Relevant bibliographies by topics / Human Induced neurons

Academic literature on the topic 'Human Induced neurons'

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Published: 15 June 2024

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  2. Dissertations / Theses
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Journal articles on the topic "Human Induced neurons":

1

Wang, Gefei, Rui Li, Zhiwu Jiang, Liming Gu, Yanxia Chen, Jianping Dai, and Kangsheng Li. "Influenza Virus Induces Inflammatory Response in Mouse Primary Cortical Neurons with Limited Viral Replication." BioMed Research International 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/8076989.

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Unlike stereotypical neurotropic viruses, influenza A viruses have been detected in the brain tissues of human and animal models. To investigate the interaction between neurons and influenza A viruses, mouse cortical neurons were isolated, infected with human H1N1 influenza virus, and then examined for the production of various inflammatory molecules involved in immune response. We found that replication of the influenza virus in neurons was limited, although early viral transcription was not affected. Virus-induced neuron viability decreased at 6 h postinfection (p.i.) but increased at 24 h p.i. depending upon the viral strain. Virus-induced apoptosis and cytopathy in primary cortical neurons were not apparent at 24 h p.i. The mRNA levels of inflammatory cytokines, chemokines, and type I interferons were upregulated at 6 h and 24 h p.i. These results indicate that the influenza virus induces inflammatory response in mouse primary cortical neurons with limited viral replication. The cytokines released in viral infection-induced neuroinflammation might play critical roles in influenza encephalopathy, rather than in viral replication-induced cytopathy.
2

Häkli, Martta, Satu Jäntti, Tiina Joki, Lassi Sukki, Kaisa Tornberg, Katriina Aalto-Setälä, Pasi Kallio, Mari Pekkanen-Mattila, and Susanna Narkilahti. "Human Neurons Form Axon-Mediated Functional Connections with Human Cardiomyocytes in Compartmentalized Microfluidic Chip." International Journal of Molecular Sciences 23, no. 6 (March 15, 2022): 3148. http://dx.doi.org/10.3390/ijms23063148.

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The cardiac autonomic nervous system (cANS) regulates cardiac function by innervating cardiac tissue with axons, and cardiomyocytes (CMs) and neurons undergo comaturation during the heart innervation in embryogenesis. As cANS is essential for cardiac function, its dysfunctions might be fatal; therefore, cardiac innervation models for studying embryogenesis, cardiac diseases, and drug screening are needed. However, previously reported neuron-cardiomyocyte (CM) coculture chips lack studies of functional neuron–CM interactions with completely human-based cell models. Here, we present a novel completely human cell-based and electrophysiologically functional cardiac innervation on a chip in which a compartmentalized microfluidic device, a 3D3C chip, was used to coculture human induced pluripotent stem cell (hiPSC)-derived neurons and CMs. The 3D3C chip enabled the coculture of both cell types with their respective culture media in their own compartments while allowing the neuronal axons to traverse between the compartments via microtunnels connecting the compartments. Furthermore, the 3D3C chip allowed the use of diverse analysis methods, including immunocytochemistry, RT-qPCR and video microscopy. This system resembled the in vivo axon-mediated neuron–CM interaction. In this study, the evaluation of the CM beating response during chemical stimulation of neurons showed that hiPSC-neurons and hiPSC-CMs formed electrophysiologically functional axon-mediated interactions.
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Cresto, Noémie, Camille Gardier, Marie-Claude Gaillard, Francesco Gubinelli, Pauline Roost, Daniela Molina, Charlène Josephine, et al. "The C-Terminal Domain of LRRK2 with the G2019S Substitution Increases Mutant A53T α-Synuclein Toxicity in Dopaminergic Neurons In Vivo." International Journal of Molecular Sciences 22, no. 13 (June 23, 2021): 6760. http://dx.doi.org/10.3390/ijms22136760.

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Alpha-synuclein (α-syn) and leucine-rich repeat kinase 2 (LRRK2) play crucial roles in Parkinson’s disease (PD). They may functionally interact to induce the degeneration of dopaminergic (DA) neurons via mechanisms that are not yet fully understood. We previously showed that the C-terminal portion of LRRK2 (ΔLRRK2) with the G2019S mutation (ΔLRRK2G2019S) was sufficient to induce neurodegeneration of DA neurons in vivo, suggesting that mutated LRRK2 induces neurotoxicity through mechanisms that are (i) independent of the N-terminal domains and (ii) “cell-autonomous”. Here, we explored whether ΔLRRK2G2019S could modify α-syn toxicity through these two mechanisms. We used a co-transduction approach in rats with AAV vectors encoding ΔLRRK2G2019S or its “dead” kinase form, ΔLRRK2DK, and human α-syn with the A53T mutation (AAV-α-synA53T). Behavioral and histological evaluations were performed at 6- and 15-weeks post-injection. Results showed that neither form of ΔLRRK2 alone induced the degeneration of neurons at these post-injection time points. By contrast, injection of AAV-α-synA53T alone resulted in motor signs and degeneration of DA neurons. Co-injection of AAV-α-synA53T with AAV-ΔLRRK2G2019S induced DA neuron degeneration that was significantly higher than that induced by AAV-α-synA53T alone or with AAV-ΔLRRK2DK. Thus, mutated α-syn neurotoxicity can be enhanced by the C-terminal domain of LRRK2G2019 alone, through cell-autonomous mechanisms.
4

Rawson, N. E., G. Gomez, B. Cowart, J. G. Brand, L. D. Lowry, E. A. Pribitkin, and D. Restrepo. "Selectivity and Response Characteristics of Human Olfactory Neurons." Journal of Neurophysiology 77, no. 3 (March 1, 1997): 1606–13. http://dx.doi.org/10.1152/jn.1997.77.3.1606.

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Rawson, N. E., G. Gomez, B. Cowart, J. G. Brand, L. D. Lowry, E. A. Pribitkin, and D. Restrepo. Selectivity and response characteristics of human olfactory neurons. J. Neurophysiol. 77: 1606–1613, 1997. Transduction mechanisms were investigated in human olfactory neurons by determining characteristics of odorant-induced changes in intracellular calcium concentration ([Ca2+]i). Olfactory neurons were freshly isolated from nasal biopsies, allowed to attach to coverslips, and loaded with the calcium-sensitive indicator fura-2. Changes in [Ca2+]i were studied in response to exposure to individual odors, or odorant mixtures composed to distinguish between transduction pathways mediated by adenosine 3′5′-monophosphate (cAMP; mix A) or inositol 1,4,5-trisphosphate (InsP3; mix B). Overall, 52% of biopsies produced one or more odorant-responsive olfactory neurons, whereas 24% of all olfactory neurons tested responded to odorant exposure with a change in [Ca2+]i. As in olfactory neurons from other species, the data suggest that odorant exposure elicited calcium influx via second-messenger pathways involving cAMP or InsP3. Unlike olfactory neurons from other species that have been tested, some human olfactory neurons responded to odorants with decreases in [Ca2+]i. Also in contrast with olfactory neurons from other species, human olfactory neurons were better able to discriminate between odorant mixtures in that no neuron responded to more than one type of odor or mixture. These results suggest the presence of a previously unreported type of olfactory transduction mechanism, and raise the possibility that coding of odor qualities in humans may be accomplished to some degree differently than in other vertebrates, with the olfactory neuron itself making a greater contribution to the discrimination process.
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Gunewardene, Niliksha, Duncan Crombie, Mirella Dottori, and Bryony A. Nayagam. "Innervation of Cochlear Hair Cells by Human Induced Pluripotent Stem Cell-Derived NeuronsIn Vitro." Stem Cells International 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/1781202.

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Induced pluripotent stem cells (iPSCs) may serve as an autologous source of replacement neurons in the injured cochlea, if they can be successfully differentiated and reconnected with residual elements in the damaged auditory system. Here, we explored the potential of hiPSC-derived neurons to innervate early postnatal hair cells, using establishedin vitroassays. We compared two hiPSC lines against a well-characterized hESC line. After ten days’ coculturein vitro, hiPSC-derived neural processes contacted inner and outer hair cells in whole cochlear explant cultures. Neural processes from hiPSC-derived neurons also made contact with hair cells in denervated sensory epithelia explants and expressed synapsin at these points of contact. Interestingly, hiPSC-derived neurons cocultured with hair cells at an early stage of differentiation formed synapses with a higher number of hair cells, compared to hiPSC-derived neurons cocultured at a later stage of differentiation. Notable differences in the innervation potentials of the hiPSC-derived neurons were also observed and variations existed between the hiPSC lines in their innervation efficiencies. Collectively, these data illustrate the promise of hiPSCs for auditory neuron replacement and highlight the need to develop methods to mitigate variabilities observed amongst hiPSC lines, in order to achieve reliable clinical improvements for patients.
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Kraskovskaya, Nina, Anastasia Bolshakova, Mikhail Khotin, Ilya Bezprozvanny, and Natalia Mikhailova. "Protocol Optimization for Direct Reprogramming of Primary Human Fibroblast into Induced Striatal Neurons." International Journal of Molecular Sciences 24, no. 7 (April 5, 2023): 6799. http://dx.doi.org/10.3390/ijms24076799.

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The modeling of neuropathology on induced neurons obtained by cell reprogramming technologies can fill a gap between clinical trials and studies on model organisms for the development of treatment strategies for neurodegenerative diseases. Patient-specific models based on patients’ cells play an important role in such studies. There are two ways to obtain induced neuronal cells. One is based on induced pluripotent stem cells. The other is based on direct reprogramming, which allows us to obtain mature neuronal cells from adult somatic cells, such as dermal fibroblasts. Moreover, the latter method makes it possible to better preserve the age-related aspects of neuropathology, which is valuable for diseases that occur with age. However, direct methods of reprogramming have a significant drawback associated with low cell viability during procedures. Furthermore, the number of reprogrammable neurons available for morphological and functional studies is limited by the initial number of somatic cells. In this article, we propose modifications of a previously developed direct reprogramming method, based on the combination of microRNA and transcription factors, which allowed us to obtain a population of functionally active induced striatal neurons (iSNs) with a high efficiency. We also overcame the problem of the presence of multinucleated neurons associated with the cellular division of starting fibroblasts. Synchronization cells in the G1 phase increased the homogeneity of the fibroblast population, increased the survival rate of induced neurons, and eliminated the presence of multinucleated cells at the end of the reprogramming procedure. We have demonstrated that iSNs are functionally active and able to form synaptic connections in co-cultures with mouse cortical neurons. The proposed modifications can also be used to obtain a population of other induced neuronal types, such as motor and dopaminergic ones, by selecting transcription factors that determine differentiation into a region-specific neuron.
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Perego, M. Chiara, Benjamin D. McMichael, Nicholas R. McMurry, Scott W. Ventrello, and Lisa J. Bain. "Arsenic Impairs Differentiation of Human Induced Pluripotent Stem Cells into Cholinergic Motor Neurons." Toxics 11, no. 8 (July 25, 2023): 644. http://dx.doi.org/10.3390/toxics11080644.

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Arsenic exposure during embryogenesis can lead to improper neurodevelopment and changes in locomotor activity. Additionally, in vitro studies have shown that arsenic inhibits the differentiation of sensory neurons and skeletal muscle. In the current study, human-induced pluripotent stem (iPS) cells were differentiated into motor neurons over 28 days, while being exposed to up to 0.5 μM arsenic. On day 6, neuroepithelial progenitor cells (NEPs) exposed to arsenic had reduced transcript levels of the neural progenitor/stem cell marker nestin (NES) and neuroepithelial progenitor marker SOX1, while levels of these transcripts were increased in motor neuron progenitors (MNPs) at day 12. In day 18 early motor neurons (MNs), choline acetyltransferase (CHAT) expression was reduced two-fold in cells exposed to 0.5 μM arsenic. RNA sequencing demonstrated that the cholinergic synapse pathway was impaired following exposure to 0.5 μM arsenic, and that transcript levels of genes involved in acetylcholine synthesis (CHAT), transport (solute carriers, SLC18A3 and SLC5A7) and degradation (acetylcholinesterase, ACHE) were all downregulated in day 18 early MNs. In day 28 mature motor neurons, arsenic significantly downregulated protein expression of microtubule-associated protein 2 (MAP2) and ChAT by 2.8- and 2.1-fold, respectively, concomitantly with a reduction in neurite length. These results show that exposure to environmentally relevant arsenic concentrations dysregulates the differentiation of human iPS cells into motor neurons and impairs the cholinergic synapse pathway, suggesting that exposure impairs cholinergic function in motor neurons.
8

Karpe, Yashashree, Zhenyu Chen, and Xue-Jun Li. "Stem Cell Models and Gene Targeting for Human Motor Neuron Diseases." Pharmaceuticals 14, no. 6 (June 12, 2021): 565. http://dx.doi.org/10.3390/ph14060565.

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Motor neurons are large projection neurons classified into upper and lower motor neurons responsible for controlling the movement of muscles. Degeneration of motor neurons results in progressive muscle weakness, which underlies several debilitating neurological disorders including amyotrophic lateral sclerosis (ALS), hereditary spastic paraplegias (HSP), and spinal muscular atrophy (SMA). With the development of induced pluripotent stem cell (iPSC) technology, human iPSCs can be derived from patients and further differentiated into motor neurons. Motor neuron disease models can also be generated by genetically modifying human pluripotent stem cells. The efficiency of gene targeting in human cells had been very low, but is greatly improved with recent gene editing technologies such as zinc-finger nucleases (ZFN), transcription activator-like effector nucleases (TALEN), and CRISPR-Cas9. The combination of human stem cell-based models and gene editing tools provides unique paradigms to dissect pathogenic mechanisms and to explore therapeutics for these devastating diseases. Owing to the critical role of several genes in the etiology of motor neuron diseases, targeted gene therapies have been developed, including antisense oligonucleotides, viral-based gene delivery, and in situ gene editing. This review summarizes recent advancements in these areas and discusses future challenges toward the development of transformative medicines for motor neuron diseases.
9

Tian, Jie L., Chia-Wei Huang, Farzad Eslami, Michael Philip Mannino, Rebecca Lee Mai, and Gerald W. Hart. "Regulation of Primary Cilium Length by O-GlcNAc during Neuronal Development in a Human Neuron Model." Cells 12, no. 11 (May 31, 2023): 1520. http://dx.doi.org/10.3390/cells12111520.

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The primary cilium plays critical roles in the homeostasis and development of neurons. Recent studies demonstrate that cilium length is regulated by the metabolic state of cells, as dictated by processes such as glucose flux and O-GlcNAcylation (OGN). The study of cilium length regulation during neuron development, however, has been an area left largely unexplored. This project aims to elucidate the roles of O-GlcNAc in neuronal development through its regulation of the primary cilium. Here, we present findings suggesting that OGN levels negatively regulate cilium length on differentiated cortical neurons derived from human-induced pluripotent stem cells. In neurons, cilium length increased significantly during maturation (after day 35), while OGN levels began to drop. Long-term perturbation of OGN via drugs, which inhibit or promote its cycling, during neuron development also have varying effects. Diminishing OGN levels increases cilium length until day 25, when neural stem cells expand and undergo early neurogenesis, before causing cell cycle exit defects and multinucleation. Elevating OGN levels induces greater primary cilia assembly but ultimately results in the development of premature neurons, which have higher insulin sensitivity. These results indicate that OGN levels and primary cilium length are jointly critical in proper neuron development and function. Understanding the interplays between these two nutrient sensors, O-GlcNAc and the primary cilium, during neuron development is important in paving connections between dysfunctional nutrient-sensing and early neurological disorders.
10

Cheng, Xueyan, Zijian Tan, Xiao Huang, Yimin Yuan, Shangyao Qin, Yakun Gu, Dan Wang, Cheng He, and Zhida Su. "Inhibition of Glioma Development by ASCL1-Mediated Direct Neuronal Reprogramming." Cells 8, no. 6 (June 11, 2019): 571. http://dx.doi.org/10.3390/cells8060571.

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Direct conversion of non-neural cells into induced neurons holds great promise for brain repair. As the most common malignant tumor in the central nervous system, glioma is currently incurable due to its exponential growth and invasive behavior. Given that neurons are irreversible postmitotic cells, reprogramming glioma cells into terminally differentiated neuron-like cells represents a potential approach to inhibit brain tumor development. We here show that human glioma cells can be directly, rapidly and efficiently reprogrammed into terminally differentiated neuron-like cells by the single transcription factor ASCL1 (Achaete-scute complex-like 1, also known as MASH1). These induced cells exhibit typical neuron-like morphology and express multiple neuron-specific markers. Importantly, ASCL1-mediated neuronal reprogramming drives human glioma cells to exit the cell cycle and results in dramatic inhibition of proliferation, both in vitro and in vivo. Taken together, this proof-of-principle study demonstrates a potential strategy for impeding brain tumor development by ASCL1-induced direct neuronal reprogramming.
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Journal articles Dissertations / Theses

Dissertations / Theses on the topic "Human Induced neurons":

1

Melo, de Farias Ana Raquel. "Probing the Alzheimer’s disease risk gene PTK2B using human-derived induced neurons." Electronic Thesis or Diss., Université de Lille (2022-....), 2023. http://www.theses.fr/2023ULILS062.

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La maladie d'Alzheimer (MA) est le principal type de démence et représente un défi majeur pour la santé publique mondiale. Elle se caractérise par un déclin progressif de la cognition, de la mémoire et des fonctions comportementales et touche plus de 55 millions de personnes dans le monde. Au niveau moléculaire, la MA se définit par la présence d'enchevêtrements neurofibrillaires agrégés dans les neurones et par l'accumulation de plaques d'amyloïde-β (Aβ) dans le cerveau. Ces caractéristiques pathologiques sont associées à des altérations de l'activité neuronale, à la perte de synapses, à la gliose et à la neuroinflammation, conduisant à une neurodégénérescence irréversible. L'étiologie et la physiopathologie de la MA impliquent une interaction complexe entre des facteurs génétiques et environnementaux. Les études d'association à l'échelle du génome ont permis d'identifier plusieurs loci porteurs de polymorphismes de nucléotides simples (SNP) associés au risque de maladie d'Alzheimer. Parmi ces loci, celui qui héberge la Protéine Tyrosine Kinase 2β (PTK2B) est mis en évidence dans le présent travail. Ce gène code pour une protéine tyrosine kinase qui est impliquée dans la régulation des canaux ioniques induite par le calcium et dans l'activation de nombreuses voies de signalisation, telles que la MAP kinase. Des variations génétiques non synonymes dans le locus PTK2B ont été associées à un risque accru de maladie d'Alzheimer et on pense qu'elles régulent l'expression de PTK2B. Cependant, les rôles physiologiques et physiopathologiques de la PTK2B ne sont pas entièrement compris. Dans le cerveau humain, l'expression de la PTK2B est principalement observée dans les neurones glutamatergiques. Au cours de la progression de la maladie d'Alzheimer, son expression diminue et peut contribuer aux dysfonctionnements neuronaux observés, tels que l'augmentation de l'excitabilité électrique et les altérations synaptiques. Par conséquent, la compréhension du rôle de la PTK2B dans les neurones humains peut contribuer à révéler les mécanismes des dysfonctionnements neuronaux dans la MA. Dans cette optique, les objectifs de cette thèse sont de découvrir les processus cellulaires et les voies moléculaires régulés par la PTK2B dans les neurones humains. Pour ce faire, nous avons utilisé des cellules souches pluripotentes induites humaines (hiPSC) isogéniques pour générer des neurones exprimant différents niveaux de PTK2B. Ensuite, nous avons utilisé des tests fonctionnels et moléculaires pour étudier les conséquences de l'altération de l'expression de la PTK2B dans un contexte physiologique et dans un contexte similaire à celui de la MA. Nous montrons qu'une réduction de l'expression de PTK2B entraîne une augmentation de la phosphorylation de TAU à divers épitopes associés à la pathologie de la MA, ce qui suggère un rôle central de PTK2B dans la régulation de l'agrégation de TAU. En utilisant la transcriptomique à noyau unique, nous montrons également que l'expression réduite de la PTK2B entraîne des altérations transcriptionnelles spécifiques liées à l'activité électrique neuronale et à la transmission synaptique, principalement dans les neurones glutamatergiques. Les expériences d'imagerie calcique indiquent que la réduction de l'expression de PTK2B contribue à augmenter la fréquence des pointes de calcium sans affecter la synchronisation, ce qui indique une activité électrique neuronale élevée. En outre, les résultats des enregistrements électrophysiologiques effectués à partir de réseaux multi-électrodes (MEA) montrent une activité électrique accrue et des schémas d'éclatement perturbés dans les neurones mutants PTK2B. Dans l'ensemble, ces travaux mettent en lumière l'implication de PTK2B dans les processus cellulaires liés à la maladie d'Alzheimer, en donnant un aperçu des mécanismes moléculaires et des altérations fonctionnelles associés à la dysrégulation de PTK2B dans les cellules neuronales humaines dérivées des iPSCs
Alzheimer's disease (AD) is the main type of dementia and poses a significant global public health challenge. It is characterized by a progressive decline in cognition, memory, and behavioral functions and affects more than 55 million people worldwide. At the molecular level, AD is defined by the presence of aggregated neurofibrillary tangles within neurons and the accumulation of amyloid-β (Aβ) plaques in the brain. These pathological features are associated with alterations in neuronal activity, synapse loss, gliosis, and neuroinflammation, leading to irreversible neurodegeneration. AD etiology and pathophysiology involves a complex interplay between genetic and environmental factors. Genome-Wide Association Studies have identified several loci carrying single nucleotide polymorphisms (SNPs) associated with AD risk. Among these loci, the one harboring the Protein Tyrosine Kinase 2β (PTK2B) is highlighted in the present work. This gene encodes a protein tyrosine kinase that is involved in calcium-induced regulation of ion channels and activation of numerous signaling pathways, such as MAP kinase. Non-synonimous genetic variations in the PTK2B locus have been associated with an increased risk of AD and are thought to regulate PTK2B expression. However, both the physiological and pathophysiological roles of PTK2B are not fully understood. In the human brain, PTK2B expression is mainly observed in glutamatergic neurons. Its expression declines during AD progression and may contribute to neuronal dysfunctions observed in the disease, such as increased electrical excitability and synaptic alterations. Therefore, understanding the role of PTK2B in human neurons may contribute to reveal the mechanisms of neuronal dysfunctions in AD. Considering that, the aims of this thesis are to uncover the cellular processes and molecular pathways regulated by PTK2B in human neurons. To that, we took advantage of isogenic human induced-pluripotent stem cells (hiPSCs) to generate neurons expressing different levels of PTK2B. Next, we employed functional and molecular assays to probe the consequences of altered PTK2B expression both in a physiological and in an AD-like context. We show that reduced PTK2B expression leads to increased TAU phosphorylation at various epitopes associated with AD pathology, suggesting a central role of PTK2B in regulating TAU aggregation. Using single-cell transcriptomics, we also show that reduced PTK2B expression leads to specific transcriptional alterations related to neuronal electrical activity and synaptic transmission mainly in glutamatergic neurons. Calcium imaging experiments indicate that PTK2B downregulation contributes to increased calcium spikes frequency without affecting synchronization, indicating an elevated neuronal electrical activity. Additionally, results from electrophysiological recordings from multi-electrode array (MEA) show increased electrical activity and disrupted bursting patterns in PTK2B mutant neurons. Overall, this work sheds light on the involvement of PTK2B in AD-related cellular processes, providing insights into the molecular mechanisms and functional alterations associated with PTK2B dysregulation in human iPSC-derived neural cells
2

Sánchez, Danés Adriana 1984. "Generation of human dopaminergic neurons from induced pluripotent stem cells to model Parkinson's disease." Doctoral thesis, Universitat Pompeu Fabra, 2012. http://hdl.handle.net/10803/96912.

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Parkinson’s disease (PD) is an incurable, chronically progressive neurodegenerative disease leading to premature invalidity and death. The locomotor disability of PD patients is mainly rooted in the gradual and insidious degeneration of dopaminergic neurons (DA) projecting from the midbrain substantia nigra (SN) to the basal ganglia striatum, a pathological process highlighted microscopically by the formation of insoluble cytosolic protein aggregates, known as Lewy bodies and Lewy neurites. The pathogenic mechanisms leading to PD remain poorly understood, arguably owing to the lack of suitable animal and cellular experimental models of the disease. Therefore, there is an urgent need for developing reliable experimental models that recapitulate the key features of PD. The recent development of induced pluripotent stem cell (iPSC) technology has enabled the generation of patient-specific iPSC and their use to model human diseases, although it is currently unclear whether this approach could be useful to successfully model age-related conditions. Importantly, disease modeling using iPSC largely relies on the existence of efficient protocols for the differentiation of disease-relevant cell types. Here, we first developed an efficient protocol for the differentiation of iPSC to authentic midbrain-specific DA neurons with SN properties by forced expression of LMX1A using a lentivirus-mediated gene delivery system. Next, we generated an iPSC-based cellular model of PD that recapitulates key phenotypic features of PD, such as DA neuron loss and α-synuclein accumulation in DA neurons from PD patients. Overall, our results demonstrate that we have developed a valuable tool for elucidating the pathogenic mechanisms leading to PD, as well as an experimental platform for screening new drugs that may prevent or rescue neurodegeneration in PD.
La malaltia de Parkinson (MP) és una malaltia neurodegenerativa incurable que causa invalidesa i mort prematura. Els pacients de la malaltia de Parkinson presenten alteracions motores degudes a una degeneració gradual de les neurones dopaminèrgiques que projecten des de la substància nigra fins a l’estriat. A nivell microscòpic s’observa la presència d’agregats proteics insolubles en el citosol de les neurones coneguts com cossos o neurites de Lewy. Els mecanismes patològics responsables de la MP no es coneixen bé, possiblement a causa de la manca de models animals i cel•lulars adequats. Per tant, existeix una gran necessitat de desenvolupar models experimentals fiables que recapitulin les característiques bàsiques de la MP. El recent desenvolupament de les cèl•lules mare pluripotents induïdes (iPSC) ha permès la generació de iPSC específiques de pacient i el seu ús per modelar malalties humanes, ara bé, no és clar si aquesta estratègia es pot utilitzar per modelar exitosament malalties d’origen tardà, com ara la MP. És important destacar que el modelatge de malalties utilitzant iPSC, es basa, en gran mesura en l'existència de protocols eficients per a la diferenciació de les iPSC cap al tipus cel•lular rellevant per a la malaltia. Durant aquest període, per primera vegada, s’ha desenvolupat un protocol per a l’eficient diferenciació de les iPSC cap a neurones dopaminèrgiques amb les propietats característiques de neurones dopaminèrgiques nigrostriatals, mitjançant l’expressió forçada de LMX1A utilitzant vectors lentivirals. A continuació, s’ha generat un model cel•lular usant iPSC derivades de pacients de MP que recapitula les principals característiques fenotípiques de la malaltia, com ara la pèrdua de neurones dopaminèrgiques i l'acumulació de α-sinucleïna en les neurones dopaminèrgiques. En general, els nostres resultats demostren que hem desenvolupat una eina valuosa per a l’estudi dels mecanismes patològics que condueixen a la MP, així com una nova plataforma pel descobriment de nous fàrmacs encaminats a prevenir o evitar la neurodegeneració.
3

GIANI, ALICE MARIA. "GENERATION OF AUTHENTIC HUMAN NEOCORTICAL NEURONS FROM INDUCED PLURIPOTENT STEM CELLS TO INVESTIGATE 7Q11.23 GENE DOSAGE IMBALANCES." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/561835.

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Questo lavoro di tesi ha avuto lo scopo di studiare lo sviluppo della neocorteccia umana ed i meccanisimi alla base della sua compromissione che risultano nell’insorgenza di patologie del neurosviluppo mediante un’analisi dei profili trascrizionali e della morfologia di neuroni neocorticali umani generati a partire da cellule staminali pluripotenti indotte (iPSCs). Data l’importanza di basarsi su un paradigma di neurogenesi in vitro riproducibile e affidabile nel generare neuroni neocoritcali umani autentici, prima di adottare questo sistema modello per lo studio di patologie del neurosviluppo, nella prima fase di questa ricerca abbiamo eseguito un’ampia caratterizzazione trascrizionale, molecolare e funzionale del protocollo di differenziamento. Le dinamiche trascrizionali che regolano il neurosviluppo in vitro sono state studiate effettuando esperimenti di RNA-sequencing sia a livello di popolazione che di singola cellula. In combinazione con diverse analisi bioinformatiche tra cui l’analisi delle componeti principali (PCA), l’analisi dei geni differenzialemtne espressi e l’analisi WGCNA. L’analisi dei profili trascrizionali è stata accompagnata da un’ampia analisi di d’immunocitochimica che ha permesso di confermare l’identità e lo stadio di sviluppo delle cellule in coltura. Inoltre, la maturità funzionale dei neuroni derivati da iPSCs è stata ulteriormente confermata dalla loro capacità di generare potenziali d’azione, sostenere pattern di scarica complessi e sviluppare attività sinaptica spontanea eccitatoria ed inibitoria. Complessivamente, i risultati ottenuti da questo ampio e diversificato pannello di analisi hanno permesso di stabilitre la riproducibilità del protocollo di differenziamento e la sua competenza nel generare con elevata efficienza principalmente neuroni neocorticali autentici. Successivamente abbiamo applicato questo protocollo di differenziamento neocorticale come sistema modello per studiare due patologie del neurosviluppo dovute alla delezione e duplicazione di una regione comprendente circa 1.5 - 1.8 Mb (megabasi) collacata sul braccio lungo (q) del cormosoma 7 nella banda 11.23. Duplicazioni e delezioni di questa regione sono di particolare interesse in quanto le due sindromi che ne risultano, rispettivamente la sindrome di Willams (WS) e la sindrome da duplicazione 7q11.23 (7q11DUP), presentano fenotipi cognitivi e comportamentali caratterizzati da profili simili e tratti simmetricamente opposti. La frequente comorbidità della sindrome da duplicazione 7q11.23 con altre patologie del neurosviluppo come l’autismo e la schizofrenia in contrasto con la sindrome di Williams che è una sindrome ben caraterizzata non associata ad altre patologie del neurosviluppo, rende lo studio dell’ alterato dosaggio genico del locus 7q11.23 estremamente interessante per identificare con precisione i meccanismi molecolari caratteristici di ciascuna condizione clinica, condivisi da entrabme le sindromi e comuni anche ad altre patologie del neurosviluppo. A questo scopo, abbiamo generato diverse linee di iPS a partire da un ampio gruppo di individui, comprendente individui sani e pazienti affetti dalla sindrome di Williams (WS) e dalla sindrome di duplizazione 7q11.23, che sono poi state differenziate in neuroni neocorticali applicando il protocollo precedentemetne caraterizzato. Confermata l’identità e l’autenticità dei neuroni neocorticali generati da iPSCs, stiamo attualmente identificando i geni ed i meccanismi molecolari disregolati in specifici sottotipi di neuroni che abbiano la maggior rilvenza clinica. Inoltre, l’analisi morfologica dei neuroni neocorticali umani ottenuti da pazienti WS e soggetti sani ha permesso di confermare nell’uomo molte alterazioni morfologiche dei neuroni neocorticali osservate in un modello murino knockout per Dnajc30, un gene ancora funzionalmente non caraterizzato compreso nel locus 7q11.23.
This research project has been aimed to investigate human neocortical development in healthy and diseased subjects by analyzing and comparing the transcriptional profiles and cellular morphologies of human neocortical cells derived from induced pluripotent stem cells (iPSCs). Given the importance to rely on a solid and highly reproducible iPSCs-based differentiation protocol that generates authentic neocortical neurons in vitro with high efficiency before applying it as a model system of human neurodevelopmental disorders, in the first phase of this study we performed a comprehensive transcriptional, cellular and physiological characterization of the in vitro neurodevelopmental paradigm. The transcriptional dynamics regulating in vitro neocortical development have been investigated by performing RNA-sequencing (RNA-seq) at both population and single- cell level in combination with several bioinformatics analyses including principal component analysis (PCA), differential gene expression analysis and weighted gene co-expression network analysis (WGCNA). The transcriptional results were corroborated by the widespread positivity for a selected panel of informative cell-fate and cell-stage specific markers detected through immunocytochemistry and the physiological maturity of our iPSCs-derived neocortical neurons was further confirmed by their ability to generate action potentials, develop complex firing patterns and sustain excitatory and inhibitory spontaneous synaptic activity. Overall, these results fully validated the reproducibility of the differentiation protocol and its efficiency and reliability in generating physiologically mature authentic neocortical neurons. Subsequently, we applied this extensively characterized neocortical differentiation paradigm to model in vitro two human neurodevelopmental disorders caused by symmetrical copy number variations (CNVs) of the Williams-Beuren syndrome chromosome region (WBSCR) located on the long arm (q) of chromosome 7 at position 11.23 (7q.11.23 locus). 7q11.23 CNVs are of special interest as the two disorders resulting from the deletion (Williams syndrome, WS) and duplication (7q.11.23 duplication syndrome, 7q11DUP) of this region exhibit cognitive and behavioral phenotypes marked by both similar features and symmetrically opposite traits. The association of 7q11DUP to complex neurodevelopmental disorders such as autism spectrum disorder and schizophrenia, while WS is a well-characterized syndrome without clear overlap to complex neurodevelopmental disorders make the study of this locus extremely interesting to identify the molecular mechanisms unique to each clinical condition, common to both syndromes and shared with other complex neurodevelopmental disorders. To this aim, we generated several iPSCs lines from a large cohort comprising WS individuals, 7q11DUP patients and healthy subjects and differentiated them into neocortical neurons by applying the previously in-depth characterized protocol. Having assessed the quality of our iPSCs-derived neocortical neurons, we are currently identifying neuronal subtypes specific genes and gene networks having the most statistically significant relationship to these disorders through single cell RNA-sequencing analysis. Furthermore, morphometric analysis of WS and control iPSCs-derived neocortical neurons has confirmed in humans many neuronal morphological abnormalities observed in a mouse knockout for Dnajc30, a previously uncharacterized gene contained in the 7q11.23 locus.
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Fenske, Pascal [Verfasser]. "Characterization of synaptic transmission in autaptic cultured neurons derived from human induced pluripotent stem cells / Pascal Fenske." Berlin : Freie Universität Berlin, 2021. http://d-nb.info/1234451611/34.

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Toli, Diana Eleni. "Directed differentiation and purification of motor neurons from human induced pluripotent stem cells to model Amyotrophic Lateral Sclerosis." Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05T044/document.

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La sclérose latérale amyotrophique (SLA) est une maladie neurodégénérative incurable de l’adulte qui affecte principalement les motoneurones. Les mécanismes conduisant à la mort des motoneurones restent mal connus, notamment du fait de l'hétérogénéité de la maladie et du manque d'accès aux neurones humains affectés. La technologie des cellules souches pluripotentes induites humaines (iPSc) est un outil prometteur pour la modélisation de la SLA, car elle offre la possibilité unique d'obtenir et d’étudier des motoneurones humains.Des clones d’iPSc de deux sujets témoins ont été générés et nous avons comparé plusieurs protocoles afin de mettre au point un protocole efficace de différenciation des iPSc en motoneurones. Les cultures obtenues étaient hétérogènes et contenaient différents types de neurones et des précurseurs neuraux. Afin de pouvoir étudier des mécanismes intrinsèques aux motoneurones dans la SLA, nous avons développé une nouvelle technique pour purifier les motoneurones. Cette technique a consisté à trier les motoneurones par FACS en combinant l'utilisation d'un vecteur lentiviral rapporteur exprimant une protéine fluorescente sous le contrôle d'un promoteur spécifique des motoneurones, et d'un anticorps monoclonal dirigé contre le récepteur aux neurotrophines p75. Cette double sélection a permis l'isolement efficace de motoneurones purs. En parallèle, la technologie iPSc a été utilisée pour établir des modèles cellulaires de la SLA. Des clones de cellules iPS ont été générés à partir d’un patient avec une forme familiale de la SLA présentant une mutation dans le gène TARDBP (codant pour une protéine de liaison à l’ADN, TDP-43) et un patient atteint d’une forme sporadique de SLA. Afin de valider nos modèles, nous avons recherché des phénotypes caractéristiques de la maladie au cours de la différenciation des iPSc : i) la formation d’agrégats cytoplasmiques, ii) des altérations de génération et de survie des motoneurones, iii) des défauts de croissance neuritique
Amyotrophic lateral sclerosis (ALS) is a fatal adult-onset neurodegenerative disorder primarily affecting motor neurons. Mechanisms leading to motor neuron death in ALS are poorly understood mostly because of disease heterogeneity and lack of access to affected cells. The induced pluripotent stem cell (iPSc) technology provides the opportunity to obtain and study human motor neurons and is therefore a promising tool for ALS modeling.IPSc clones from control subjects were generated, and we compared several protocols in order to set up an efficient protocol for iPSc differentiation into motor neurons. The obtained cultures were heterogenous, comprising different neuron subtypes and neural precursors. To allow investigation of intrinsic disease mechanisms in ALS motor neurons, we developed a new technique to purify motor neurons by FACS sorting. By combining the use of a lentiviral vector expressing a fluorescent protein under control of a motoneuron-specific promoter and of a monoclonal antibody directed against the p75 neurotrophin receptor, isolation of exquisitely pure motor neurons was achieved. In parallel, iPSc technology was used to establish cellular models of ALS. IPSc were generated from one patient with familial ALS carrying a mutation in the TARDBP gene (encoding a DNA-binding protein, TDP-43) and one patient with sporadic ALS. To validate our models, we investigated characteristic disease phenotypes during iPSc differentiation, including i) cytoplasmic aggregate formation, ii) motor neuron generation and survival defects, iii) neurite growth alterations
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Hermann, Andreas, Jeong Beom Kim, Sumitra Srimasorn, Holm Zaehres, Peter Reinhardt, Hans R. Schöler, and Alexander Storch. "Factor-Reduced Human Induced Pluripotent Stem Cells Efficiently Differentiate into Neurons Independent of the Number of Reprogramming Factors." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-203366.

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Reprogramming of somatic cells into induced pluripotent stem cells (iPSCs) by overexpression of the transcription factors OCT4, SOX2, KLF4, and c-Myc holds great promise for the development of personalized cell replacement therapies. In an attempt to minimize the risk of chromosomal disruption and to simplify reprogramming, several studies demonstrated that a reduced set of reprogramming factors is sufficient to generate iPSC. We recently showed that a reduction of reprogramming factors in murine cells not only reduces reprogramming efficiency but also may worsen subsequent differentiation. To prove whether this is also true for human cells, we compared the efficiency of neuronal differentiation of iPSC generated from fetal human neural stem cells with either one (OCT4; hiPSC1F-NSC) or two (OCT4, KLF4; hiPSC2F-NSC) reprogramming factors with iPSC produced from human fibroblasts using three (hiPSC3F-FIB) or four reprogramming factors (hiPSC4F-FIB). After four weeks of coculture with PA6 stromal cells, neuronal differentiation of hiPSC1F-NSC and hiPSC2F-NSC was as efficient as iPSC3F-FIB or iPSC4F-FIB. We conclude that a reduction of reprogramming factors in human cells does reduce reprogramming efficiency but does not alter subsequent differentiation into neural lineages. This is of importance for the development of future application of iPSC in cell replacement therapies.
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Miyawaki, Yoshifumi. "Zonisamide promotes survival of human induced pluripotent stem cell-derived dopaminergic neurons in the striatum of female rats." Kyoto University, 2020. http://hdl.handle.net/2433/259730.

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Beevers, Joel Edward. "Investigating the function of microtubule-associated protein tau (MAPT) and its genetic association with Parkinson's using human iPSC-derived dopamine neurons." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:7a94919a-73a1-4a9f-b04d-cdf5b9c64be7.

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Parkinson's disease (PD) primarily manifests as loss of motor control through the degeneration of nigrostriatal dopaminergic neurons. The microtubule-associated protein tau (MAPT) locus is highly genetically associated with PD, wherein the H1 haplotype confers disease risk and the H2 haplotype is protective. As this haplotype variation does not alter the amino acid sequence, disease risk may be conferred by altered gene expression, either of total MAPT or of specific isoforms, of which there are six in adult human brain. To investigate haplotype-specific control of MAPT expression in the neurons that die in PD, induced pluripotent stem cells (iPSCs) from H1/H2 heterozygous individuals were differentiated into dopaminergic neuronal cultures that expressed all six mature isoforms of MAPT after six months' maturation. A reporter construct using the human tyrosine hydroxylase locus was also generated to identify human dopaminergic neurons in mixed cultures. Haplotype-specific differences in the inclusion of exon 3 and total MAPT were observed in iPSC-derived dopaminergic neuronal cultures and a novel variant in MAPT intron 10 increased the inclusion of exon 10 by two-fold. RNA interference tools were generated to knockdown total MAPT or specific isoforms, wherein knockdown of the 4-repeat isoform of tau protein increased the velocity of axonal transport in iPSC-derived neurons. MAPT knockdown also reduced p62 levels, suggesting an impact of tau on macroautophagy, likely through altered axonal transport. These results demonstrate how variation at a disease susceptibility locus can alter gene expression, thereby impacting on neuronal function.
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Burton, Mark P., Declan J. McKeefry, Brendan T. Barrett, Chara Vakrou, and A. B. Morland. "Disruptions to human speed perception induced by motion adaptation and transcranial magnetic stimulation." Wiley, 2009. http://hdl.handle.net/10454/4731.

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To investigate the underlying nature of the effects of transcranial magnetic stimulation (TMS) on speed perception, we applied repetitive TMS (rTMS) to human V5/MT+ following adaptation to either fast- (20 deg/s) or slow (4 deg/s)-moving grating stimuli. The adapting stimuli induced changes in the perceived speed of a standard reference stimulus moving at 10 deg/s. In the absence of rTMS, adaptation to the slower stimulus led to an increase in perceived speed of the reference, whilst adaptation to the faster stimulus produced a reduction in perceived speed. These induced changes in speed perception can be modelled by a ratio-taking operation of the outputs of two temporally tuned mechanisms that decay exponentially over time. When rTMS was applied to V5/MT+ following adaptation, the perceived speed of the reference stimulus was reduced, irrespective of whether adaptation had been to the faster- or slower-moving stimulus. The fact that rTMS after adaptation always reduces perceived speed, independent of which temporal mechanism has undergone adaptation, suggests that rTMS does not selectively facilitate activity of adapted neurons but instead leads to suppression of neural function. The results highlight the fact that potentially different effects are generated by TMS on adapted neuronal populations depending upon whether or not they are responding to visual stimuli.
BBSRC
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Kikuchi, Tetsuhiro. "Survival of human induced pluripotent stem cell-derived midbrain dopaminergic neurons in the brain of a primate model of Parkinson's disease." Kyoto University, 2012. http://hdl.handle.net/2433/159389.

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Books on the topic "Human Induced neurons":

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Nat, Roxana, and Andreas Eigentler. Cell Culture, iPS Cells and Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0013.

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Somatic reprogramming technology, which enables the conversion of adult human non-neural cells into neurons, has progressed rapidly in recent years. The derivation of patient-specific induced pluripotent stem (iPS) cells has become routine. The inherent broad differentiation potential of iPS cells makes possible the generation of diverse types of human neurons. This constitutes a remarkable step in facilitating the development of more appropriate and comprehensive preclinical human disease models, as well as for high throughput drug screenings and cell therapy. This chapter reviews recent progress in the human iPS cell culture models related to common and rare NDDs, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, spinal muscular atrophy, and degenerative ataxias. It focuses on the pathophysiological features revealed in cell cultures, and the neuronal subtypes most affected in NDDs. The chapter discusses the validity, limitation, and improvements of this system in faithfully and reproducibly recapitulating disease pathology.
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Seth, Rohit. Zinc deficiency induces apoptosis via mitochondrial p53- and caspase-dependent pathways in human neuronal precursor cells. Elseveir, 2014.

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Bisschops, Raf. Ligand & Electrically Induced Activation Patterns in Myenteric Neuronal Networks: Confocal Calcium Imaging As a Bridge Between Basic & Human Physiology (Acta Biomedica Lovaniensia). Leuven Univ Pr, 2005.

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Ziemann, Ulf. Pharmacology of TMS measures. Edited by Charles M. Epstein, Eric M. Wassermann, and Ulf Ziemann. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780198568926.013.0013.

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This article discusses various aspects of the pharmacology of transcranial magnetic stimulator (TMS) measures. TMS measures reflect axonal, or excitatory or inhibitory synaptic excitability in distinct interneuron circuits. TMS measures can be employed to study the effects of a drug with unknown or multiple modes of action, and hence to determine its main mode of action at the systems level of the motor cortex. TMS experiments can also study acute drug effects that may be different from chronic drug effects. TMS or repetitive TMS may induce changes in endogenous neurotransmitter or neuromodulator systems. This allows for the study of neurotransmission along defined neuronal projections in health and disease. This article describes pharmacological experiments that have characterized the physiology of TMS measures of motor cortical excitability. Pharmacological challenging of TMS measures has opened a broad window into human cortical physiology.

Book chapters on the topic "Human Induced neurons":

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Zhou-Yang, Lucia, Sophie Eichhorner, Lukas Karbacher, Lena Böhnke, Larissa Traxler, and Jerome Mertens. "Direct Conversion of Human Fibroblasts to Induced Neurons." In Methods in Molecular Biology, 73–96. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1601-7_6.

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Legault, Emilie M., and Janelle Drouin-Ouellet. "Generation of Induced Dopaminergic Neurons from Human Fetal Fibroblasts." In Methods in Molecular Biology, 97–115. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1601-7_7.

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Tofoli, Fabiano Araújo, Ana Teresa Silva Semeano, Ágatha Oliveira-Giacomelli, Maria Carolina Bittencourt Gonçalves, Merari F. R. Ferrari, Lygia Veiga Pereira, and Henning Ulrich. "Midbrain Dopaminergic Neurons Differentiated from Human-Induced Pluripotent Stem Cells." In Methods in Molecular Biology, 97–118. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9007-8_8.

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Fernandes, Sofia R., Mariana Pereira, Sherif M. Elbasiouny, Yasin Y. Dhaher, Mamede de Carvalho, and Pedro C. Miranda. "Interplay Between Electrical Conductivity of Tissues and Position of Electrodes in Transcutaneous Spinal Direct Current Stimulation (tsDCS)." In Brain and Human Body Modelling 2021, 101–22. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-15451-5_7.

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AbstractTranscutaneous Spinal Direct Current Stimulation (tsDCS) is a neuromodulatory technique that applies low intensity (2–4 mA) direct currents to the spinal cord through electrodes placed above or near the vertebral column. As in transcranial electric stimulation, tsDCS induces an electric field in the spinal cord that can transiently change the transmembrane potential of spinal neurons or influence synaptic communication. Anatomical features near the electrodes or in the current path can originate local variations of the electric field magnitude and orientation that result in different effects generated at neuronal and synaptic level. Accurate realistic models of the spinal cord and surrounding tissues can provide a deeper understanding on how and why these variations occur.Our research aims at studying how electrode placement interacts with electrical conductivities of the tissues located in the current path. Using a realistic human model of the spinal cord and surrounding tissues, we estimated the electric field induced by tsDCS, considering different combinations of electrode positions and electrical conductivity of relevant tissues. Our study started from a homogeneous conductivity paradigm up to a full heterogeneous model. The results show that electrode placement influences the electric field orientation, while the conductivities of vertebral bone and CSF can lead to local electric field hotspots in spinal segments located in the current path. Understanding the interplay between these two effects can provide a solid framework to target specific spinal circuits in terms of magnitude and field orientation towards a more personalized approach.
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Falco, Amel, Rocío Bartolomé-Cabrero, and Sergio Gascón. "Bcl-2-Assisted Reprogramming of Mouse Astrocytes and Human Fibroblasts into Induced Neurons." In Methods in Molecular Biology, 57–71. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1601-7_5.

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Silva, M. Catarina, Ghata Nandi, and Stephen J. Haggarty. "Differentiation of Human Induced Pluripotent Stem Cells into Cortical Neurons to Advance Precision Medicine." In Methods in Molecular Biology, 143–74. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1979-7_10.

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Buchholz, Sarah, Michael Bell-Simons, Cagla Cakmak, Jennifer Klimek, Li Gan, and Hans Zempel. "Cultivation, Differentiation, and Lentiviral Transduction of Human-Induced Pluripotent Stem Cell (hiPSC)-Derived Glutamatergic Neurons for Studying Human Tau." In Methods in Molecular Biology, 533–49. New York, NY: Springer US, 2024. http://dx.doi.org/10.1007/978-1-0716-3629-9_31.

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Salvador, R., M. C. Biagi, O. Puonti, M. Splittgerber, V. Moliadze, M. Siniatchkin, A. Thielscher, and G. Ruffini. "Personalization of Multi-electrode Setups in tCS/tES: Methods and Advantages." In Brain and Human Body Modeling 2020, 119–35. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-45623-8_7.

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AbstractTranscranial current stimulation (tCS or tES) protocols yield results that are highly variable across individuals. Part of this variability results from differences in the electric field (E-field) induced in subjects’ brains during stimulation. The E-field determines how neurons respond to stimulation, and it can be used as a proxy for predicting the concurrent effects of stimulation, like changes in cortical excitability, and, ultimately, its plastic effects. While the use of multichannel systems with small electrodes has provided a more precise tool for delivering tCS, individually variable anatomical parameters like the shape and thickness of tissues affect the E-field distribution for a specific electrode montage. Therefore, using the same montage parameters across subjects does not lead to the homogeneity of E-field amplitude over the desired targets. Here we describe a pipeline that leverages individualized head models combined with montage optimization algorithms to reduce the variability of the E-field distributions over subjects in tCS. We will describe the different steps of the pipeline – namely, MRI segmentation and head model creation, target specification, and montage optimization – and discuss their main advantages and limitations.
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Young, Jessica E., and Raul Delgado-Morales. "Human-Induced Pluripotent Stem Cell-Derived Neurons to Model and Gain Insights into Alzheimer’s Disease Pathogenesis." In Stem Cell Genetics for Biomedical Research, 3–12. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90695-9_1.

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Mehta, Arpan R., Siddharthan Chandran, and Bhuvaneish T. Selvaraj. "Assessment of Mitochondrial Trafficking as a Surrogate for Fast Axonal Transport in Human Induced Pluripotent Stem Cell–Derived Spinal Motor Neurons." In Methods in Molecular Biology, 311–22. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1990-2_16.

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AbstractAxonal transport is essential for the development, function, and survival of the nervous system. In an energy-demanding process, motor proteins act in concert with microtubules to deliver cargoes, such as organelles, from one end of the axon to the other. Perturbations in axonal transport are a prominent phenotype of many neurodegenerative diseases, including amyotrophic lateral sclerosis. Here, we describe a simple method to fluorescently label mitochondrial cargo, a surrogate for fast axonal transport, in human induced pluripotent stem cell–derived motor neurons. This method enables the sparse labeling of axons to track directionality of movement and can be adapted to assess not only the cell autonomous effects of a genetic mutation on axonal transport but also the cell non-autonomous effects, through the use of conditioned medium and/or co-culture systems.

Conference papers on the topic "Human Induced neurons":

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Schmieder, F., R. Habibey, V. Busskamp, J. W. Czarske, and L. Büttner. "Adaptive Holographic Optogenetic Illumination for Human Neural Network Analysis." In Digital Holography and Three-Dimensional Imaging. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/dh.2022.w4a.7.

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A two-wavelength optogenetic stimulation platform with high spatiotemporal resolution and inherent aberration correction is presented. By stimulating single neurons, we investigated the temporal evolution of connectivity in human induced pluripotent stem cell-derived neuronal networks in-vitro.
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Pitta, Marina Galdino da Rocha, Jordy Silva de Carvalho, Luzilene Pereira de Lima, and Ivan da Rocha Pitta. "iPSC therapies applied to rehabilitation in parkinson’s disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.022.

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Background: Parkinson’s disease (PD) is a neurological disorder that affects movement, mainly due to damage and degeneration of the nigrostriatal dopaminergic pathway. The diagnosis is made through a clinical neurological analysis where motor characteristics are considered. There is still no cure, and treatment strategies are focused on symptoms control. Cell replacement therapies emerge as an alternative. Objective: This review focused on current techniques of induced pluripotent stem cells (iPSCs). Methods: The search terms used were: “Parkinson’s Disease”, “Stem cells” and “iPSC”. Open articles written in English, from 2016-21 were selected in the Pubmed database, 10 publications were identified. Results: With the modernization of iPSC, it was possible to reprogram pluripotent human somatic cells and generate dopaminergic neurons and individual-specific glial cells. To understand the molecular basis, cell and animal models of neurons and organelles are currently being employed. Organoids are derived from stem cells in a three-dimensional matrix, such as matrigel or hydrogels derived from animals. The neuronal models are: α-synuclein (SNCA), leucine-rich repeat kinase2 (LRRK2), PARK2, putative kinase1 induced by phosphatase and tensin homolog (PINK1), DJ-1. Both models offer opportunities to investigate pathogenic mechanisms of PD and test compounds on human neurons. Conclusions: Cell replacement therapy is promising and has great capacity for the treatment of neurodegenerative diseases. Studies using iPSC neuron and PD organoid modeling is highly valuable in elucidating relevants neuronal pathways and therapeutic targets, moreover providing important models for testing future therapies.
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Murata, Masaaki, Hidekatsu Ito, Teppei Taenaka, and Suguru N. Kudoh. "Modification of activity pattern induced by synaptic enhancements in a semi-artificial network of living neurons." In 2011 International Symposium on Micro-NanoMechatronics and Human Science (MHS). IEEE, 2011. http://dx.doi.org/10.1109/mhs.2011.6102187.

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Komatsu, Masaaki, Heather E. Wheeler, Claudia Wing, Shannon Delaney, and M. Eileen Dolan. "Abstract 3489: A novel investigation into chemotherapy-induced peripheral neuropathy using iPSC-derived human neurons." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3489.

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Foisset, F., C. Lehalle, A. Nasri, C. Bourdais, I. Vachier, S. Assou, Q. Muller, et al. "Development of a bronchial epithelium model innervated by sensory neurons from human induced pluripotent stem cells." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.2394.

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Ferreira, João, Manuel de Sousa Ribeiro, Ricardo Gonçalves, and João Leite. "Looking Inside the Black-Box: Logic-based Explanations for Neural Networks." In 19th International Conference on Principles of Knowledge Representation and Reasoning {KR-2022}. California: International Joint Conferences on Artificial Intelligence Organization, 2022. http://dx.doi.org/10.24963/kr.2022/45.

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Abstract:
Deep neural network-based methods have recently enjoyed great popularity due to their effectiveness in solving difficult tasks. Requiring minimal human effort, they have turned into an almost ubiquitous solution in multiple domains. However, due to the size and complexity of typical neural network models' architectures, as well as the sub-symbolical nature of the representations generated by their neuronal activations, neural networks are essentially opaque, making it nearly impossible to explain to humans the reasoning behind their decisions. We address this issue by developing a procedure to induce human-understandable logic-based theories that attempt to represent the classification process of a given neural network model, based on the idea of establishing mappings from the values of the activations produced by the neurons of that model to human-defined concepts to be used in the induced logic-based theory. Exploring the setting of a synthetic image classification task, we provide empirical results to assess the quality of the developed theories for different neural network models, compare them to existing theories on that task, and give evidence that the theories developed through our method are faithful to the representations learned by the neural networks that they are built to describe.
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Courellis, Hristos, Juri Minxha, Araceli Cardenas, Taufik Valiante, Adam Mamelak, Ralph Adolphs, Stefano Fusi, and Ueli Rutishauser. "Abstract representations encoded by human hippocampal neurons support behavioral inference and can be induced through verbal instruction." In 2023 Conference on Cognitive Computational Neuroscience. Oxford, United Kingdom: Cognitive Computational Neuroscience, 2023. http://dx.doi.org/10.32470/ccn.2023.1668-0.

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Cotter, Laurent, Romane A. Lahaye, Wei Chou Tseng, Yuanjing Liu, Aude Lemesle, Sophie Lenoir, Elena Dale, Frédéric Saudou, and Anselme L. Perrier. "I07 Selective lowering of mutant-huntingtin by antisense oligonucleotides (ASOs) in human cortical neurons derived from patient-specific induced pluripotent stem cells (HD-IPSC)." In EHDN 2022 Plenary Meeting, Bologna, Italy, Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jnnp-2022-ehdn.233.

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"Human induced stem cells (hiPSCs)-derived motor neurons model applied for the study of the aryl hydrocarbon receptor mediated signaling by the induction of environmental pollutant." In INTERNATIONAL CONFERENCE ON BIOLOGICAL RESEARCH AND APPLIED SCIENCE. Jinnah University for Women, 2024. http://dx.doi.org/10.37962/ibras/2024/57.

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Martens, William L., Philip Poronnik, and Darren Saunders. "Hypothesis-Driven Sonification of Proteomic Data Distributions Indicating Neurodegredation in Amyotrophic Lateral Sclerosis." In The 22nd International Conference on Auditory Display. Arlington, Virginia: The International Community for Auditory Display, 2016. http://dx.doi.org/10.21785/icad2016.024.

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Three alternative sonifications of proteomic data distributions were compared as a means to indicate the neuropathology associated with Amyotrophic Lateral Sclerosis (ALS) via auditory display (through exploration of the differentiation of induced pluripotent stem cell derived neurons). Pure visual displays of proteomic data often result in ”visual overload” such that detailed or subtle data important to describe ALS neurodegradation may be glossed over, and so three competing approaches to the sonification of proteomic data were designed to capitalize upon human auditory capacities that complement the visual capacities engaged by more conventional graphic representations. The auditory displays resulting from hypothesis-driven design of three alternative sonifications were evaluated by naïve listeners, who were instructed to listen for differences between the sonifications produce from proteomic data associated with three different types of cells. One of the sonifications was based upon the hypothesis that auditory sensitivity to regularities and irregularities in spatio-temporal patterns in the data could be heard through spatial distribution of sonification components. The design of a second sonification was based upon the hypothesis that variation in timbral components might create a distinguishable sound for each of three types of cells. A third sonification was based upon the hypothesis that redundant variation in both spatial and timbral components would be even more powerful as a means for identifying spatio-temporal patterns in the dynamic, multidimensional data generated in current proteomic studies of ALS.

Reports on the topic "Human Induced neurons":

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Yu, Mei, Pengyu Wang, Binbin Li, Qiaoling Ruan, Jingzi ZhangBao, Lei Wu, Xiaoshuang Zhang, Zhaolin Liu, and Fang Huang. NRSF Negatively Regulates Microglial Pro-Inflammatory Activation. Progress in Neurobiology, May 2024. http://dx.doi.org/10.60124/j.pneuro.2024.20.02.

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Microglial activation contributes to neurological disorders like Parkinson’s disease (PD), and modulating this activation is a potential therapeutic approach. The neuron-restrictive silencer factor (NRSF) functions as a negative regulator of gene transcription through epigenetic modifications. While previous research has primarily examined the role of NRSF in neuronal differentiation and injury, emerging evidence indicates that NRSF also plays a significant role in maintaining the phenotype of glial cells. In this study, we explored the role and underlying mechanisms of NRSF in lipopolysaccharide (LPS)-induced pro-inflammatory or interleukin-4 (IL4)-induced anti-inflammatory phenotype of microglial activation. Following LPS stimulation, the nuclear localization of NRSF increased in BV2 microglial cells, primary mouse microglia, and microglia within the substantia nigra of PD mice. Knockdown of NRSF enhanced the expression of inflammation-related factors induced by LPS via the mitogen-activated protein kinase-extracellular signal-regulated kinase (MAPK-ERK) and nuclear factor-κB (NF-κB) p65 signalling pathways in BV2 cells. Moreover, the culture medium from LPS-treated NRSF knockdown BV2 cells exerted greater toxic effects on human neuroblastoma SH-SY5Y cells compared to the control. However, NRSF knockdown exerted inconsistent effects on the expression of anti-inflammatory-related genes in IL4-treated BV2 cells. Our findings suggest that NRSF knockdown promotes microglial pro-inflammatory activation.

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