Gotowe bibliografie tematyczne / Neurogenesis

Gotowa bibliografia na temat „Neurogenesis”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 13 lipca 2024

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Artykuły w czasopismach na temat "Neurogenesis"

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Morgun, A. V., E. D. Osipova, E. B. Boytsova, A. N. Shuvaev, Yu K. Komleva, L. V. Trufanova, E. F. Vais i A. B. Salmina. "Astroglia-mediated regulation of cell development in the model of neurogenic niche in vitro treated with Aβ1-42". Biomeditsinskaya Khimiya 65, nr 5 (2019): 366–73. http://dx.doi.org/10.18097/pbmc20196505366.

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Neurogenesis is a complex process which governs embryonic brain development and is importants for brain plasticity throughout the whole life. Postnatal neurogenesis occurs in neurogenic niches that regulate the processes of proliferation and differentiation of stem and progenitor cells under the action of stimuli that trigger the mechanisms of neuroplasticity. Cells of glial and endothelial origin are the key regulators of neurogenesis. It is known that physiological neurogeneses is crucial for memory formation, whereas reparative neurogenesis provides partial repair of altered brain structure and compensation of neurological deficits caused by brain injury. Dysregulation of neurogenesis is a characteristics of various neurodevelopmental and neurodegenerative diseases, particularly, Alzheimer's disease which is very important medical and social problem. In the in vitro model of the neurogenic niche using hippocampal neurospheres as a source of stem/progenitor cells and astrocytes, we studied effects of astrocyte activation on the expression of markers of different stages of cell proliferation and differentiation. We found that aberrant mechanisms of development of stem and progenitor cells, caused by the beta-amyloid (Aβ1-42), can be partially restored by targeted activation of GFAP-expressing cells in the neurogenic niche.
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Kowalczyk, Anna, Robert K. Filipkowski, Marcin Rylski, Grzegorz M. Wilczynski, Filip A. Konopacki, Jacek Jaworski, Maria A. Ciemerych, Piotr Sicinski i Leszek Kaczmarek. "The critical role of cyclin D2 in adult neurogenesis". Journal of Cell Biology 167, nr 2 (25.10.2004): 209–13. http://dx.doi.org/10.1083/jcb.200404181.

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Adult neurogenesis (i.e., proliferation and differentiation of neuronal precursors in the adult brain) is responsible for adding new neurons in the dentate gyrus of the hippocampus and in the olfactory bulb. We describe herein that adult mice mutated in the cell cycle regulatory gene Ccnd2, encoding cyclin D2, lack newly born neurons in both of these brain structures. In contrast, genetic ablation of cyclin D1 does not affect adult neurogenesis. Furthermore, we show that cyclin D2 is the only D-type cyclin (out of D1, D2, and D3) expressed in dividing cells derived from neuronal precursors present in the adult hippocampus. In contrast, all three cyclin D mRNAs are present in the cultures derived from 5-day-old hippocampi, when developmental neurogenesis in the dentate gyrus takes place. Thus, our results reveal the existence of molecular mechanisms discriminating adult versus developmental neurogeneses.
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Talan, Jamie. "Neurogenesis". Neurology Today 18, nr 7 (kwiecień 2018): 62–66. http://dx.doi.org/10.1097/01.nt.0000532356.12905.0c.

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Valeri, Andrea, i Emanuela Mazzon. "Cannabinoids and Neurogenesis: The Promised Solution for Neurodegeneration?" Molecules 26, nr 20 (19.10.2021): 6313. http://dx.doi.org/10.3390/molecules26206313.

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The concept of neurons as irreplaceable cells does not hold true today. Experiments and evidence of neurogenesis, also, in the adult brain give hope that some compounds or drugs can enhance this process, helping to reverse the outcomes of diseases or traumas that once were thought to be everlasting. Cannabinoids, both from natural and artificial origins, already proved to have several beneficial effects (e.g., anti-inflammatory, anti-oxidants and analgesic action), but also capacity to increase neuronal population, by replacing the cells that were lost and/or regenerate a damaged nerve cell. Neurogenesis is a process which is not highly represented in literature as neuroprotection, though it is as important as prevention of nervous system damage, because it can represent a possible solution when neuronal death is already present, such as in neurodegenerative diseases. The aim of this review is to resume the experimental evidence of phyto- and synthetic cannabinoids effects on neurogenesis, both in vitro and in vivo, in order to elucidate if they possess also neurogenetic and neurorepairing properties.
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Wang, Ning, Yang Lu, Kui Wang, Wei-song Li, Pan Lu, Shan Lei, Rong Li i in. "Simvastatin Attenuates Neurogenetic Damage and Improves Neurocongnitive Deficits Induced by Isoflurane in Neonatal Rats". Cellular Physiology and Biochemistry 46, nr 2 (2018): 618–32. http://dx.doi.org/10.1159/000488630.

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Background/Aims: Isoflurane inhibited neurogenesis and induced subsequent neurocognitive deficits in developing brain. Simvastatin exerts neuroprotection in a wide range of brain injury models. In the present study, we investigated whether simvastatin could attenuate neurogenetic inhibition and cognitive deficits induced by isoflurane exposure in neonatal rats. Methods: Sprague-Dawley rats at postnatal day (PND) 7 and neural stem cells (NSCs) were treated with either gas mixture, isoflurane, or simvastatin 60 min prior to isoflurane exposure, respectively. The rats were decapitated at PND 8 and PND 10 for detection of neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ) of the hippocampus by immunostaining. NSC proliferation, viability and apoptosis were assessed by immunohistochemistry, CCK-8 and TUNEL, respectively. The protein expressions of caspase-3, p-Akt and p-GSK-3β both in vivo and vitro were assessed by western blotting. Cognitive functions were assessed by Morris Water Maze test and context fear conditioning test at the adult. Results: Isoflurane exposure inhibited neurogenesis in the SVZ and SGZ, decreased NSC proliferation and viability, promoted NSC apoptosis and led to late cognitive deficits. Furthermore, isoflurane increased caspase-3 expression and decreased protein expressions of p-Akt and p-GSK-3β both in vivo and in vitro. Pretreatment with simvastatin attenuated isoflurane-elicited changes in NSCs and cognitive function. Co-treatment with LY294002 reversed the effect of simvastatin on NSCs in vitro. Conclusion: We for the first time showed that simvastatin, by upregulating Akt/GSK-3β signaling pathway, alleviated isoflurane-induced neurogenetic damage and neurocognitive deficits in developing rat brain.
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Walton, R. M. "Postnatal Neurogenesis". Veterinary Pathology 49, nr 1 (8.08.2011): 155–65. http://dx.doi.org/10.1177/0300985811414035.

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Crusio, Wim E. "Adult Neurogenesis". Genes, Brain and Behavior 7, nr 7 (październik 2008): 831–32. http://dx.doi.org/10.1111/j.1601-183x.2008.00424_6.x.

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Farley, Suzanne. "Exciting neurogenesis". Nature Reviews Neuroscience 5, nr 7 (lipiec 2004): 514. http://dx.doi.org/10.1038/nrn1446.

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Whalley, Katherine. "Upsetting neurogenesis". Nature Reviews Neuroscience 9, nr 4 (kwiecień 2008): 250–51. http://dx.doi.org/10.1038/nrn2358.

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de Souza, Natalie. "Predicting neurogenesis". Nature Methods 8, nr 8 (28.07.2011): 616–17. http://dx.doi.org/10.1038/nmeth0811-616a.

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Rozprawy doktorskie na temat "Neurogenesis"

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Charbord, Jérémie. "Criblage à haut débit d'inhibiteurs du répresseur de transcription REST dans des progénies neurales issues de cellules souches embryonnaires humaines". Thesis, Evry-Val d'Essonne, 2012. http://www.theses.fr/2012EVRY0004.

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Nous avons identifié des inhibiteurs pharmacologiques de REST capables d’augmenter l’expression d’un ensemble de gènes cibles de REST (gènes RE1) neuronaux dans des cellules souches neurales (NSC) issues de cellules souches embryonnaires humaines (HESC). De tels composés ont pour intérêt de constituer un nouveau type d’outil pour étudier la fonction de REST dans la prolifération et la différenciation des NSC normales ou pathologiques et pourraient posséder des propriétés thérapeutiques dans les maladies ou une sur-activation de REST participe ou marque la pathologie cellulaire telles que la maladie de Huntington ou certaines tumeurs du cerveau. L’identification des inhibiteurs de REST a été réalisée grâce à la technologie puissante du criblage à haut débit (HTS). Le succès de cette méthode a reposé sur l’élaboration d’un test cellulaire fonctionnel robuste de l’activité de REST dans les NSC. Un système rapporteur de cette activité a été construit autour d’une cassette d’expression de la Luciferase Renilla placée sous le contrôle d’un promoteur constitutif fort. Plusieurs sites RE1 ont été insérés en amont de cette cassette afin de rendre l’expression de la Luciferase dépendante de l’activité de REST. Nous avons ainsi isolé le compose x5050, un benzimidazole qui entraîne, comme montre par l’étude transcriptomique, la surexpression spécifique des gènes RE1 neuronaux. x5050 ne modifie ni la transcription de REST ni la fixation de REST sur une séquence oligonucléotidique RE1 marquée. En revanche, x5050 entraîne la diminution du niveau de la protéine REST, vraisemblablement en modulant la dégradation de REST par le système ubiquitine-protéasome
Our goal was to identify pharmacological inhibitors of REST that would be able to increase the expression of a set of neuronal gene targets of REST (RE1 genes) in human neural stem cells (NSCS) derived from human embryonic stem cells (HESC). These compounds would at first provide a new type of tool to better understand REST action on proliferation and differentiation in normal or pathological NSCS and could have therapeutical properties for diseases in which an over-activation of REST is implicated in or influences cellular pathology such as huntington’s disease or some brain tumors. Identification of REST inhibitors was performed using the powerful technology of high throughput screening (HTS). Success of this method was based on the set up of a robust functional cell assay of REST activity in NSCS. A reporter system of this activity has been constructed using an expression cassette of the renilla luciferase placed under control of a strong constitutive promoter. Several RE1 sites have been inserted upstream of this cassette to make the expression of Luciferase dependent on REST activity. We have isolated x5050 compound, a benzimidazole which leads to upregulation of RE1 genes as shown by transcriptomic studies. x5050 modified neither rest transcription nor rest fixation on a labeled nucleotidic RE1 sequence. On the contrary, x5050 treatment induced the decrease in rest protein level, probably by modulating REST degradation by the ubiquitin-proteasome system
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Sandberg, Magnus. "Sox proteins and neurogenesis". Stockholm, 2010. http://diss.kib.ki.se/2010/978-91-7409-873-0/.

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Brill, Monika. "Regionalization of adult neurogenesis". Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-101449.

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Aaku-Saraste, E. (Eeva). "A prelude to neurogenesis". Doctoral thesis, University of Oulu, 1999. http://urn.fi/urn:isbn:9514253655.

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Abstract All neurons and macroglial cells of vertebrates derive from the neuroepithelium. Neuroepithelial (NE) cells first proliferate and, after closure of the neural tube, some cells start generating neurons. It is still unclear what triggers differentiation but apparently there is interplay between extrinsic (secreted or transmembrane signals) and intrinsic factors. Diriving from the embryonic ectoderm, the NE cells inherit epithelial characteristics. It has been shown in other developmental systems that epithelial determinants, such as cell-cell contacts and contact to basal laminar components can guide differentiation. The key epithelial features include cell polarity, and tight junctions. We studied these in the NE at two developmental stages, the neural plate, a proliferative stage and the neural tube, a differentiative stage. The polarity of membrane proteins in NE cells was studied with polarly budding viruses. Mouse embryos were infected with Fowl plague- and vesicular stomatitis viruses and cultured in a whole embryo culture system. Viral envelope proteins (HA and G-protein) were localized by indirect immunofluorescence and immunoelectron microscopy. HA was polarized in the plate stage neuroepithelial cells, whereas in the tube it was not polarized anymore. It is also shown by penetrance of apically injected horseradish peroxidase that in the neural plate, NE cells have functional tight junctions. At this stage, they also express occludin, a transmembrane protein of tight junctions, as shown by indirect immunofluorescence. In the neural tube, the paracellular barrier is lost and there is no occludin expression. In contrast, expression of ZO-1, a cytoplasmic protein binding to occiudin, is upregulated. The downregulation of these epithelial features occurs in all NE cells, irrespective of their mode of division and before any neurons are generated in the NE. The change is initiated already at the plate stage and coincides with the switch from E- to N-cadherin. Later, with birth of neurons, the proliferative cell layer also looses contact to basal lamina. This is probably an important step in the regulation of neurogenesis. Furthermore, lack of apico-basolateral polarity of non-anchored membrane proteins may contribute to the mechanism of rapid neuron generation. Until now, it has been impossible to distinguish a neuroepithelial cell preparing for neuron generation from the surrounding cells that give rise to two precursor cells. In this study, the immediate neuron precursors are shown to express the antiproliferative gene TIS2 1. Using this new marker and ISH in serial sections, we show that the switch to differentiation is initiated in single NE cells.
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Tosti, Claudia. "NEUROGENESIS IN UTERINE DISORDERS". Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1095599.

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Endometriosis, adenomyosis and uterine fibroids represent benign gynecologic diseases, affecting women of reproductive age associated with chronic pelvic pain, dysmenorrhea, dyspareunia and infertility. The present knowledge indicates that hormonal function (estrogen and progesterone receptors), immunological and neuroinflammatory factors are critically altered in every of uterine disorders. The aggressive behaviour of deep infiltrating endometriosis may be explained by the highly decreased apoptosis, by the increased proliferation activity related to oxidative stress and by invasive neurogenic mechanisms and inflammatory patterns that explain its correlation with chronic pelvic pain. Adenomyotic nodules are novel site of protein expression of inflammatory and neurogenic factors, probably involved in the pathogenesis of adenomyosis: endometrial cells invade and proliferate within myometrium, and inflammatory mediators participate to the intense painful symptoms. The increased expression of neurogenic factors in uterine fibroids and endometrium may contribute to explain the painful stimuli; in addition, NGF hyperexpression, in both fibroids and endometrium, may be associated with infertility. Accordingly, in the future, these neurogenic factors may represent potential therapeutic avenues to treat the fibroid-related symptoms. 
 In conclusion, our results give new insights into the neurogenic characteristics of uterine disorders showing that endometriosis, adenomyosis and fibroids has distinct molecular patterns. With further advances in our understanding of uterine disorders, preventive strategies, novel non-surgical diagnostic modalities, and targeted therapeutics hold great promise of becoming realities and help to treat our patients. The future research may contribute to a better phenotyping of these benign gynaecological diseases in order to give a specific efficient management to each disorder. Basic science approach is necessary to increase pathogenesis knowledge of endometriosis, adenomyosis and uterine fibroids, and new medical treatment, and the clinical and diagnostic approach is necessary for planning an accurate surgical or medical treatment.
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Vaculik, Michael. "Beclin1 Regulates Adult Hippocampal Neurogenesis". Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32994.

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Adult neurogenesis is a process that produces neurons in the adult brain and garners potential for the development of novel therapeutic interventions to combat neurodegenerative and other brain related diseases. With the hope of increasing neurogenesis, active investigations are defining the cellular and molecular mechanisms that regulate adult neural precursor cell (NPC) survival, and thus maintain neurogenesis. Recently, autophagy, an intracellular recycling pathway, has been implicated in regulating adult NPCs in embryonic knockout mice models. Whether autophagy has a similar effect within the adult and how autophagy regulates development of adult NPC remains unknown. Here, we investigate the role of Beclin1, a gene responsible for autophagy induction, in adult hippocampal NPC function in mice. Retroviral-mediated removal of Beclin1 from proliferating adult NPCs in vivo led to a reduction in the survival of adult-born neurons. In addition, Beclin1 was removed specifically from nestin-expressing adult neural stem- and progenitor-cells through the development of a Beclin1 nestin-inducible knockout mouse. Beclin1 nKO mice had a reduction in NPC proliferation and development, and overall fewer adult-generated neurons. Together, these findings reveal Beclin1 is required for adult hippocampal neurogenesis through regulating the proliferation and survival of the NPCs, in the absence of changing NPC fate.
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Dhaliwal, Jagroop. "Regulators of Adult Hippocampal Neurogenesis". Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/35712.

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One mechanism of plasticity within the adult mammalian brain is the dynamic process of adult neurogenesis that is functionally important in physiological and pathological conditions. During this process, neurons develop from adult neural stem cells (NSCs) via intermediate neural progenitors (NPCs) through several processes including proliferation, survival, differentiation, migration and integration. Despite neurogenesis during development sharing these same processes, there is growing evidence highlighting unique mechanisms that regulate adult versus embryonic neurogenesis. The studies in this thesis test the cell-intrinsic function of genes that have defined roles in embryonic neurogenesis and undefined roles in adult hippocampal neurogenesis using a combination of transgenic inducible mice and in vivo retroviral techniques. The first study examines the microtubule associated protein Doublecortin (DCX), which is transiently expressed by NPCs and is critical for neuronal migration. Our results show that, in the context of adult hippocampal neurogenesis, DCX is not required for the survival or differentiation of the NPCs within the subgranular zone (SGZ). The second study examines the functional role of the autophagy-associated gene 5 (Atg5) which is critical for embryonic neurogenesis and survival. Our findings demonstrate that the intracellular recycling process of autophagy is active throughout maturation of adult hippocampal NPCs and that ablation of Atg5 produces a drastic reduction in NPC survival, without altering the neuronal fate of these cells. The third study examines the requirement of the familial-Alzheimer’s disease associated genes, presenilin 1 and presenilin 2 (PS1 & PS2), which are critical for embryonic NSC maintenance and differentiation. Similar to the findings with DCX, our results demonstrate that presenilins are dispensable for adult neurogenesis. Altogether, these studies add to the growing evidence suggesting differences in the regulation of adult versus embryonic neurogenesis, and highlight autophagy as a novel regulator of survival for adult generated granule neurons in the hippocampus.
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Teutenberg, Kevin. "Glucose, glucose transporters and neurogenesis". Thesis, University of Ottawa (Canada), 2008. http://hdl.handle.net/10393/28026.

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Since the pioneering work of Altman in the late 60's, much has been learned about the generation of neurons in the adult brains of several species, including mice, rats, and humans. An underlying assumption is that these newborn neurons acquire their energy, in the form of glucose, in a similar manner to mature neurons: via glucose transporters. Using BRDU and double immunohistochemistry, we investigated the relationship between hippocampal neurogenesis and glucose transporters, as well as monocarboxylate transporters. Unexpectedly, the results suggest that newborn neurons do not acquire their energy via the major glucose transporters (1, 3, 4, and 8), nor via either monocarboxylate transporter tested (1 and 2). Future studies will have to resolve whether lesser known glucose transporters carry this function or if other mechanisms are used to provide metabolic energy to newborn neurons.
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Wright, Rupert. "Engineering surfaces to control neurogenesis". Thesis, Keele University, 2015. http://eprints.keele.ac.uk/2350/.

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Producing therapeutic neural cell populations in vitro to treat neurodegenerative diseases is a key aim of regenerative medicine. Various protocols have been developed to produce a wide range of neural cell types in vitro, but the protocols are labour and resource intensive. Lower costs will take the cell therapy closer to clinical adoption. Cell-material interactions can be used to control cellular processes and behaviours in the place of expensive reagents. The thesis went about developing superior materials to culture neurons in vitro by using simple surface parameters. By using simple surfaces findings could be leveraged by incorporation in to other materials, and protocols to culture neurons. We have investigated the responses of primary neural tissue derived from rat ventral mesencephalon (VM), interacting with a range of surface chemical functionalities and net molecular properties by using silanes. Specific substrate functionality leads to higher ratios of neurons, longer neurites and neurosphere spreading capacity. All of these characteristics indicate a high neuro-regenerative capacity. Next it became important to optimize the amine functionalised surface with the addition of secondary amines in to the surface. The rational of adding secondary amines to the surface would produce functionalities which have a closer resemblance to biological molecules. The biomimicry in the surfaces provides extra scope for selective surface interactions to provide more control over neural cell culture which could steer protocols away from the use of expensive surfaces which are coated in extra cellular matrix molecules such as laminin. Controlling differentiation with surfaces has long been an aim in regenerative medicine to deliver productive production protocols. It has been shown that surfaces can induce differentiation of stem cells; however there is little control where stem cells and adult cells are simultaneously cultured. To achieve controlled differentiation of neural stem cells a surface gradient of amine polymer lengths, and polymer densities. That is in contrast to the surfaces used in previous chapters which had homogeneous presentations of surface chemistries.
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Lyons, David Anthony. "Neurogenesis in the zebrafish hindbrain". Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407357.

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Książki na temat "Neurogenesis"

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Adult neurogenesis. Wyd. 2. New York: Oxford University Press, 2011.

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1950-, Gage F., Kempermann Gerd, Song Hongjun i Cold Spring Harbor Laboratory, red. Adult neurogenesis. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2008.

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P, Klausen Martina, red. Neurogenesis research advances. New York: Nova Biomedical Books, 2008.

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P, Klausen Martina, red. Neurogenesis research advances. New York: Nova Biomedical Books, 2008.

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P, Klausen Martina, red. Neurogenesis research advances. New York: Nova Biomedical Books, 2008.

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Belzung, Catherine, i Peter Wigmore, red. Neurogenesis and Neural Plasticity. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-36232-3.

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Barker, Jennifer M. Hippocampal neurogenesis and spatial memory: Postnatal neurogenesis in yellow-pine chipmunks and eastern grey squirrels. Ottawa: National Library of Canada, 2004.

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Gravanis, Achille G., i Synthia H. Mellon, red. Hormones in Neurodegeneration, Neuroprotection, and Neurogenesis. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527633968.

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Seki, Tatsunori, Kazunobu Sawamoto, Jack M. Parent i Arturo Alvarez-Buylla, red. Neurogenesis in the Adult Brain I. Tokyo: Springer Japan, 2011. http://dx.doi.org/10.1007/978-4-431-53933-9.

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Seki, Tatsunori, Kazunobu Sawamoto, Jack M. Parent i Arturo Alvarez-Buylla, red. Neurogenesis in the Adult Brain II. Tokyo: Springer Japan, 2011. http://dx.doi.org/10.1007/978-4-431-53945-2.

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Części książek na temat "Neurogenesis"

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Jessberger, Sebastian, i Gerd Kempermann. "Neurogenesis". W Neuroprotection, 261–89. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2005. http://dx.doi.org/10.1002/3527603867.ch13.

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Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea i in. "Neurogenesis". W Encyclopedia of Psychopharmacology, 851–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_400.

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Bessa, João M., Osborne F. X. Almeida i Nuno Sousa. "Neurogenesis". W Encyclopedia of Psychopharmacology, 1067–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-36172-2_400.

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Hamburger, Viktor. "Neurogenesis". W Neuroembryology, 143–61. Boston, MA: Birkhäuser Boston, 1990. http://dx.doi.org/10.1007/978-1-4899-6743-5_8.

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Lyle, Randall R. "Neurogenesis". W Encyclopedia of Child Behavior and Development, 1011–12. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-0-387-79061-9_1950.

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Clausen, Torben, José Luis Trejo, Mark P. Mattson, Alexis M. Stranahan, Joanna Erion, Rosa Maria Bruno, Stefano Taddei i Melinda M. Manore. "Neurogenesis". W Encyclopedia of Exercise Medicine in Health and Disease, 640. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2750.

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Kumar, Ankit. "Neurogenesis". W Encyclopedia of Animal Cognition and Behavior, 1–3. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47829-6_176-1.

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Kumar, Ankit. "Neurogenesis". W Encyclopedia of Animal Cognition and Behavior, 4653–55. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-319-55065-7_176.

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Bessa, João M., Osborne F. X. Almeida i Nuno Sousa. "Neurogenesis". W Encyclopedia of Psychopharmacology, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27772-6_400-2.

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Twyman, R. M. "Neurogenesis". W BIOS Instant Notes in Developmental Biology, 296–301. London: Taylor & Francis, 2023. http://dx.doi.org/10.1201/9781003416371-55.

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Streszczenia konferencji na temat "Neurogenesis"

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Martin, Charles E., i Praveen K. Pilly. "Probabilistic Program Neurogenesis". W The 2019 Conference on Artificial Life. Cambridge, MA: MIT Press, 2019. http://dx.doi.org/10.1162/isal_a_00199.

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Martin, Charles E., i Praveen K. Pilly. "Probabilistic Program Neurogenesis". W The 2019 Conference on Artificial Life. Cambridge, MA: MIT Press, 2019. http://dx.doi.org/10.1162/isal_a_00199.xml.

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Akay, Metin. "Neurogenesis, neurocontrol and neurochips". W 2008 International Conference on Technology and Applications in Biomedicine (ITAB). IEEE, 2008. http://dx.doi.org/10.1109/itab.2008.4570494.

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Wilson, Dennis, Sylvain Cussat-Blanc i Hervé Luga. "The Evolution of Artificial Neurogenesis". W GECCO '16: Genetic and Evolutionary Computation Conference. New York, NY, USA: ACM, 2016. http://dx.doi.org/10.1145/2908961.2931671.

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Pandit, Tej, i Dhireesha Kudithipudi. "Relational Neurogenesis for Lifelong Learning Agents". W NICE '20: Neuro-inspired Computational Elements Workshop. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3381755.3381766.

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Palmer, Michael E. "Evolved neurogenesis and synaptogenesis for robotic control". W the 13th annual conference. New York, New York, USA: ACM Press, 2011. http://dx.doi.org/10.1145/2001576.2001780.

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Fortino, V. R., D. Pawley, D. Pelaez i H. S. Cheung. "Novel Pluripotent Adult Stem Cell Source for Neurogenesis". W 2013 29th Southern Biomedical Engineering Conference (SBEC 2013). IEEE, 2013. http://dx.doi.org/10.1109/sbec.2013.16.

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Khodanovich, M. Yu. "Reparative neurogenesis after cerebral ischemia: Clinical application prospects". W NEW OPERATIONAL TECHNOLOGIES (NEWOT’2015): Proceedings of the 5th International Scientific Conference «New Operational Technologies». AIP Publishing LLC, 2015. http://dx.doi.org/10.1063/1.4935997.

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MAEKAWA, MOTOKO, i NORIKO OSUMI. "THE ROLE OF Pax6 IN POSTNATAL HIPPOCAMPAL NEUROGENESIS". W Proceedings of the Final Symposium of the Tohoku University 21st Century Center of Excellence Program. IMPERIAL COLLEGE PRESS, 2006. http://dx.doi.org/10.1142/9781860948800_0013.

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Kurhekar, Manish, i Umesh Deshpande. "A Deterministic Model of the Adult Subventricular Neurogenesis". W 8th International Conference on Bio-inspired Information and Communications Technologies (formerly BIONETICS). ACM, 2015. http://dx.doi.org/10.4108/icst.bict.2014.257892.

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Raporty organizacyjne na temat "Neurogenesis"

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Stratton, Kalera. Fetal Stress and Neurogenesis in Thamnophis sirtalis parietalis. Portland State University Library, styczeń 2016. http://dx.doi.org/10.15760/honors.330.

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Harris, James, Shannon Kinkead, Dylan Fox i Yang Ho. Continual Learning for Pattern Recognizers using Neurogenesis Deep Learning. Office of Scientific and Technical Information (OSTI), wrzesień 2021. http://dx.doi.org/10.2172/1855019.

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Draelos, Timothy John, Nadine E. Miner, Christopher C. Lamb, Craig Michael Vineyard, Kristofor David Carlson, Conrad D. James i James Bradley Aimone. Neurogenesis Deep Learning: Extending deep networks to accommodate new classes. Office of Scientific and Technical Information (OSTI), grudzień 2016. http://dx.doi.org/10.2172/1505351.

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Owens, Greg D., Nafisa M. Jadavji i Patrice D. Smith. Neurogenesis Unchanged by MTHFR Deficiency in Three-Week-Old Mice. Journal of Young Investigators, grudzień 2016. http://dx.doi.org/10.22186/jyi.31.6.39-43.

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Fike, John R. Effects of Low Level Radiation exposure on Neurogenesis and Cognitive Function: Mechanisms and Prevention. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2005. http://dx.doi.org/10.21236/ada443579.

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Fike, John R. Effects of Low Level Radiation Exposure on Neurogenesis and Cognitive Function: Mechanisms and Prevention. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2004. http://dx.doi.org/10.21236/ada428521.

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Vineyard, Craig Michael, Stephen Joseph Verzi, Conrad D. James i James Bradley Aimone. Quantifying neural information content: a case study of the impact of hippocampal adult neurogenesis. Office of Scientific and Technical Information (OSTI), marzec 2016. http://dx.doi.org/10.2172/1561002.

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Aimone, James Bradley, i Rita Betty. Using High Performance Computing to Examine the Processes of Neurogenesis Underlying Pattern Separation/Completion of Episodic Information. Office of Scientific and Technical Information (OSTI), marzec 2015. http://dx.doi.org/10.2172/1172176.

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Aimone, James Bradley, Michael Lewis Bernard, Craig Michael Vineyard i Stephen Joseph Verzi. Using High Performance Computing to Examine the Processes of Neurogenesis Underlying Pattern Separation and Completion of Episodic Information. Office of Scientific and Technical Information (OSTI), październik 2014. http://dx.doi.org/10.2172/1162373.

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Henderson, Brian E. ,. M. D. Development of Structural Neurobiology and Genomics Programs in the Neurogenetic Institute. Office of Scientific and Technical Information (OSTI), listopad 2006. http://dx.doi.org/10.2172/894898.

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