Relevant bibliographies by topics / Human neurogenesis

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Human neurogenesis'

Author: Grafiati
Published: 16 November 2024

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Journal articles on the topic "Human neurogenesis"

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Snyder, Jason S. "Questioning human neurogenesis." Nature 555, no. 7696 (March 2018): 315–16. http://dx.doi.org/10.1038/d41586-018-02629-3.

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Murrell, Wayne, Gillian R. Bushell, Jonathon Livesey, John McGrath, Kelli P. A. MacDonald, Paul R. Bates, and Alan Mackay-Sim. "Neurogenesis in adult human." NeuroReport 7, no. 6 (April 1996): 1189–94. http://dx.doi.org/10.1097/00001756-199604260-00019.

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Sugano, Hidenori, Madoka Nakajima, Ikuko Ogino, and Hajime Arai. "Neurogenesis in Human Epileptic Hippocampus." Journal of the Japan Epilepsy Society 26, no. 1 (2008): 16–25. http://dx.doi.org/10.3805/jjes.26.16.

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Flor-García, Miguel, Julia Terreros-Roncal, Elena P. Moreno-Jiménez, Jesús Ávila, Alberto Rábano, and María Llorens-Martín. "Unraveling human adult hippocampal neurogenesis." Nature Protocols 15, no. 2 (January 8, 2020): 668–93. http://dx.doi.org/10.1038/s41596-019-0267-y.

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Lucassen, Paul J., Nicolas Toni, Gerd Kempermann, Jonas Frisen, Fred H. Gage, and Dick F. Swaab. "Limits to human neurogenesis—really?" Molecular Psychiatry 25, no. 10 (January 7, 2019): 2207–9. http://dx.doi.org/10.1038/s41380-018-0337-5.

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Liu, He, and Ni Song. "Molecular Mechanism of Adult Neurogenesis and its Association with Human Brain Diseases." Journal of Central Nervous System Disease 8 (January 2016): JCNSD.S32204. http://dx.doi.org/10.4137/jcnsd.s32204.

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Recent advances in neuroscience challenge the old dogma that neurogenesis occurs only during embryonic development. Mounting evidence suggests that functional neurogenesis occurs throughout adulthood. This review article discusses molecular factors that affect adult neurogenesis, including morphogens, growth factors, neurotransmitters, transcription factors, and epigenetic factors. Furthermore, we summarize and compare current evidence of associations between adult neurogenesis and human brain diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and brain tumors.
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Inta, agos, and Peter Gass. "Is Forebrain Neurogenesis a Potential Repair Mechanism after Stroke?" Journal of Cerebral Blood Flow & Metabolism 35, no. 7 (May 13, 2015): 1220–21. http://dx.doi.org/10.1038/jcbfm.2015.95.

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The use of adult subventricular zone (SVZ) neurogenesis as brain repair strategy after stroke represents a hot topic in neurologic research. Recent radiocarbon-14 dating has revealed a lack of poststroke neurogenesis in the adult human neocortex; however, adult neurogenesis has been shown to occur, even under physiologic conditions, in the human striatum. Here, these results are contrasted with experimental poststroke neurogenesis in the murine brain. Both in humans and in rodents, the SVZ generates predominantly calretinin (CR)-expressing GABAergic interneurons, which cannot replace the broad spectrum of neuronal subtypes damaged by stroke. Therefore, SVZ neurogenesis may represent a repair mechanism only after genetic manipulation redirecting its differentiation.
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Mustafin, Rustam N., and Elza K. Khusnutdinova. "Postnatal neurogenesis in the human brain." Morphology 159, no. 2 (August 1, 2022): 37–46. http://dx.doi.org/10.17816/1026-3543-2021-159-2-37-46.

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Recently, a lot of data has been gathered which demonstrates neurogenesis in the brain of adult humans. In genetics, findings have been obtained that not only prove, but also elucidate the molecular mechanisms of neurogenesis. In some publications, however, morphology disputes neuronal renewal in adulthood. Therefore, this review presents the modern achievements of epigenetics, morphology, and physiology, which confirm and characterize postnatal neurogenesis in detail. We suggest that the introduction of molecular genetic technologies into morphological studies will be the starting point for the integration of these areas, complementing each other for the introduction of targeted therapy in clinical practice. Numerous evidence has been obtained of the presence of postnatal neurogenesis in adult humans in studies using bromodeoxyuridine, a carbon isotope of 14C, and 3H-thymidine, in comparative analyses of experimental data from animals. Neuronal stem cells, represented by radial glia present in the subventricular and subgranular zones of the human brain, are morphologically similar to neuroepithelial cells. They express marker proteins for astrocytes, which suggests that the proliferation of neuroglia found in adults can also indicate the regeneration of neurons. To prove this, further studies are required, with the exact identification of newly-formed cells, using specific molecular markers, and data from modern epigenetics. The integration of molecular genetic methods into morphology will facilitate not only the accurate determination of the classification of cells to a specific subpopulation but also to study the effects of various agents on the proliferation of neurons in the adult brain.
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Kessaris, Nicoletta. "Human cortical interneuron development unraveled." Science 375, no. 6579 (January 28, 2022): 383–84. http://dx.doi.org/10.1126/science.abn6333.

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Lewis, Sian. "Human olfaction is not neurogenesis-dependent." Nature Reviews Neuroscience 13, no. 7 (June 20, 2012): 451. http://dx.doi.org/10.1038/nrn3286.

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Dissertations / Theses on the topic "Human neurogenesis"

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Andersson, Annika. "Studies on neurogenesis in the adult human brain." Thesis, Södertörn University College, School of Life Sciences, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:sh:diva-3646.

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Many studies on neurogenesis in adult dentate gyrus (DG) have been performed on rodents and other mammalian species, but only a few on adult human DG.  This study is focusing on neurogenesis in adult human DG. To characterize the birth of cells in DG, the expression of the cell proliferation marker Ki67 was examined using immunohistochemistry. Ki67-positive labelling was indeed observed in the granular cell layer and the molecular layer of dentate gyrus and in the hilus of hippocampus, as well as in the subgranular zone (SGZ). The Ki67 positive nuclei could be divided into three groups, based on their morphology and position, suggesting that one of the groups represents neuronal precursors. Fewer Ki67 positive cells were seen in aged subjects and in subjects with an alcohol abuse. When comparing the Ki67 positive cells and the amount of blood vessels as determined by anti factor VIII, no systematic pattern could be discerned. To identify possible stem/progenitor cells in DG a co-labelling with nestin and glial fibrillary acid protein was carried out. Co-labelling was found in the SGZ, but most of the filaments were positive for just one of the two antibodies. Antibodies to detect immature/mature neurons were also used to investigate adult human neurogenesis in DG. The immature marker βIII-tubulin showed a weak expression. The other two immature markers (PSA-NCAM and DCX) used did not work, probably since they were not cross-reacting against human tissue. In summary, this study shows that new cells are continuously formed in the adult human hippocampus, but at a slower pace compared to the rat, and that some of these new cells may represent neuronal precursors.

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Yu, Chieh. "Heparan sulfate proteoglycans in human models of Neurogenesis." Thesis, Queensland University of Technology, 2020. https://eprints.qut.edu.au/203960/1/Chieh_Yu_Thesis.pdf.

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This thesis examined cell surface glycoproteins the heparan sulfate proteoglycans, as regulators of the human nervous system and identified a number of potentially novel stem cell targets for use in treating neurological disorders. Due to the poor outcome of current stem cell transplantation therapies for brain injury and neurodegeneration, this project aimed to understand the fundamentals of human neurogenesis with implications in improving stem cell therapy, understanding brain development, and the factors mediating neurodegeneration.
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Komuro, Yutaro. "Altered adult neurogenesis in a mouse model of human tauopathy." Case Western Reserve University School of Graduate Studies / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=case1434743393.

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Ahmad, Ruhel [Verfasser], and Albrecht [Akademischer Betreuer] Müller. "Neurogenesis from parthenogenetic human embryonic stem cells / Ruhel Ahmad. Betreuer: Albrecht Müller." Würzburg : Universitätsbibliothek der Universität Würzburg, 2013. http://d-nb.info/1031379878/34.

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Wei, Yulei. "Genetic Knowledge-based Artificial Control over Neurogenesis in Human Cells Using Synthetic Transcription Factor Mimics." Kyoto University, 2018. http://hdl.handle.net/2433/232265.

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Garnett, Shaun. "Generating a proteomic profile of neurogenesis, through the use of human foetal neural stem cells." Doctoral thesis, Faculty of Science, 2019. http://hdl.handle.net/11427/31143.

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Introduction Neurogenesis, the development of new neurons, starts soon after the formation of the neural tube and is largely completed by birth. Development of the brain after birth is mainly reliant on the formation of new connections between surviving neurons. However, adult neurogenesis does continue in the subgranular zone of the hippocampus from quiescent adult neural stem cells. Traditionally neural stem cells were cultured as neurospheres, a heterogeneous agglomeration of neural cells at various stages of differentiation. This heterogeneity prevented accurate quantitative analysis. In 2008 Sun et al produced the first non-immortalised human foetal neural stem (NS) cell line from nine week old human foetal cortex. These cells are cultured as monolayers, have a radial glia like appearance, self renew and form all three neural cell types, neurons, astrocytes and oligodendrocytes upon differentiation. More recently human foetal neuroepithelial like (NES) stem cells have been produced from five week old human foetal hind-brain, they resemble neuroepithelial cells, with characteristic rosettes, upon differentiation they appear to form a pure population of neurons. These homogeneous monolayer cultures enable quantitative proteomic analysis, to increase our understanding of early brain development Methods Three NES and two NS cell lines were available for analysis. They proliferate by stimulation from FGF and EGF, removal of these growth factors results in spontaneous differentiation. Proliferating NES and NS cells were compared using SILAC labelling. In addition, each cell line was differentiated for 12 days, 6 timepoints were taken and compared using label free quantitation. Results 4677 proteins were quantitated with 473 differentially expressed, revealing fundamental differences between NES and NS cells. NES cells are less differentiated, expressing SOX2 and LIN28, have active cell cycle processes, DNA elongation, histone modification and miRNA mediated gene silencing. Whereas NS cells are more developmentally defined, express multiple membrane proteins, have activated focal adhesion, thereby increasing their binding and interaction with their environment. NS metabolism is more oxidative, utilises lipid metabolism, the pentose phosphate pathway and produces creatine phosphate. Upon differentiation the cell cycle processes are downregulated and neurogenic and gliogenic processes increased. Conclusion This work represent a detailed in vitro characterisation of non immortalised human foetal neural stem cells, it describes the regulatory, metabolic and structural changes occurring within neural stem cells in early brain development. The information herein points towards de-differentiation potentially through LIN28-let7, as a means to produce more neurogenic neural stem cells in vitro thus aiding regenerative therapies, as well as provides a wealth of information for better understanding neurological developmental disorders.
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Bramwell, Thomas William. "Investigations into the use of human embryonal carcinoma stem cells as a model to study dopaminergic neurogenesis." Thesis, Durham University, 2009. http://etheses.dur.ac.uk/2071/.

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Parkinson's disease in reality arises as a result of a complex series of events, however it is strongly linked to the loss of a specific cellular population of midbrain dopaminergic neurons making it a candidate for stem cell based research. Stem cells can be cultured in vitro and via asymmetric cell division possess the capacity for both self renewal and the production of differentiated derivatives. The use of specific molecules and culture conditions can be applied to promote the differentiation of them towards particular cellular fates, in turn facilitating the possibility of producing enriched populations of cells displaying characteristics of a certain phenotype of interest. There has been much research focussed on the in vitro generation of dopaminergic neurons from various stem cell types. In this work the Tera2.cl.SP12 embryonal carcinoma stem cell line was the primary vehicle investigated for its ability to produce cells that were reflective of a dopaminergic phenotype. Retinoic acid was found to be able to up regulate the expression of a range of dopaminergic markers in the Tera2.cl.SP12 cell line over time. However it was clear that lowered oxygen culture, a method known to promote the production of neurons reflective of a dopaminergic phenotype in mesencephalic cultures, had no effect on the dopaminergic differentiation capacity of the embryonal carcinoma stem cells. The glycoprotein Wnt1 when applied to Tera2.cl.SP12 cultures in concert with retinoic acid was shown to increase the number and percentage of cells positive for the neuronal marker Beta III tubulin approximately 1.5 fold. This was accompanied by a concomitant rise in the mRNA expression of this marker, thus suggesting that the use of Wnt1 may be a means to produce cultures derived from embryonal carcinoma cells that are more neuronal, based on marker expression data. Other established methods to achieve dopaminergic differentiation such as suspension culture, stromal cell co-culture and the application of Sonic hedgehog and Fibroblast growth factor 8 are also able to induce a degree of neuronal and dopaminergic marker expression in Tera2.cl.SPI2 cultures. Overall these results suggest that the Tera2.cl.SP12 cell line might be one vehicle for the study of dopaminergic neurogenesis in vitro, in particular when Wnt1 and retinoic acid are used as a means to favourably enrich the population of cells displaying neuronal characteristics.
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Oikari, Lotta Emilia. "Regulation of human neural stem cell fate determination by proteoglycans." Thesis, Queensland University of Technology, 2017. https://eprints.qut.edu.au/103844/8/Lotta_Emilia_Oikari_Thesis.pdf.

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This thesis investigated how human neural stem cells are regulated, focusing specifically on heparan sulfate proteoglycans, the key proteins of the extracellular space. The findings of this study identified central roles for proteoglycans in mediating neural stem cell events, including self-renewal and differentiation. This research has improved our understanding of human stem cell and human neurogenesis biology and provided novel approaches for the development of improved neural stem cell applications, including using these cells for brain damage therapy.
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GUARNIERI, GIULIA. "Human cholinergic neurons from nucleus basalis of Meynert: a new promising tool to study pathogenetic mechanisms affecting neurogenesis." Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1072770.

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The degeneration of basal forebrain cholinergic neurons within the nucleus basalis of Meynert (NBM) is responsible for the cognitive decline in neurodegenerative disorders, including Alzheimer’s disease (AD) and Parkinson’s disease (PD). Indeed, the major therapeutic strategies have been directed toward the cholinergic system. However, no effective therapies exist to contrast NBM cholinergic neuron loss and investigations in the field are strongly restricted by the lack of human models. Thus, the work of this thesis firstly contributed to establish and characterise a novel primary culture of cholinergic neurons from the human foetal NBM (hfNBM). An extensive phenotypic and functional characterization confirmed the cholinergic identity of hfNBM cells, including positivity for specific markers (ChAT, VAChT and AChE) and acetylcholine release as well as the presence of functional cholinergic receptors. Treatment with Nerve Growth Factor (NGF), the main neurotrophin for NBM neurons, activated the specific NGF/TrkA signalling pathway and promoted differentiation of hfNBM cells. Moreover, when intravenously injected in a NBM-lesioned rat model, hfNBM cells led to a significant improvement in cognitive and memory functions, confirming the functional value of these cells. Given the key role of neuroinflammation in the onset and progression of neurodegenerative diseases, another objective of this work was to investigate the effects of the main pro-inflammatory cytokine, tumor necrosis factor α (TNF-α), on cholinergic neuron development and plasticity. TNF-α exposure reduced immature neuronal markers (nestin, β-tubulin III) and increased the mature marker MAP2 along with neurite elongation. Interestingly, TNF-α treatment significantly reduced the number of neurons expressing primary cilium, a non-motile sensory antenna required for neurogenesis. Furthermore, a significant reduction of TrkA along with an increase of p75NTR, the high- and low-affinity NGF receptors, essential for survival or apoptotic signals, respectively, were observed upon TNF-α stimulation. Lastly, based on the emerging evidences demonstrating inflammation-driven epigenetic modifications, a significant increase of DNMT1, one of the key enzymes regulating DNA methylation, was detected after TNF-α stimulation. Interestingly, the genome-wide methylome analysis of hfNBM cells revealed an alteration of methylation pattern after the inflammatory insult. In particular, TNF-α exposure for 48 hours led to promoter hypermethylation of genes involved in neuronal development, such as chordin like-1 (CHRDL1) and mesoderm specific transcript (MEST). Accordingly, the mRNA levels of both genes were significantly reduced by TNF-α treatment. Overall, these results suggest that TNF-α-mediated inflammation may affect hfNBM cell development and maturation most likely interfering with the DNA methylation status. In conclusion, our findings indicate that hfNBM cells may represent a proven powerful in vitro model for studying disorders of the human nervous system, such as those affecting the differentiation and maintenance of cholinergic NBM neurons.
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Pigeon, Julien. "The role of NEUROG2 T149 phosphorylation site in the developing human neocortex." Electronic Thesis or Diss., Sorbonne université, 2024. http://www.theses.fr/2024SORUS092.

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Le développement des fonctions cognitives supérieures observée au cours de l'évolution des mammifères, repose sur la capacité des progéniteurs corticaux à augmenter leur production neuronale et ainsi étendre la surface du neocortex. Chez les mammifères dit gyrencéphaliques, où la période de production neuronale est allongée, la régulation du type de division, proliférative ou neurogénique, des progéniteurs corticaux est d'autant plus importante pour garantir l'accumulation de neurones. Dans le télencéphale dorsal, à l'origine du néocortex, c'est l'articulation de la voie de signalisation Notch et du gène proneural Neurogenin2 (NEUROG2) qui contrôle le choix de division. L'expression de NEUROG2 à elle seule étant suffisante pour induire la production de neurones dans le néocortex, sa régulation au niveau génique a déjà fait l'objet d'études approfondies chez la souris. Cependant, de nouveaux travaux démontrent qu'au niveau protéique, les modifications post-traductionnelles peuvent aussi influencer profondément l'activité et la stabilité des protéines. Ainsi, la modulation du site de phosphorylation T149 de NEUROG2 dans le néocortex murin perturbe les proportions de progéniteurs corticaux et les différents sous types de neurones des couches profondes et superficielles qu'ils produisent. Toutefois, il n'est pas connu comment ces régulations pourraient moduler l'activité de NEUROG2 sous des niveaux endogènes et comment cela pourrait affecter le développement du néocortex humain.Nous avons donc supposé que la régulation de l'activité de NEUROG2 via la modulation du site de phosphorylation T149 pourrait réguler la différenciation des progéniteurs corticaux en neurones dans le développement cortical humain.Afin de tester cette hypothèse, nous avons utilisé des organoïdes corticaux issus de la différenciation de cellules iPS génétiquement remodifiées. Nous avons commencé par étudier le rôle de NEUROG2 dans la différenciation neuronale des progéniteurs en induisant la perte d'expression de NEUROG2 grâce aux ciseaux moléculaires CRISPR/Cas9. Nous avons observé une diminution des proportions de neurones à des stades intermédiaire et avancé du développement des organoïdes corticaux. A cela s'ajoute une ventralisation des progéniteurs corticaux via la diminution de l'expression de gènes leur conférant une idendité dorsale et une augmentation de ceux leur conférant une identité ventrale. Ainsi, grâce à la validation du rôle crucial de NEUROG2 dans la neurogénèse corticale chez l'humain, nous avons étudié comment la perte du site de phosphorylation T149 de NEUROG2 via son remplacement par une Alanine, T149A affecte la production neuronale dans le néocortex humain.Pour cela, nous avons combiné de l'imagerie sur cellules vivantes et fixées dont nous avons quantifiés les proportions avec des algorithmes d'apprentissage profond combinées à des techniques de reprogrammtion cellulaire ainsi que du séquencage ARN et de la ChIP pour étudier les propriétés de notre NEUROG2 T149A mutant sur la neurogeneses corticale. Nous avons observé que la mutation T149A homozygote ne change ni l'expression de NEUROG2 dans les cellules de la glie radiaire ni dans les progéniteurs intermédiaires, ni sa capacité à se lier à l'ADN et à activer l'expression de ses gènes cibles. Cependant, nous avons observé que les cellules de la glie radiaire effectuent plus de divisions neurogéniques, produisant donc plus de neurones, aux stades intermédiaire et avancé du développement des organoïdes corticaux. On note d'autre part que ce phénotype s'accompagne d'une augmentation de l'expression des gènes responsables de l'organisation structurale et fonctionnelle du cil des cellules de la glie radiaire. Or, ces gènes sont moins exprimés dans les mutants NEUROG2 KO suggérant un lien fort entre ce cil, NEUROG2, son profil de phosphorylation, et la régulation de la neurogénèse corticale chez l'humain ce qui pourrait donc constituer un potentiel mécanisme moléculaire
Neocortical expansion throughout evolution has been responsible for higher-order cognitive abilities and relies on the increased proliferative capacities of cortical progenitors to increase neuronal production. Therefore, in gyrencephalic species such as humans and primates, where the neurogenic period is protracted, the regulation of the balance between progenitor maintenance and differentiation is of key importance for the right neuronal production. The control of this balance in the dorsal telencephalon, which gives rise to the neocortex, is mediated by feedback regulation between Notch signaling and the proneural transcription factor Neurogenin2 (NEUROG2). As the expression of NEUROG2 alone is sufficient to induce neurogenesis in the neocortex, its regulation at the gene level has been extensively studied in mice. However, recent findings highlight that regulation at the protein level through post-translational modifications can profoundly influence protein activity and stability. Indeed, the modulation of the conserved NEUROG2 T149 phosphorylation site in the developing mouse neocortex results in an altered pool of progenitors and number of neurons in the deep and upper layers. Nevertheless, it is not known how such post-translation modification regulates NEUROG2 activity in the development of the human neocortex under endogenous levels and its contribution to the development of the neocortex.We hypothesize that modulation of the activity of the transcription factor NEUROG2 through this T149 phosphorylation site may regulate the pace of the temporal advance of human cortical progenitors down the differentiation landscape.To test this hypothesis in humans, we used 3D cortical organoids derived from CRISPR/Cas9 engineered iPSCs lines to study cortical neurogenesis. Before diving into the role of post translational modifications regulating NEUROG2 activity we started by confirming, for the first time in humans that Neurogenin2 is indeed the gateway gene of neuronal differentiation. In differentiated iPSCs NEUROG2 KO clones, we observed reduced proportions of neurons after 70 and 140 days in vitro at both the mid and late stages of cortical organoid development. This phenotype is accompanied by a ventralization of these dorsal forebrain organoids with a downregulation of the genes encoding for the dorsal forebrain identity and an upregulation of the genes encoding for the ventral forebrain identity. Knowing that Neurogenin2 is required for cortical neurogenesis, we next studied how the loss of NEUROG2 phosphorylation site T149 by its replacement with an Alanine (T149A) at endogenous levels alters neuronal production. To this end we combined live imaging of radial glial clones, immunohistochemistry for key cell fate markers, machine-learning based cell type quantification, transcriptional activation and stem cell reprogramming assays, RNA sequencing and chromatin immunoprecipitation to analyze cortical neurogenesis. We found, on the one hand, the TA/TA mutant does not change the pattern of NEUROG2 expression in both radial glial cells and intermediate progenitors, nor its ability to bind and activate target genes or reprogram human stem cells to neurons. However, the TA/TA mutant radial glia switch their division mode from proliferative to neurogenic and generate more neurons at both the mid and late stages of cortical development in organoids. Mechanistically, we found that this phenotype is accompanied by an upregulation of the genes encoding the organization and the movements of the primary cilium of radial glial cells, which are downregulated in the NEUROG2 KO clones. These results suggest a strong link between the primary cilium, Neurogenin2, and its phosphorylation profile with the regulation of neurogenesis in human cortical organoids
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Books on the topic "Human neurogenesis"

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Winter, Robin M. London dysmorphology database: &, London neurogenetics database. 2nd ed. Oxford: Oxford University Press, 1998.

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Winter, Robin M. London dysmorphology database. 2nd ed. Oxford: Oxford University Press, 1996.

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R, Hayden Michael, and Rubinsztein D. C, eds. Analysis of triplet repeat disorders. Oxford: Bios Scientific Publishers, 1998.

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Sutcliffe, Alastair. Congenital anomalies: Case studies and mechanisms. Rijeka, Croatia: InTech, 2012.

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D, Wells R., Warren Stephen T, and Sarmiento Marion, eds. Genetic instabilities and hereditary neurological diseases. San Diego, Calif: Academic Press, 1998.

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1946-, Oostra Ben A., ed. Trinucleotide diseases and instability. Berlin: Springer, 1998.

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Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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Cryan, John F., and Andreas Reif. Behavioral Neurogenetics. Springer, 2014.

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Cryan, John F., and Andreas Reif. Behavioral Neurogenetics. Springer, 2012.

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Cryan, John F., and Andreas Reif. Behavioral Neurogenetics. Springer London, Limited, 2012.

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Book chapters on the topic "Human neurogenesis"

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Bédard, Andréanne, Patrick J. Bernier, and André Parent. "Neurogenesis in Monkey and Human Adult Brain." In Neurogenesis in the Adult Brain II, 1–21. Tokyo: Springer Japan, 2011. http://dx.doi.org/10.1007/978-4-431-53945-2_1.

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Sachan, Nalani, Mousumi Mutsuddi, and Ashim Mukherjee. "Notch Signaling: From Neurogenesis to Neurodegeneration." In Insights into Human Neurodegeneration: Lessons Learnt from Drosophila, 185–221. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-2218-1_7.

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Suzuki, Masatoshi, Jacalyn McHugh, and Narisorn Kitiyanant. "Human Neural Progenitor Cells: Mitotic and Neurogenic Effects of Growth Factors, Neurosteroids, and Excitatory Amino Acids." In Hormones in Neurodegeneration, Neuroprotection, and Neurogenesis, 331–45. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527633968.ch19.

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Vineyard, Craig M., Stephen J. Verzi, Thomas P. Caudell, Michael L. Bernard, and James B. Aimone. "Adult Neurogenesis: Implications on Human And Computational Decision Making." In Foundations of Augmented Cognition, 531–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-39454-6_57.

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Ølstørn, Håvard, Morten C. Moe, Mercy Varghese, and Iver A. Langmoen. "Neurogenesis and Potential Use of Stem Cells from Adult Human Brain." In Stem Cells, Human Embryos and Ethics, 41–53. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6989-5_4.

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de los Rios, Maria Elizabeth. "Reflections on neurogenetic challenges to human dignity and social doctrine of the Catholic Church." In Interreligious Perspectives on Mind, Genes and the Self, 112–16. Abingdon, Oxon ; New York, NY : Routledge, 2019. | Series: Routledge science and religion series: Routledge, 2018. http://dx.doi.org/10.4324/9780429456145-12.

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Bhaduri, Aparna, Madeline G. Andrews, and Arnold R. Kriegstein. "Human neurogenesis." In Patterning and Cell Type Specification in the Developing CNS and PNS, 751–67. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-814405-3.00029-1.

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"Timespans of Neurogenesis." In Atlas of Human Central Nervous System Development, 490–97. CRC Press, 2007. http://dx.doi.org/10.1201/9781420003284.ax1.

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Gong, Jing, Jiahui Kang, Minghui Li, Xiao Liu, Jun Yang, and Haiwei Xu. "Applications of Neural Organoids in Neurodevelopment and Regenerative Medicine." In Organoids [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.104044.

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Recent advances in stem cell technologies have enabled the application of three-dimensional neural organoids for exploring the mechanisms of neurodevelopment and regenerative medicine. Over the past decade, series of studies have been carried out to investigate the cellular and molecular events of human neurogenesis using animal models, while the species differences between animal models and human being prevent a full understanding of human neurogenesis. Human neural organoids provide a new model system for gaining a more complete understanding of human neural development and their applications in regenerative medicine. In this chapter, the recent advances of the neural organoids of the brain and retina as well as their applications in neurodevelopment and regenerative medicine are reviewed.
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Cho, Kyung-Ok, and Jenny Hsieh. "Adult Neurogenesis in Epileptogenesis and Comorbidities." In Jasper's Basic Mechanisms of the Epilepsies, edited by Annamaria Vezzani and Helen E. Scharfman, 523–38. 5th ed. Oxford University PressNew York, 2024. http://dx.doi.org/10.1093/med/9780197549469.003.0025.

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Abstract Epilepsy is a lifelong, devastating disease that affects all ages. Epileptic seizures generate abnormal adult-born granule cells (abGCs) in the dentate gyrus, which can contribute to the development of epilepsy and comorbidities. In this chapter, we present the characteristic features and potential significance of abGC abnormalities: increased proliferation and subsequent reduction of neural progenitors, persistent hilar basal dendrites, sprouting of mossy fibers, production of hilar ectopic granule cells, and dispersion of granule cells. We also describe several key molecules that regulate seizure-induced aberrant neurogenesis. We then discuss the role of reactive astrocytes and microglia in each step of hippocampal neurogenesis during the epileptogenesis. Finally, we review the crucial findings regarding the functional implications of abnormal abGCs in epileptogenesis and summarize comorbid illnesses such as cognitive impairment and mood disturbances. Seizure-generated abGCs represent an attractive target for treating epilepsy and associated psychiatric dysfunction. Therefore, developing novel and selective antiepileptic drugs will require more basic research on the molecular mechanisms governing aberrant hippocampal neurogenesis, as well as exploiting human and non-human primate models.
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Conference papers on the topic "Human neurogenesis"

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Proshchina, Alexandra, Anastasia Kharlamova, Olga Godovalova, Evgeniya Grushetskaya, and Sergey Saveliev. "IMMUNOPHENOTYPIC PROFILES OF NEUROGENESIS IN THE DEVELOPMENT OF THE HUMAN CEREBRAL CORTEX." In XX INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY, 230–31. LCC MAKS Press, 2024. http://dx.doi.org/10.29003/m4000.sudak.ns2024-20/230-231.

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Bobkova, Natalia Victorovna, Rimma Alekseevna Poltavtseva, Daria Jurievna Zhdanova, Vladimir Igorevich Kovalev, and Alina Vadimovna Chaplygina. "THE EFFECT OF YB-1 PROTEIN IN СHIMERIC MODEL OF ALZHEIMER’S DISEASE." In NEW TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2021. http://dx.doi.org/10.47501/978-5-6044060-1-4.10.

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The paper focuses on the molecular cell interaction of human mesenchymal stromal cells with the hippocampal primary culture of transgenic XFAD mice and the effect of multifunctional YB-1 protein on the memory and state of adult neurogenesis niches in animals with a chi-meric model of Alzheimer's disease. The results suggest the usefulness of a comprehensive use of cell therapy in combination with YB-1 to activate compensatory mechanisms in patients with Alzheimer's disease.
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Yildirim, Murat, Danielle Feldman, Tianyu Wang, Dimitre G. Ouzounov, Stephanie Chou, Justin Swaney, Kwanghun Chung, Chris Xu, Peter T. C. So, and Mriganka Sur. "Third harmonic generation imaging of intact human cerebral organoids to assess key components of early neurogenesis in Rett Syndrome (Conference Presentation)." In Multiphoton Microscopy in the Biomedical Sciences XVII, edited by Ammasi Periasamy, Peter T. So, Xiaoliang S. Xie, and Karsten König. SPIE, 2017. http://dx.doi.org/10.1117/12.2256182.

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Porcino, Caterina. "NEUROTROPHINS, TRK-RECEPTORS AND CALCIUM BINDING PROTEIN LOCALIZATION IN MECHANOSENSORY SYSTEMS AND RETINA OF NOTHOBRANCHIUS GUENTHERI." In Dubai International Conference on Research in Life-Science & Healthcare, 22-23 February 2024. Global Research & Development Services, 2024. http://dx.doi.org/10.20319/icrlsh.2024.4243.

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Neurotrophins are growth factors playing a crucial role in the survival, differentiation, development, and plasticity of neurons. They exert their effects by binding to specific receptors (Trks) in the central and peripheral nervous systems, including sensory organs. Calcium-binding proteins (CaBPs) are also present in these systems. They are involved in essential physiological functions related to calcium ions, such as nerve impulse transmission, neurogenesis, synaptic plasticity, and transmission. Further, CaBPs are supposed to be involved in neuron protection. Neurotrophins and CaBPs perform their roles in various vertebrates, including fish. Nonetheless, based on existing knowledge, there is no record of the presence of neurotrophins in the sensory organs of Nothobranchius guentheri. Due to its relatively short lifespan, N. guentheri has emerged as a valuable model for aging studies, holding significant relevance in the field of translational medicine. As a teleost, its sensory systems share several morphological and functional similarities with mammals, including humans. However, unlike mammals, fish sensory organs keep the regeneration capability. In light of this, the present research sought to identify the neurotrophin-receptor systems and calcium-binding proteins (CaBPs) in the mechanosensory organs and retina of N. guentheri. Utilizing immunoperoxidase, single, and double immunofluorescence methods, the investigation unveiled the localization of neurotrophins and CaBPs in the inner ear, neuromasts of the lateral line system, and retinal cells of N. guentheri. This newfound information indicates the influence of these proteins on the biology of N. guentheri, reinforcing its suitability as a model for aging studies. The implications of these findings could significantly contribute to research on age-related neurodegeneration within the realm of translational medicine.
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