortical cultured neurons.

Previous studies suggest the protective potentiality of Ginkgo biloba (EGb 761) against apoptotic cell death induced by hydroxyl radicals, staurosporine, serum deprivation and beta-amyloid (betaA) peptide. We have extended these observations to cultured cortical neurons and studied the effect of EGb 761 on neuronal survival (evaluated as MTT reduction), the presence of condensed nuclei (monitored as Hoechst staining), the time-course of caspase-1, caspase-3 and caspase-9 activation (measured by cleavage of specific fluorescent substrates) and superoxide anion production (evaluated by hydroethidine staining) after the exposure to staurosporine. Results show that 200 microg/ml of EGb 761 increased cell survival and reduced the number of condensed nuclei after the exposure to 200 nM staurosporine.

Expression of the small heat-shock protein Hsp16-2 in Caenorhabditis elegans is suppressed by Ginkgo biloba extract EGb 761.

EGb 761, a standardized extract of Ginkgo biloba leaves, has been shown to have antioxidative properties. We have previously demonstrated that EGb 761 increases stress resistance and mean life span in the model organism Caenorhabditis elegans. In this study, the molecular mechanism of EGb 761 on alleviating effects of oxidative stress is further investigated using transgenic C.

[Environmental factors of longevity].

A PROBABLE ROLE: The great increase in life expectancy over the past decades and too short a time lapse for any major genetic mutations to intervene, are arguments in favour of the intervention of environmental factors in longevity. A FAIRLY LONG LIST: Various environmental factors can be envisaged: prenatal environment, pollution, radiation and oncogenic agents, notably tobacco, food (quantitatively and qualitatively), medicinal products, stress, education and socio-professional life style, isolation, number of children and sexual activity, sports and exercising, etc. It is highly likely that all these factors, or at least some of them, have a real effect on longevity, although this is difficult to demonstrate directly.

Induction of heme oxygenase 1 by Ginkgo biloba in neuronal cultures and potential implications in ischemia.

Ginkgo biloba extract (EGb 761) is a standardized extract originating in traditional Chinese medicine. Ginkgo biloba dried leaves have been used for centuries to treat various neurological conditions. The constituents from the extract are likely to have synergistic effects that have been shown to be protective against oxidative stress injury.

Egb 761 in the postgenomic era: new tools from molecular biology for the study of complex products such as Ginkgo biloba extract.

The decoding of the human genome has completely changed our views on medicine. Beyond sequencing, tools of the postgenomic era may lead to a better understanding of various therapies, especially those with a complex effect on numerous cellular components and functions. The development of high-density oligonucleotide microarrays led to pioneer studies on the multiple gene expression effects exhibited by Ginkgo biloba extract EGb 761, changing traditional pharmacology and medicine concepts.

[Proteins and mutations: a new vision (molecular) of neurodegenerative diseases].

Neurodegenerative diseases have long been considered to be poorly defined, misunderstood, and inadequately treated. In recent years, research on Alzheimer's disease has led to numerous advances that have improved our understanding of this form of dementia and also of the entire category of neurodegenerative diseases. It now appears that numerous neurodegenerative diseases of the central nervous system correspond to the aggregation of specific proteins: beta-amyloid in Alzheimer disease, tau protein in Alzheimer disease, fronto-temporal dementia, progressive supranuclear palsy and corticobasal degeneration, alpha-synuclein in Parkinson disease and Lewy body dementia, PrP protein in prion diseases, SOD in amyotrophic lateral sclerosis, polyglutamine expansions in Huntington's disease and other diseases, etc.