Purification of a new neurotrophic factor from mammalian brain.

Barde, Yves‐Alain; Edgar, David; Thoenen, H.

doi:10.1002/j.1460-2075.1982.tb01207.x

Cited by 1,614 publications

(757 citation statements)

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“…Specifically, soluble Aβ oligomers are fundamental to promote neurotoxicity (Klein, 2001; Walsh & Selkoe, 2007) through different ways (Ferreira & Klein, 2011; Pearson‐Leary & McNay, 2012), including altered levels of neurotrophic factors (NTFs) (Calissano et al ., 2010; Budni et al ., 2015). Among these, brain‐derived neurotrophic factor (BDNF) (Barde et al ., 1982) is essential in sustaining physiological processes of the normal adult brain (Nagahara & Tuszynski, 2011), by tuning: (i) dendritic branching and spine morphology (Horch & Katz, 2002) and (ii) synaptic plasticity and long‐term potentiation (Figurov et al ., 1996) and therefore learning and memory. Interestingly, postmortem studies have shown that BDNF mRNA and protein decrease not only in end‐stage disease, but also in patients diagnosed with mild cognitive impairment (MCI) (Peng et al ., 2005), suggesting that a BDNF loss could be involved in the early synaptic dysfunctions.…”

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confidence: 99%

Amyloid Beta monomers regulate cyclic adenosine monophosphate response element binding protein functions by activating type‐1 insulin‐like growth factor receptors in neuronal cells

et al. 2017

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SummaryAlzheimer's disease (AD) is a progressive neurodegenerative disorder associated with synaptic dysfunction, pathological accumulation of β‐amyloid (Aβ), and neuronal loss. The self‐association of Aβ monomers into soluble oligomers seems to be crucial for the development of neurotoxicity (J. Neurochem., 00, 2007 and 1172). Aβ oligomers have been suggested to compromise neuronal functions in AD by reducing the expression levels of the CREB target gene and brain‐derived neurotrophic factor (BDNF) (J. Neurosci., 27, 2007 and 2628; Neurobiol. Aging, 36, 2015 and 20406 Mol. Neurodegener., 6, 2011 and 60). We previously reported a broad neuroprotective activity of physiological Aβ monomers, involving the activation of type‐1 insulin‐like growth factor receptors (IGF‐IRs) (J. Neurosci., 29, 2009 and 10582, Front Cell Neurosci., 9, 2015 and 297). We now provide evidence that Aβ monomers, by activating the IGF‐IR‐stimulated PI3‐K/AKT pathway, induce the activation of CREB in neurons and sustain BDNF transcription and release.

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Section: Introductionmentioning

confidence: 99%

Amyloid Beta monomers regulate cyclic adenosine monophosphate response element binding protein functions by activating type‐1 insulin‐like growth factor receptors in neuronal cells

et al. 2017

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“…This brainderived neurotrophic factor (BDNF) has a molecular weight of 12,000 Da and an isoelectric point of about 10. It is known to support the survival of a variety of primary sensory neurons (connected to the CNS by their central axons) and to be inactive on both ciliary and sympathetic neurons (Barde et al, 1982;Davies et al, 1986;Lindsay et al, 1985).The current studies were conducted to determine if there is a population of CNS neurons that responds to BDNF in culture. The retina was chosen for these studies since we have previously shown that an extract prepared from pig brain stimulates neurite outgrowth from fetal rat retinal explants in culture (Turner et al, 1983).…”

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Brain-derived neurotrophic factor supports the survival of cultured rat retinal ganglion cells

Johnson¹,

Barde²,

Schwab³

et al. 1986

J. Neurosci.

488

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Brain-derived neurotrophic factor (BDNF) is a small, basic protein purified from the mammalian brain that has been shown previously to support the survival of cultured spinal sensory neurons (Barde et al., 1982). In current studies, BDNF was tested for its ability to support the survival of cultured CNS cells isolated from the perinatal rat retina. Both immunofluorescent labeling of Thy-l and prior retrograde labeling with HRP were used as retinal ganglion cell markers in vitro. With embryonic day (E) 17 retinas, it was found that BDNF allowed the survival of a small subpopulation of neurons (about 7% of the cells plated at this age) identified by the immunofluorescent labeling of Thy-1. No detectable effects were seen when either the total number of cells or the number of tetanus toxin-positive neurons was measured. BDNF also had an effect on cultured neurons retrogradely labeled after HRP injections in the superior colliculi of neonatal rats. The BDNF-responsive population was therefore detected only in retinal cultures with specific markers and identified as consisting of retinal ganglion cells. These cells could be enriched about 80-fold by density gradient centrifugation, and purified ganglion cell cultures were shown to be responsive to BDNF. Whereas with El7 retinas, the number of surviving Thy-l positive neurons could be kept constant for at least 4 d, the survival of postnatal neurons was only transiently increased by BDNF.We conclude that in the retina, BDNF affects only the survival of ganglion cells in vitro by a direct action on these cells. The results are discussed in terms of target-derived neurotrophic support during development.The death of a substantial proportion of many different types of neurons is a common feature of the normal development of the vertebrate nervous system. It is generally believed to serve in the appropriate quantitative matching of a neuronal population with its respective terminal field .In vertebrates, evidence for the epigenetic regulation of neuronal cell death in the CNS as well as in the PNS has arisen from both target transplantation and ablation experiments. There is good evidence for molecular agents that serve to regulate neuronal cell death, the clearest being provided by the protein nerve growth factor (NGF). Treatment of developing mammals with antibodies against NGF results in the selective elimination of a large proportion of the peripheral sympathetic and sensory neurons. On the other hand, the treatment of animals with Received Jan. 7, 1986; revised Apr. 7, 1986; accepted Apr. 11, 1986. We wish to thank Dr. Hermann Rohrer for helpful suggestions and Mrs. C. Cap for technical assistance. This work was supported in part by fellowships from the Alexander von Humboldt Foundation, the Kempton Foundation and an NRSA from NIH, NINCDS (PHS-5F32-NSO7332-02X1) awarded to J.E.J.Correspondence should be addressed to Dr. James E. Thoenen and Barde, 1980). Results from in vitro assays have indicated that several other proteins with a similar function, but a differen...

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“…De nombreuses observations faites lors du déve-loppement de la moelle épinière, de la rétine ou du cervelet, suggéraient depuis longtemps l'existence de mécanismes équivalents dans le SNC. La découverte de molécules structurellement semblables au NGF, en particulier du BDNF qui est la neurotrophine de loin la plus abondante dans le SNC [5], a contribué à renforcer l'hypothèse selon laquelle les mécanis-mes contrôlant la survie des neurones dans le SNC pourraient être similaires à ceux opérant dans le SNP. Cependant, un nombre croissant d'observations ont montré de plus en plus clairement que même en l'absence complète de BDNF ou d'autres facteurs de croissance, le SNC se développe sans perte massive de neurones [6].…”

Section: Rôle Et Mode D'action Des Neurotrophinesunclassified