Relevant bibliographies by topics / Neural progenitor

Academic literature on the topic 'Neural progenitor'

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Published: 4 June 2021
Last updated: 22 February 2023

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Journal articles on the topic "Neural progenitor"

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Easterday, Mathew C., Joseph D. Dougherty, Robert L. Jackson, Jing Ou, Ichiro Nakano, Andres A. Paucar, Babak Roobini, et al. "Neural progenitor genes." Developmental Biology 264, no. 2 (December 2003): 309–22. http://dx.doi.org/10.1016/j.ydbio.2003.09.003.

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Allen, Nicholas D. "Temporal and epigenetic regulation of neurodevelopmental plasticity." Philosophical Transactions of the Royal Society B: Biological Sciences 363, no. 1489 (February 20, 2007): 23–38. http://dx.doi.org/10.1098/rstb.2006.2010.

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The anticipated therapeutic uses of neural stem cells depend on their ability to retain a certain level of developmental plasticity. In particular, cells must respond to developmental manipulations designed to specify precise neural fates. Studies in vivo and in vitro have shown that the developmental potential of neural progenitor cells changes and becomes progressively restricted with time. For in vitro cultured neural progenitors, it is those derived from embryonic stem cells that exhibit the greatest developmental potential. It is clear that both extrinsic and intrinsic mechanisms determine the developmental potential of neural progenitors and that epigenetic, or chromatin structural, changes regulate and coordinate hierarchical changes in fate-determining gene expression. Here, we review the temporal changes in developmental plasticity of neural progenitor cells and discuss the epigenetic mechanisms that underpin these changes. We propose that understanding the processes of epigenetic programming within the neural lineage is likely to lead to the development of more rationale strategies for cell reprogramming that may be used to expand the developmental potential of otherwise restricted progenitor populations.
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Shih, Hung-Yu, Chia-Wei Chang, Yi-Chieh Chen, and Yi-Chuan Cheng. "Identification of the Time Period during Which BMP Signaling Regulates Proliferation of Neural Progenitor Cells in Zebrafish." International Journal of Molecular Sciences 24, no. 2 (January 15, 2023): 1733. http://dx.doi.org/10.3390/ijms24021733.

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Bone morphogenetic protein (BMP) signaling regulates neural induction, neuronal specification, and neuronal differentiation. However, the role of BMP signaling in neural progenitors remains unclear. This is because interruption of BMP signaling before or during neural induction causes severe effects on subsequent neural developmental processes. To examine the role of BMP signaling in the development of neural progenitors in zebrafish, we bypassed the effect of BMP signaling on neural induction and suppressed BMP signaling at different time points during gastrulation using a temporally controlled transgenic line carrying a dominant-negative form of Bmp receptor type 1aa and a chemical inhibitor of BMP signaling, DMH1. Inhibiting BMP signaling from 8 hpf could bypass BMP regulation on neural induction, induce the number of proliferating neural progenitors, and reduce the number of neuronal precursors. Inhibiting BMP signaling upregulates the expression of the Notch downstream gene hairy/E(spl)-related 2 (her2). Inhibiting Notch signaling or knocking down the Her2 function reduced neural progenitor proliferation, whereas inactivating BMP signaling in Notch-Her2 deficient background restored the number of proliferating neural progenitors. These results reveal the time window for the proliferation of neural progenitors during zebrafish development and a fine balance between BMP and Notch signaling in regulating the proliferation of neural progenitor cells.
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Lillien, Laura. "Neural progenitors and stem cells: mechanisms of progenitor heterogeneity." Current Opinion in Neurobiology 8, no. 1 (February 1998): 37–44. http://dx.doi.org/10.1016/s0959-4388(98)80006-8.

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Mitra, Siddhartha S., Abdullah H. Feroze, Sharareh Gholamin, Chase Richard, Rogelio Esparza, Michael Zhang, Tej D. Azad, et al. "Neural Placode Tissue Derived From Myelomeningocele Repair Serves as a Viable Source of Oligodendrocyte Progenitor Cells." Neurosurgery 77, no. 5 (July 29, 2015): 794–802. http://dx.doi.org/10.1227/neu.0000000000000918.

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Abstract BACKGROUND: The presence, characteristics, and potential clinical relevance of neural progenitor populations within the neural placodes of myelomeningocele patients remain to be studied. Neural stem cells are known to reside adjacent to ependyma-lined surfaces along the central nervous system axis. OBJECTIVE: Given such neuroanatomic correlation and regenerative capacity in fetal development, we assessed myelomeningocele-derived neural placode tissue as a potentially novel source of neural stem and progenitor cells. METHODS: Nonfunctional neural placode tissue was harvested from infants during the surgical repair of myelomeningocele and subsequently further analyzed by in vitro studies, flow cytometry, and immunofluorescence. To assess lineage potential, neural placode-derived neurospheres were subjected to differential media conditions. Through assessment of platelet-derived growth factor receptor α (PDGFRα) and CD15 cell marker expression, Sox2+Olig2+ putative oligodendrocyte progenitor cells were successfully isolated. RESULTS: PDGFRαhiCD15hi cell populations demonstrated the highest rate of self-renewal capacity and multipotency of cell progeny. Immunofluorescence of neural placode-derived neurospheres demonstrated preferential expression of the oligodendrocyte progenitor marker, CNPase, whereas differentiation to neurons and astrocytes was also noted, albeit to a limited degree. CONCLUSION: Neural placode tissue contains multipotent progenitors that are preferentially biased toward oligodendrocyte progenitor cell differentiation and presents a novel source of such cells for use in the treatment of a variety of pediatric and adult neurological disease, including spinal cord injury, multiple sclerosis, and metabolic leukoencephalopathies.
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Feng, Shiqing, Juan Xiao, Fabin Han, Lin Chen, Wenyong Gao, Gengsheng Mao, and Hongyun Huang. "Neurorestorative clinical application standards for the culture and quality control of neural progenitor/precursor cells (version 2017)." Journal of Neurorestoratology 1, no. 1 (2018): 32–36. http://dx.doi.org/10.2147/jn.s147917.

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In order to promote the clinical use of neural progenitor or precursor cells for treating neurological diseases and damage, we need to standardize culture procedures for these cells. The Chinese Association of Neurorestoratology put forward these standards for training operators, standardized use and management of materials and equipment, standardized isolation and culture for neural progenitor/precursor cells, and the standardized management in preservation, transport, and related safe operation procedures of the neural progenitors. These cultures and quality control standards also include the Good Manufacturing Practice environment, routine maintenance as well as the monitoring and reporting of the clinical-grade neural progenitor cells. The aim of these standards is to improve the therapeutic efficacy and minimize the possible side effects from lake of quality control.
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Hill, Justin, and John Cave. "Targeting the vasculature to improve neural progenitor transplant survival." Translational Neuroscience 6, no. 1 (January 1, 2015): 162–67. http://dx.doi.org/10.1515/tnsci-2015-0016.

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AbstractNeural progenitor transplantation is a promising therapeutic option for several neurological diseases and injuries. In nearly all human clinical trials and animal models that have tested this strategy, the low survival rate of progenitors after engraftment remains a significant challenge to overcome. Developing methods to improve the survival rate will reduce the number of cells required for transplant and will likely enhance functional improvements produced by the procedure. Here we briefly review the close relationship between the blood vasculature and neural progenitors in both the embryo and adult nervous system. We also discuss previous studies that have explored the role of the vasculature and hypoxic pre-conditioning in neural transplants. From these studies, we suggest that hypoxic pre-conditioning of a progenitor pool containing both neural and endothelial cells will improve engrafted transplanted neuronal survival rates.
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Sánchez-González, Rebeca, María Figueres-Oñate, Ana Cristina Ojalvo-Sanz, and Laura López-Mascaraque. "Cell Progeny in the Olfactory Bulb after Targeting Specific Progenitors with Different UbC-StarTrack Approaches." Genes 11, no. 3 (March 13, 2020): 305. http://dx.doi.org/10.3390/genes11030305.

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The large phenotypic variation in the olfactory bulb may be related to heterogeneity in the progenitor cells. Accordingly, the progeny of subventricular zone (SVZ) progenitor cells that are destined for the olfactory bulb is of particular interest, specifically as there are many facets of these progenitors and their molecular profiles remain unknown. Using modified StarTrack genetic tracing strategies, specific SVZ progenitor cells were targeted in E12 mice embryos, and the cell fate of these neural progenitors was determined in the adult olfactory bulb. This study defined the distribution and the phenotypic diversity of olfactory bulb interneurons from specific SVZ-progenitor cells, focusing on their spatial pallial origin, heterogeneity, and genetic profile.
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Alshawaf, Abdullah J., Ana Antonic, Efstratios Skafidas, Dominic Chi-Hung Ng, and Mirella Dottori. "WDR62 Regulates Early Neural and Glial Progenitor Specification of Human Pluripotent Stem Cells." Stem Cells International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/7848932.

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Mutations in WD40-repeat protein 62 (WDR62) are commonly associated with primary microcephaly and other developmental cortical malformations. We used human pluripotent stem cells (hPSC) to examine WDR62 function during human neural differentiation and model early stages of human corticogenesis. Neurospheres lacking WDR62 expression showed decreased expression of intermediate progenitor marker, TBR2, and also glial marker, S100β. In contrast, inhibition of c-Jun N-terminal kinase (JNK) signalling during hPSC neural differentiation induced upregulation of WDR62 with a corresponding increase in neural and glial progenitor markers, PAX6 and EAAT1, respectively. These findings may signify a role of WDR62 in specifying intermediate neural and glial progenitors during human pluripotent stem cell differentiation.
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Ruan, Xiangbin, Bowei Kang, Cai Qi, Wenhe Lin, Jingshu Wang, and Xiaochang Zhang. "Progenitor cell diversity in the developing mouse neocortex." Proceedings of the National Academy of Sciences 118, no. 10 (March 1, 2021): e2018866118. http://dx.doi.org/10.1073/pnas.2018866118.

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In the mammalian neocortex, projection neuron types are sequentially generated by the same pool of neural progenitors. How neuron type specification is related to developmental timing remains unclear. To determine whether temporal gene expression in neural progenitors correlates with neuron type specification, we performed single-cell RNA sequencing (scRNA-Seq) analysis of the developing mouse neocortex. We uncovered neuroepithelial cell enriched genes such as Hmga2 and Ccnd1 when compared to radial glial cells (RGCs). RGCs display dynamic gene expression over time; for instance, early RGCs express higher levels of Hes5, and late RGCs show higher expression of Pou3f2. Interestingly, intermediate progenitor cell marker gene Eomes coexpresses temporally with known neuronal identity genes at different developmental stages, though mostly in postmitotic cells. Our results delineate neural progenitor cell diversity in the developing mouse neocortex and support that neuronal identity genes are transcriptionally evident in Eomes-positive cells.
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Dissertations / Theses on the topic "Neural progenitor"

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Distasio, Andrew. "Novel Regulators of Neural Crest and Neural Progenitor Survival." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1593170783550813.

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Farnsworth, Dylan. "Temporal changes in neural progenitor competence." Thesis, University of Oregon, 2017. http://hdl.handle.net/1794/22280.

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Drosophila neural stem cells (neuroblasts) are a powerful model system for investigating stem cell self-renewal, specification of temporal identity, and progressive restriction in competence. Notch signaling is a conserved cue that is an important determinant of cell fate in many contexts across animal development; for example mammalian T cell differentiation in the thymus and neuroblast specification in Drosophila are both regulated by Notch signaling. However, Notch also functions as a mitogen, and constitutive Notch signaling potentiates T cell leukemia as well as Drosophila neuroblast tumors. While the role of Notch signaling has been studied in these and other cell types, it remains unclear how stem cells and progenitors change competence to respond to Notch over time. Notch is required in type II neuroblasts for normal development of their transit amplifying progeny, intermediate neural progenitors (INPs). Here we find that aging INPs lose competence to respond to constitutively active Notch signaling. Moreover, we show that reducing the levels of the old INP temporal transcription factor Eyeless/Pax6 allows Notch signaling to promote the de-differentiation of INP progeny into ectopic INPs, thereby creating a proliferative mass of ectopic progenitors in the brain. These findings provide a new system for studying progenitor competence, and identify a novel role for the conserved transcription factor Eyeless/Pax6 in blocking Notch signaling during development. This dissertation includes previously published, co-authored material
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Leeson, Hannah Caitlin. "P2X7 Receptor Regulation of Hippocampal Neural Progenitor Cells." Thesis, Griffith University, 2017. http://hdl.handle.net/10072/373045.

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Adult hippocampal neurogenesis plays an essential role in the formation and consolidation of new memories, spatial processing and some forms of learning. Identifying the molecular mechanisms that regulate hippocampal neural progenitor cells as they proliferate, differentiate, and are selected for either survival or cell death will provide a fundamental understanding of how this neurogenic niche coordinates these activities. Here, the roles of P2X7 receptors are examined for their influence over neural progenitor cell biology, particularly cell death, proliferation, and phagocytosis of apoptotic progenitors that have undergone programmed cell death. As a purinergic cation channel, P2X7 receptors are exceptionally versatile; their primary role is as ATP-gated calcium channels, and they have notable roles in the immune system, where they regulate cytokine release and form large transmembrane pores resulting in cell death. By acting as scavenger receptors, they can also mediate phagocytosis. These diverse roles were investigated in neural progenitor cells of the adult murine hippocampal neurogenic niche. Primary cultures of hippocampal neural progenitor cells were derived from adult female C57BL/6 mice and characterised using multimarker immunocytochemistry as P2X7 receptor positive type 2 neural progenitor cells, as defined by Sox2pos, nestinpos, BLBPpos, Mash1pos/neg, vimentinpos, Pax6pos, Prox1pos, DCXneg, GFAPneg staining patterns. For some experiments, cultures derived from P2X7 knock out mice (Pfizer) were also used. Calcium influx assays using the indicator dye Fluo-8-AM demonstrated functional activity of P2X7 receptors with the general agonist ATP (1 mM) and the more specific agonist BzATP (100 μM). Ethidium bromide uptake demonstrated that P2X7 receptors were able to form large transmembrane pores, a canonical function unique to this receptor, and confirmed the presence of a full length protein, as opposed to various splice variants. Live cell confocal microscopy revealed hippocampal neural progenitors are capable of phagocytosing fluorescent latex beads, and flow cytometry in conjunction with specific inhibitors demonstrated that P2X7 receptors are capable of facilitating this phagocytosis. The effects of purinergic signalling on neural progenitor proliferation were assessed using the thymidine analogue EdU. P2X7 receptors activated with either extracellular ATP or BzATP showed a significant dose-dependent decrease in proliferation. Cell death was not observed under these conditions and proliferation could be rescued upon exchange of medium. P2X7 receptor inhibition reduced the effects of extracellular ATP on proliferation, and use of neural progenitor cultures derived from genetically null mice corroborated this observation. Convergence with growth factor signalling pathways was also explored. The data presented here provides good evidence that P2X7 receptors function as scavenger receptors in the absence of ATP, allowing neural progenitor cells to phagocytose their apoptotic peers during target-independent programmed cell death, as well as governing rates of proliferation in the presence of ATP, possibly by regulating calcium dependent downstream signalling. Effector molecules of calcium signalling pathways were investigated following P2X7 receptor activation to determine some of the downstream mechanisms involved in P2X7 receptor mediated decreases in proliferation. Live cell calcium imaging identified the instigation of secondary calcium oscillations following extracellular ATP application; it was hypothesised that the decrease in proliferation was due to calcium dependent signalling cascades, involving calcium release from internal stores. Using confocal microscopy, calcium dependent transcription factors NFκB and NFAT1 were evaluated for their potential to translocate to the nucleus following purinergic stimulation. Extracellular ATP did not cause translocation of NFκB or NFAT1. A possible convergence with growth factor signalling pathways was investigated as the growth factors present in culture conditions exert powerful regulation over the cells and also utilise calcium and endoplasmic reticulum signalling to exert their effects. Inhibition of proteins involved in endoplasmic reticulum signalling caused a decrease in proliferation, as did growth factor withdrawal. Transcription factor analysis revealed that withdrawal of both EGF and bFGF caused NFAT1, but not NFκB, to translocate to the nucleus, a novel finding in these cells. The data presented here is among the first to examine the dichotomous signalling roles of P2X7 receptors in adult hippocampal neural progenitor cells. In mature neurons, P2X7 receptors have been implicated in various pathologies, and may present a therapeutic target for a number of neurological disorders. Understanding how these receptors regulate the physiology of stem and progenitor cells is an important first step in developing any regenerative therapies. Given the crucial role neurogenesis plays in both memory formation and hippocampal function, understanding these biological mechanisms is essential to addressing significant questions regarding neurogenesis and regeneration.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Natural Sciences
Science, Environment, Engineering and Technology
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Nunn, A. C. "The role of SOX9 in neural progenitor identity." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1372652/.

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Recent evidence has shown that SOX9 is required for the proliferation and multipotentiality of neural progenitors in the developing CNS. Notably, these findings suggest that in contrast to previous studies, SOX9 is important for differentiation along the neuronal lineage, both in the adult and embryonic CNS. Here, a phenotypic analysis of the CNS-specific Sox9-null forebrain, including detailed analysis of cortical lamination, shows that neurons of the appropriate layer-identity are born and migrate to their destined layers. All other parameters in this analysis were normal, with the exception of the formation of glia from the ventral and dorsal telencephalons, and midline glial structures, which were absent in the mutant. Since Sox9 is expressed long before the onset of gliogenesis in these brain regions, the possibility that Sox9 may ‘prime’ the progenitors of the ventricular zone to respond to a gliogenic signal arose. To investigate this, populations of Sox9-deficient and wild-type dorsal telencephalon cells were enriched for progenitors and subjected to transcriptional profiling. Bioinformatic analysis revealed that ‘vascular endothelial growth factor’ receptors, which are important for gliogenesis, were down-regulated, in addition to two transcription factors. Previously, Sox9-deficient neural progenitors have been shown to generate neurospheres poorly, and so the dataset of potential targets was used to identify candidates that might mediate this reduced neurosphere-forming ability. Thirteen down-regulated targets were confirmed by qPCR, six of which were expressed in the same distribution as Sox9 in the embryonic telencephalon; three were also expressed in neurosphere cultures. Of these, one encoded a K+ channel (Kir4.1), and the other a modulator of the GABAA channel (DBI). In order to show that reduced expression of one of these might contribute to the Sox9-deficient neurosphere phenotype, pharmacological modulators were used and showed that blockade of Kir4.1 or enhancement of GABAA channels mimicked the effect of Sox9 loss, leaving open the possibility that Kir4.1 or DBI expression might mediate this effect.
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Dause, Tyler. "Investigating Neural Stem and Progenitor Cell Intracrine Signaling." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1555618643450352.

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Buscarlet, Manuel. "The neural progenitor to neuron transition : role and regulation of GrouchoTLE proteins." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115670.

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Groucho/transducin-like Enhancer of split (Gro/TLE) family proteins are corepressors found as part of multiple transcriptional complexes that play significant roles during many developmental processes, including neurogenesis. This thesis sought to characterize the molecular mechanisms underlying the biological activity of Gro/TLE1. More specifically, the aim was to clarify the contribution of different transcriptional cofactors, as well as phosphorylation events induced by cofactor binding, to Gro/TLE1 ability to inhibit neuronal differentiation from proliferating neural progenitor cells.
By characterizing specific point mutations within the C-terminal domain of Gro/TLE1, we were able to selectively impair binding of Gro/TLE1 to different classes of DNA-binding proteins and then assess the effect of those mutations on Gro/TLE1 anti-neurogenic function. These studies showed that the inhibition of cerebral cortex (cortical) neuron differentiation by Gro/TLE1 requires interaction with transcription factors that use short tetrapeptide sequences, WRP(W/Y), to recruit Gro/TLE1. In contrast, interactions with proteins that either interact with the C-terminal domain of Gro/TLE1 using a different type of binding sequence, termed engrailed homology 1 (Eh1) motif, or bind to the N-terminal part of the protein, are not required for Gro/TLE1 anti-neurogenic function.
Using a similar strategy based on mutation analysis, we characterized point mutations that block the hyperphosphorylation of Gro/TLE1 induced by transcription cofactor binding ("cofactor-activated phosphorylation") without impairing cofactor binding and transcriptional corepression ability. These mutations map at phosphorylatable serine residues, Ser-286, Ser-289, and Ser298. Mutation of those residues to alanine blocks/reduces both cofactor-activated phosphorylation and anti-neurogenic activity of Gro/TLE1, demonstrating that cofactor-activated phosphorylation is required for that function. Tandem mass spectroscopy analysis showed further that Ser-286 is phosphorylated. Taken together, these findings characterize the role of cofactor-activated phosphorylation and identify residues important for this mechanism.
Our studies also showed that homeodomain-interacting protein kinase 2 (HIPK2) mediates phosphorylation of Gro/TLE1 when the latter is complexed with transcriptional partners of the WRP(W/Y) motif family. However, HIPK2 is not involved in Gro/TLE1 cofactor-activated phosphorylation. Rather, HIPK2--mediated phosphorylation is antagonistic to the latter and decreases the ability of Gro/TLE1 to interact and repress transcription with WRP(W/Y) motif proteins.
Taken together, these results improve significantly our understanding of the mechanisms underlying the anti-neurogenic function of Gro/TLE1. This information provides new insight into the regulation of mammalian neuronal development and, possibly, other developmental processes controlled by Gro/TLE proteins.
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Curtis, Maurice A. "Neural progenitor cells in the Huntington's Disease human brain." Thesis, University of Auckland, 2004. http://hdl.handle.net/2292/3114.

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The recent demonstration of endogenous progenitor cells in the adult mammalian brain raises the exciting possibility that these undifferentiated cells may be able to generate new neurons for cell replacement in diseases such as Huntington's disease (HD). Previous studies have shown that neural stem cells in the rodent brain subependymal layer (SEL), adjacent to the caudate nucleus, proliferate and differentiate into neurons and glial cells but no previous study has characterised the human SEL or shown neurogenesis in the diseased human brain. In this study, histochemical and immunohistochemical techniques were used to demonstrate the regional anatomy and staining characteristics of the normal and HD brain SEL using light and laser scanning confocal microscopy. The results demonstrated that the normal and HD SEL contained migrating neuroblasts, glial cells and precursor cells but there were more of each cell type present in the HD brain, and that the increase in cell numbers correlated with HD neuropathological grade. The normal and HD SEL was stained with a proliferative marker, proliferating cell nuclear antigen (PCNA), to label dividing cells. The results showed a significant increase in the number of dividing cells in the HD brain that correlated with HD grade and with CAG repeat length. Furthermore, the results showed that neurogenesis had occurred in the SEL as evidenced by co-localisation of PCNA and the neuronal marker βIII-tubulin. Also, gliogenesis had occurred in the SEL as evidenced by the co-localisation of PCNA with the glial marker GFAP. These studies also revealed a 2.6 fold increase in the number of new neurons in the HD SEL. PCNA positive cells were distributed throughout the SEL overlying the caudate nucleus but most notably the ventral and central regions of the SEL adjacent to the caudate nucleus contained the highest number of proliferating cells. I examined the SEL for mature cell markers and demonstrated many of the same cell types that are present in the normal striatum. With the exception of neuropeptide Y (NPY) neurons, there was a reduction in the number of mature neurons in the HD SEL. The NPY neurons were more abundant in the HD SEL suggesting they play a role in progenitor cell proliferation. The results in this thesis provide evidence of increased progenitor cell proliferation and neurogenesis in the diseased adult human brain and indicate the regenerative potential of the human brain. These findings may be of major relevance to the development of therapeutic approaches in the treatment of neurodegenerative diseases.
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Smith, Edward John. "Establishing a neural progenitor cell model of Huntington's disease." Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/establishing-a-neural-progenitor-cell-model-of-huntingtons-disease(5bcdd521-e71a-4dcb-b833-971f32576c2a).html.

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Huntington's disease (HD) is caused by the expansion of a CAG repeat in the huntingtin (HTT) gene The R6/2 transgenic mouse model exhibits a rapid onset of Huntington's disease-like phenotypes including neurodegeneration and aggregation of mutant huntingtin protein (mHTT). Neural progenitor cells (NPCs) are a pool of cells with stem cell-like properties and are responsible for self-renewal and differentiation into the cells of the central nervous system and mature brain. In this thesis, NPC lines were established from cells extracted from foetal R6/2 and wildtype mouse embryos and cultured in optimised culture media. NPCs were successfully maintained in a mitotic state as monolayer cultures for multiple passages without effects to karyotype or CAG repeat length. Cultures were differentiated by removal of growth factors, into mixed neurons and glia populations that expressed proteins indicative of mature cell types; neurons showed evidence of synaptophysin expression at junctions between cell neurites, suggesting synaptic functionality and formation of rudimentary neural networks. After differentiation, mHTT aggregation was detectable using immunohistochemistry from 14 days of differentiation in 5% of R6/2 cell nuclei, rising to 20% by 28 days, recapitulating an HD-like phenotype found in vivo. Detection of detergent insoluble mHTT-aggregated protein was also validated via western blotting. Super high resolution cell imaging showed aggregation of mHTT is also present in the cytoplasm. High-content imaging analysis system was performed using the Operetta system to explore morphological differences between WT and R6/2 cultures, as well as within the subset of cells with detectable aggregation. R6/2 nuclei were found to be larger than those of WT cells. Novel compounds known to affect protein aggregation were applied to the cell lines to assess their potential use in screening for approaches to modulation mHTT aggregation. The cells developed in this thesis are a novel and useful complement to the R6/2 mouse; phenotypes observed in vivo can be interrogated at the molecular level in terms of how mHTT protein misfolding and aggregation occur and how this affects cellular function.
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Hemmati, Houman David Rothenberg Ellen V. "Neural stem and progenitor cells in cancer and development /." Diss., Pasadena, Calif. : Caltech, 2006. http://resolver.caltech.edu/CaltechETD:etd-05232006-140457.

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Robins, Sarah. "Neural stem/progenitor cells in the adult mouse hypothalamus." Thesis, University of Sheffield, 2009. http://etheses.whiterose.ac.uk/111/.

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Adult neural stem cells are now widely accepted to exist in the neurogenic regions of the subventricular zone and dentate gyrus; however there is increasing evidence to suggest that neurogenesis may also occur in other brain regions. It has been proposed that one such population of neural stem cells resides in the hypothalamus, more specifically in the ependymal lining of the third ventricle. In this thesis, I tested the hypothesis that stem cells exist in defined regions of the adult mouse hypothalamus. My work confirms the presence of stem/progenitor cells in the adult mouse hypothalamus. Analysis of neural 'stem cell markers', both in vivo and in vitro, suggests the presence of different populations of stem/progenitor cells occupying discrete territories of the ependymal zone. Some markers are common to those found in other adult neural stem cell niches, whilst others are unique to the hypothalamus. I have isolated hypothalamic stem/progenitor cells, and assayed their character and potential for both self-renewal and differentiation using the neurosphere assay. I show that hypothalamic neurospheres can be propagated in culture for extended periods of time, and that they can differentiate into cells of all three neural lineages. I have also determined the precise location of neurosphere-forming cells in the hypothalamus, showing that proliferative capacity is restricted to defined regions. Within these regions, I have also identified separate populations of proliferating cells that vary in their capacity for self-renewal, and correlated this with marker profiles. This data supports previous reports suggesting that tanycytes act as neural stem cells in the hypothalamus. Finally, I have started work investigating the control of hypothalamic stem/progenitor proliferation by fibroblast growth factors. I demonstrate that FGF signalling is necessary for in vitro proliferation. Finally, my studies suggest that endogenous FGFs may regulate hypothalamic stem cell proliferation.
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Books on the topic "Neural progenitor"

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Deleyrolle, Loic P., ed. Neural Progenitor Cells. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1783-0.

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Reynolds, Brent A., and Loic P. Deleyrolle, eds. Neural Progenitor Cells. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-574-3.

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Reynolds, Brent A., and Loic P. Deleyrolle. Neural progenitor cells: Methods and protocols. New York: Humana Press, 2013.

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Garcia-Verdugo, Jose Manuel, Arturo Alvarez-Buylla, and Sara Gil-Perotín. Identification and Characterization of Neural Progenitor Cells in the Adult Mammalian Brain. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-88719-5.

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Arturo, Álvarez-Buylla, and García-Verdugo José Manuel, eds. Identification and characterization of neural progenitor cells in the adult mammalian brain. Berlin: Springer, 2009.

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Reynolds, Brent A., and Loic P. Deleyrolle. Neural Progenitor Cells: Methods and Protocols. Humana Press, 2016.

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Deleyrolle, Loic P. Neural Progenitor Cells: Methods and Protocols. Springer, 2021.

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Deleyrolle, Loic P. Neural Progenitor Cells: Methods and Protocols. Springer, 2022.

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Costa, Marcos R., Cecilia Hedin-Pereira, and Caroline Rouaux, eds. Progenitor Diversity and Neural Cell Specification in the Central Nervous System. Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-683-8.

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Seaberg, Raewyn M. Mammalian brain development: The role of distinct neural stem and progenitor cells from embryonic neural induction to adult neurogenesis. 2004.

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Book chapters on the topic "Neural progenitor"

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Horie, Nobutaka. "Neural Stem Cells/Neuronal Progenitor Cells." In Cell Therapy Against Cerebral Stroke, 27–37. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56059-3_3.

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Lindholm, Dan, Johanna Mäkelä, and Laura Korhonen. "PACAP and Neural Progenitor Cells." In Current Topics in Neurotoxicity, 53–63. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-35135-3_5.

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Kelly, Stephen, Maeve Caldwell, Matthew P. Keasey, Jessica A. Cooke, and James B. Uney. "Identifying Neural Progenitor Cells in the Adult Brain." In Neural Cell Transplantation, 217–30. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-931-4_15.

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Nedachi, Taku. "Neural Stem/Progenitor Cells and Progranulin." In Progranulin and Central Nervous System Disorders, 127–38. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-6186-9_8.

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Vestergaard, Jacob S., Anders L. Dahl, Peter Holm, and Rasmus Larsen. "Pipeline for Tracking Neural Progenitor Cells." In Medical Computer Vision. Recognition Techniques and Applications in Medical Imaging, 155–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-36620-8_16.

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Muotri, Alysson R. "L1 Retrotransposition in Neural Progenitor Cells." In Methods in Molecular Biology, 157–63. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3372-3_11.

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Martins, Antonio H., Jose L. Roig-Lopez, and Maxine Nicole Gonzalez. "Neural Differentiation of Rodent Neural Progenitor Cells and Isolation and Enrichment of Human Neural Progenitor/Stem Cells." In Working with Stem Cells, 57–77. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30582-0_4.

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Profico, Daniela Celeste, Giada Sgaravizzi, Massimo Projetti Pensi, Gianmarco Muzi, Claudia Ricciolini, Maurizio Gelati, and Angelo Luigi Vescovi. "Cryopreservation of Human Neural Stem and Progenitor Cells." In Neural Stem Cell Assays, 61–65. Hoboken, NJ, USA: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118308295.ch6.

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Kondo, Yoichi, and Ian D. Duncan. "Transplantation of Oligodendrocyte Progenitor Cells in Animal Models of Leukodystrophies." In Neural Cell Transplantation, 175–85. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-931-4_12.

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Liao, Ronglih, and Regina L. Sohn. "Cardiac Stem and Progenitor Cells." In Cell Cycle Regulation and Differentiation in Cardiovascular and Neural Systems, 79–103. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-60327-153-0_5.

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Conference papers on the topic "Neural progenitor"

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Abasi, Sara, John R. Aggas, and Anthony Guiseppi-Elie. "Permissive Electroconductive Nanocomposites for Neuronal Progenitor Cells." In 2019 9th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2019. http://dx.doi.org/10.1109/ner.2019.8716893.

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Vestergaard, Jacob S., Anders L. Dahl, Peter Holm, and Rasmus Larsen. "Dynamically constrained pipeline for tracking neural progenitor cells." In SPIE Medical Imaging, edited by Metin N. Gurcan and Anant Madabhushi. SPIE, 2013. http://dx.doi.org/10.1117/12.2006996.

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Lee, Y.-S., G. Collins, and T. Livingston Arinzeh. "Neural differentiation of human neural stem/progenitor cells on piezoelectric scaffolds." In 2010 36th Annual Northeast Bioengineering Conference. IEEE, 2010. http://dx.doi.org/10.1109/nebc.2010.5458264.

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Hwang, C. M., S. K. Kim, J. H. Kim, A. Khademhosseini, and S. H. Lee. "Differentiation of human neural progenitor cells on PLGA microfibers." In 2009 IEEE 35th Annual Northeast Bioengineering Conference. IEEE, 2009. http://dx.doi.org/10.1109/nebc.2009.4967758.

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Smith, Edward, Kirupa Sathasivam, and Gillian Bates. "B17 Establishing a neural progenitor cell model of huntington’s disease." In EHDN 2018 Plenary Meeting, Vienna, Austria, Programme and Abstracts. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/jnnp-2018-ehdn.69.

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San, Isabelle V. Leefa Chong, Gaelle Prost, and Ulrike Nuber. "Abstract A09: Effects of Podocalyxin on neural stem/progenitor cells." In Abstracts: AACR Special Conference: Advances in Brain Cancer Research; May 27-30, 2015; Washington, DC. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.brain15-a09.

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Tandon, Nina, Elisa Cimetta, Alanna Taubman, Nicolette Kupferstein, Uday Madaan, Jason Mighty, Stephen Redenti, and Gordana Vunjak-Novakovic. "Biomimetic electrical stimulation platform for neural differentiation of retinal progenitor cells." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6610836.

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Jiang, Bo, Xinyuan Wang, Jianzhong Luo, Xiao Zhang, Yucui Xiong, and Hongwen Pang. "Convolutional Neural Networks in Automatic Recognition of Trans-differentiated Neural Progenitor Cells under Bright-Field Microscopy." In 2015 Fifth International Conference on Instrumentation & Measurement, Computer, Communication and Control (IMCCC). IEEE, 2015. http://dx.doi.org/10.1109/imccc.2015.33.

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Chen, Keren, William Ong, Sing Yian Chew, and Quan Liu. "Raman spectroscopy for discrimination of neural progenitor cells and their lineages (Conference Presentation)." In Advanced Biomedical and Clinical Diagnostic and Surgical Guidance Systems XV, edited by Tuan Vo-Dinh, Anita Mahadevan-Jansen, and Warren S. Grundfest. SPIE, 2017. http://dx.doi.org/10.1117/12.2250146.

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Gore, Kalea, and Deanna M. Thompson. "Effect of flow-stimulated vascular endothelial cell extracellular matrix on neural progenitor cell fate." In 2015 41st Annual Northeast Biomedical Engineering Conference (NEBEC). IEEE, 2015. http://dx.doi.org/10.1109/nebec.2015.7117100.

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Reports on the topic "Neural progenitor"

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Mangner, Thomas J. Radiopharmaceutical Tracers for Neural Progenitor Cells. Office of Scientific and Technical Information (OSTI), September 2006. http://dx.doi.org/10.2172/892567.

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Jones, Erin Boote. Effects of Substrate and Co-Culture on Neural Progenitor Cell Differentiation. Office of Scientific and Technical Information (OSTI), January 2008. http://dx.doi.org/10.2172/939376.

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Sullivan, Genevieve M. The Regenerative Response of Endogenous Neural Stem/Progenitor Cells to Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ad1012867.

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