Готові списки джерел за темами / IPSC-derived neurons

Добірка наукової літератури з теми "IPSC-derived neurons"

Автор: Grafiati

Опубліковано: 14 березня 2023

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Статті в журналах з теми "IPSC-derived neurons"

Allison, Reilly L., Jacob W. Adelman, Jenica Abrudan, Raul A. Urrutia, Michael T. Zimmermann, Angela J. Mathison, and Allison D. Ebert. "Microglia Influence Neurofilament Deposition in ALS iPSC-Derived Motor Neurons." Genes 13, no. 2 (January 27, 2022): 241. http://dx.doi.org/10.3390/genes13020241.

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease in which upper and lower motor neuron loss is the primary phenotype, leading to muscle weakness and wasting, respiratory failure, and death. Although a portion of ALS cases are linked to one of over 50 unique genes, the vast majority of cases are sporadic in nature. However, the mechanisms underlying the motor neuron loss in either familial or sporadic ALS are not entirely clear. Here, we used induced pluripotent stem cells derived from a set of identical twin brothers discordant for ALS to assess the role of astrocytes and microglia on the expression and accumulation of neurofilament proteins in motor neurons. We found that motor neurons derived from the affected twin which exhibited increased transcript levels of all three neurofilament isoforms and increased expression of phosphorylated neurofilament puncta. We further found that treatment of the motor neurons with astrocyte-conditioned medium and microglial-conditioned medium significantly impacted neurofilament deposition. Together, these data suggest that glial-secreted factors can alter neurofilament pathology in ALS iPSC-derived motor neurons.

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Matsui, Toshikatsu, Norimasa Miyamoto, Fumiyo Saito, and Tadahiro Shinozawa. "Molecular Profiling of Human Induced Pluripotent Stem Cell-Derived Cells and their Application for Drug Safety Study." Current Pharmaceutical Biotechnology 21, no. 9 (June 9, 2020): 807–28. http://dx.doi.org/10.2174/1389201021666200422090952.

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Drug-induced toxicity remains one of the leading causes of discontinuation of the drug candidate and post-marketing withdrawal. Thus, early identification of the drug candidates with the potential for toxicity is crucial in the drug development process. With the recent discovery of human- Induced Pluripotent Stem Cells (iPSC) and the establishment of the differentiation protocol of human iPSC into the cell types of interest, the differentiated cells from human iPSC have garnered much attention because of their potential applicability in toxicity evaluation as well as drug screening, disease modeling and cell therapy. In this review, we expanded on current information regarding the feasibility of human iPSC-derived cells for the evaluation of drug-induced toxicity with a focus on human iPSCderived hepatocyte (iPSC-Hep), cardiomyocyte (iPSC-CMs) and neurons (iPSC-Neurons). Further, we CSAHi, Consortium for Safety Assessment using Human iPS Cells, reported our gene expression profiling data with DNA microarray using commercially available human iPSC-derived cells (iPSC-Hep, iPSC-CMs, iPSC-Neurons), their relevant human tissues and primary cultured human cells to discuss the future direction of the three types of human iPSC-derived cells.

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Avazzadeh, Sahar, Jara Maria Baena, Cameron Keighron, Yajaira Feller-Sanchez, and Leo R. Quinlan. "Modelling Parkinson’s Disease: iPSCs towards Better Understanding of Human Pathology." Brain Sciences 11, no. 3 (March 14, 2021): 373. http://dx.doi.org/10.3390/brainsci11030373.

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Parkinson’s Disease (PD) is a chronic neurodegenerative disorder characterized by motor and non-motor symptoms, among which are bradykinesia, rigidity, tremor as well as mental symptoms such as dementia. The underlying cause of Parkinson disease is degeneration of dopaminergic neurons. It has been challenging to develop an efficient animal model to accurately represent the complex phenotypes found with PD. However, it has become possible to recapitulate the myriad of phenotypes underlying the PD pathology by using human induced pluripotent stem cell (iPSC) technology. Patient-specific iPSC-derived dopaminergic neurons are available and present an opportunity to study many aspects of the PD phenotypes in a dish. In this review, we report the available data on iPSC-derived neurons derived from PD patients with identified gene mutations. Specifically, we will report on the key phenotypes of the generated iPSC-derived neurons from PD patients with different genetic background. Furthermore, we discuss the relationship these cellular phenotypes have to PD pathology and future challenges and prospects for iPSC modelling and understanding of the pathogenesis of PD.

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Guyett, Paul, Mike Hendrickson, and Kurt Laha. "CNS Drug Discovery Using iPSC-Derived Neurons." Genetic Engineering & Biotechnology News 38, no. 20 (November 15, 2018): 14–15. http://dx.doi.org/10.1089/gen.38.20.08.

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Ichise, Eisuke, Tomohiro Chiyonobu, Mitsuru Ishikawa, Yasuyoshi Tanaka, Mami Shibata, Takenori Tozawa, Yoshihiro Taura, et al. "Impaired neuronal activity and differential gene expression in STXBP1 encephalopathy patient iPSC-derived GABAergic neurons." Human Molecular Genetics 30, no. 14 (May 7, 2021): 1337–48. http://dx.doi.org/10.1093/hmg/ddab113.

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Abstract Syntaxin-binding protein 1 (STXBP1; also called MUNC18–1), encoded by STXBP1, is an essential component of the molecular machinery that controls synaptic vesicle docking and fusion. De novo pathogenic variants of STXBP1 cause a complex set of neurological disturbances, namely STXBP1 encephalopathy (STXBP1-E) that includes epilepsy, neurodevelopmental disorders and neurodegeneration. Several animal studies have suggested the contribution of GABAergic dysfunction in STXBP1-E pathogenesis. However, the pathophysiological changes in GABAergic neurons of these patients are still poorly understood. Here, we exclusively generated GABAergic neurons from STXBP1-E patient-derived induced pluripotent stem cells (iPSCs) by transient expression of the transcription factors ASCL1 and DLX2. We also generated CRISPR/Cas9-edited isogenic iPSC-derived GABAergic (iPSC GABA) neurons as controls. We demonstrated that the reduction in STXBP1 protein levels in patient-derived iPSC GABA neurons was slight (approximately 20%) compared to the control neurons, despite a 50% reduction in STXBP1 mRNA levels. Using a microelectrode array–based assay, we found that patient-derived iPSC GABA neurons exhibited dysfunctional maturation with reduced numbers of spontaneous spikes and bursts. These findings reinforce the idea that GABAergic dysfunction is a crucial contributor to STXBP1-E pathogenesis. Moreover, gene expression analysis revealed specific dysregulation of genes previously implicated in epilepsy, neurodevelopment and neurodegeneration in patient-derived iPSC GABA neurons, namely KCNH1, KCNH5, CNN3, RASGRF1, SEMA3A, SIAH3 and INPP5F. Thus, our study provides new insights for understanding the biological processes underlying the widespread neuropathological features of STXBP1-E.

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Hedegaard, Anne, Jimena Monzón-Sandoval, Sarah E. Newey, Emma S. Whiteley, Caleb Webber, and Colin J. Akerman. "Pro-maturational Effects of Human iPSC-Derived Cortical Astrocytes upon iPSC-Derived Cortical Neurons." Stem Cell Reports 15, no. 1 (July 2020): 38–51. http://dx.doi.org/10.1016/j.stemcr.2020.05.003.

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Miletta, Maria Consolata, and Tamas L. Horvath. "Patient-Derived iPSC-Hypothamic Neurons: The Ultimate Protocol." Cell Stem Cell 22, no. 5 (May 2018): 615–16. http://dx.doi.org/10.1016/j.stem.2018.04.019.

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Lee, Sebum, and Eric J. Huang. "Modeling ALS and FTD with iPSC-derived neurons." Brain Research 1656 (February 2017): 88–97. http://dx.doi.org/10.1016/j.brainres.2015.10.003.

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Vangeel, Laura. "TRP Channel Function in iPSC-Derived Sensory Neurons." Biophysical Journal 112, no. 3 (February 2017): 135a. http://dx.doi.org/10.1016/j.bpj.2016.11.750.

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Pierson, Tyler M., Yogesh K. Kushwaha, Hiral Oza, and Maria G. Otero. "Modeling CLN6 with IPSC-derived neurons and glia." Molecular Genetics and Metabolism 138, no. 2 (February 2023): 107269. http://dx.doi.org/10.1016/j.ymgme.2022.107269.

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Дисертації з теми "IPSC-derived neurons"

Zambon, Federico. "Studying α-Synuclein pathology using iPSC-derived dopaminergic neurons". Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:2856dcf3-0f38-4a37-9242-8c685d1c2c3a.

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Parkinson's disease (PD) is characterised by the loss of dopaminergic neurons in the Substantia Nigra pars compacta in the midbrain and the presence of intracellular aggregates, known as Lewy bodies (LBs), in the surviving neurons. The aetiology of PD is unknown but a causative role for α-Synuclein (SNCA) has been proposed. Although the function of αSyn is not well understood, a number of pathological mechanisms associated with αSyn toxicity have been proposed. In this study, nine induced pluripotent stem cells (iPSCs) lines from healthy individuals and PD patients carrying the A53T SNCA mutation or a triplication of SNCA were differentiated to dopaminergic neurons (iDAn). All iPSC lines differentiated with similar efficiency to iDAn, indicating that they could be used for phenotypic analysis. Quantification of αSyn expression showed increased αSyn intracellular staining and the novel detection of increased αSyn oligomerization in PD iDAn. Analysis of mitochondrial respiration found a decrease in basal respiration, maximal respiration, ATP production and spare capacity in PD iDAn, but not in undifferentiated iPSCs, indicating the cell-type specificity of these defects. Decreased phosphorylation of dynamin-1-like protein at Ser616 (DRP1^Ser616) and increased levels of Peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC-1α) in A53T SNCA iDAn suggest a new pathological mechanism linking αSyn to the imbalance in mitochondria homeostasis. Markers of endoplasmic reticulum (ER) stress were found to be up-regulated, along with increased β- Glucocerebrosidase (GBA) activity, perturbation of autophagy and decreased expression of fatty acids binding protein 7 (FAPB7) in PD iDAn. Lastly, lentiviral vectors for RNAi-mediated knockdown of αSyn were developed and these reduced αSyn protein levels in iDAn, resulting in increased expression of FABP7. These results describe a novel functional link between αSyn and FABP7. This work demonstrates that iDAn are a promising and relevant in vitro cell model for studying cellular dysfunctions in PD pathology, and the phenotypic analysis of A53T SNCA and SNCA triplication iDAn enabled the detection of novel pathological mechanisms associated with PD.

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Booth, Heather D. E. "Modelling and analysis of LRRK2 mutations in iPSC-derived dopaminergic neurons and astrocytes." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:d85d164e-e9d4-4911-8aa0-831d4519a5a2.

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Parkinson's disease (PD) is a common neurodegenerative disorder, characterised by preferential loss of ventral midbrain dopaminergic (vmDA) neurons in the substantia nigra pars compacta (SNc). The majority of PD cases have unknown aetiology; however, between 5-10% arise due to known genetic mutations, the most common of which are found in the LRRK2 gene. LRRK2 is expressed in neurons and glia in the human brain; therefore, cell-autonomous and/or non-cell autonomous effects may participate in LRRK2-mutation-mediated degeneration of vmDA neurons. This study set out to understand the effects of LRRK2 mutations on human vmDA neurons and midbrain astrocytes, and to shed new light on the mechanisms of PD pathogenesis. To achieve this goal, differentiation protocols were generated to produce vmDA neurons and midbrain patterned (MP) astrocytes from induced pluripotent stem cells (iPSCs). iPSCs from patients carrying the LRRK2-G2019S mutation were differentiated into both cell types, and hypothesis-driven analysis of cellular functions including autophagy, mitochondrial respiration, glycolysis, and cellular migration was conducted; however, no disease phenotypes were observed. Following this, proteomics and transcriptomics techniques were then used to analyse the effects of the LRRK2-G2019S mutation in an unbiased manner. In the iPSC-derived MPastrocyte cultures, this technique highlighted stochastic X-chromosome reactivation events that led to difficulties in interpreting the resulting data; however, in the iPSC-derived vmDA-neuron cultures, LRRK2-G2019S-mediated inhibition of endocytosis and axon guidance was identified. These findings were found to be consistent in iPSC-derived vmDA-neuron cultures carrying the LRRK2-R1441C mutation, suggesting that these two mutations exert their pathogenic effects through similar mechanisms. Finally, phosphoproteomics analysis of iPSC-derived vmDA-neuron cultures was conducted to identify bone fide LRRK2-kinase substrates. Eleven potential LRRK2- kinase substrates were identified, nine of which have been previously shown to participate in endocytic vesicle trafficking, neurite outgrowth, and synaptic function. The findings of this study suggest that LRRK2 has neuron-specific functions, and that its mutations contribute to neurodegeneration in a cell-autonomous manner.

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Samata, Bumpei. "Purification of functional human ES and iPSC-derived midbrain dopaminergic progenitors using LRTM1." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225509.

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Landucci, Elisa. "Modeling Rett syndrome with iPSCs-derived neurons." Doctoral thesis, Università di Siena, 2018. http://hdl.handle.net/11365/1051069.

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Rett syndrome is a severe neurodevelopmental disorder. The condition affects approximately one in every 10.000 females and is only rarely seen in males. Causative mutations in the transcriptional regulator MeCP2 have been identified in more than 95% of classic Rett patients; mutations in CDKL5 are responsible for the early onset seizures Rett variant and mutations in FOXG1 gene lead to the congenital Rett variant. To shed light on molecular mechanisms underlying Rett syndrome onset and progression in disease-relevant cells, we took advantage of the breakthrough genetic reprogramming technology and we investigated changes in iPSC-derived neurons from patients with different MECP2 and FOXG1 mutations and in the brain of Foxg1+/- mice. In total brains from Foxg1+/ − mutants we noticed a statistically significant overexpression of a group of neuropeptides expressed in the basal ganglia, cortex, hippocampus and hypothalamus: Oxytocin (Oxt), Arginine vasopressin (Avp) and Neuronatin (Nnat).Moreover, in iPSC-derived neuronal precursors and neurons mutated in FOXG1 and in Foxg1+/− mouse embryonic brain (E11.5) compared to wild type controls we found an increase in the expression of GluD1 and inhibitory synaptic markers, such as GAD67 and GABA AR-α1 and a decreased expression of excitatory synaptic markers, such as VGLUT1, GluA1, GluN1 and PSD-95, suggesting an excitation/inhibition imbalance in the developing brain of the congenital RTT variant. Furthermore, we investigated transcriptome changes in neurons differentiated from MECP2 mutated iPSC-derived neurons and we noticed a prominent GABAergic circuit disruption and a perturbation of cytoskeleton dynamics. In particular, in MECP2-mutated neurons we identified a significant decrease of acetylated α-tubulin which can be reverted by treatment with a selective inhibitor of HDAC6, the main α-tubulin deacetylase. Taken togheter, these findings contribute to shed light on Rett pathogenic mechanisms and provide hints for the definition of new therapeutic strategies for Rett syndrome.

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Srikanth, Priya. "Schizophrenia-Relevant DISC1 Interruption Alters Wnt Signaling and Cell Fate in Human iPSC-Derived Neurons." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:23845068.

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The advent of human induced pluripotent stem cell (iPSC) technology has allowed for unprecedented investigation into the pathophysiology of human neurological and psychiatric diseases. Use of human iPSC-derived neural cells to study disease is complicated by the genetic heterogeneity of cell lines and diversity of differentiation protocols. Here, I address issues surrounding neuropsychiatric disease modeling with human iPSCs. Dozens of published protocols exist to differentiate iPSCs into forebrain neuronal cultures. Among the factors that distinguish these methods are: use of small molecules, monolayer vs. aggregate culture, choice of plating substrates, method of NPC isolation, and glial co-culture. Each of these factors is evaluated here, creating a resource that directly compares a variety of differentiation procedures. The most efficient and reproducible method was an embryoid aggregate differentiation protocol, including aggregate plating onto a Matrigel substrate, enzymatic neural rosette selection, and neuronal dissociation and plating onto Matrigel. This optimized protocol is used to model a schizophrenia-relevant mutation in human neural cells. Genetic and clinical association studies have identified disrupted-in-schizophrenia 1 (DISC1) as a strong candidate risk gene for major mental illness. DISC1 was initially associated with mental illness upon the discovery that its coding sequence is interrupted by a balanced chr(1;11) translocation in a Scottish family, in which the translocation cosegregates with psychiatric disorders. I investigate the functional and biochemical consequences of DISC1 interruption in human neurons using TALENs or CRISPR-Cas9 to introduce DISC1 frameshift mutations into iPSCs. I show that disease-relevant DISC1 targeting results in decreased DISC1 protein expression by nonsense-mediated decay, increases baseline Wnt signaling in neural progenitor cells, and causes a shift in neural cell fate. DISC1-dependent Wnt signaling and cell fate changes can be reversed by antagonizing the Wnt pathway during a critical window in neural progenitor development. These experiments suggest that DISC1-disruption increases Wnt signaling, which alters the balance and identity of neural progenitors, thereby subtly modifying cell fate. These studies evaluate the use of multiple differentiation procedures in neural disease modeling, shed light on the roles of DISC1 during human brain development, and further our understanding of the pathogenesis of major mental illness.
Medical Sciences

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Grunwald, Lena-Marie [Verfasser], and Hans-Georg [Akademischer Betreuer] Rammensee. "iPSC-derived cortical neurons from patients with schizophrenia exhibit changes in early neuronal development / Lena-Marie Grunwald ; Betreuer: Hans-Georg Rammensee." Tübingen : Universitätsbibliothek Tübingen, 2019. http://d-nb.info/120091614X/34.

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Klaus, Johannes [Verfasser], and Magdalena [Akademischer Betreuer] Götz. "Modeling neuronal heterotopias using iPSC derived neural stem cells, neurons and cerebral organoids derived from patients with mutations in FAT4 and DCHS1 / Johannes Klaus ; Betreuer: Magdalena Götz." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1148275789/34.

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Mosaku, Olukunbi Eniola. "The use of the CRISPR-Cas9 system and iPSC-derived neurons with a SNCA mutation to model neurodegeneration." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10062570/.

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Parkinson's disease (PD) is characterised by the selective loss of dopaminergic neurons of the substantia nigra pars compacta. Patients suffer from a progressive motor disorder, defined by the presence of rigidity, resting tremor and bradykinesia. Current treatment options, relieve symptoms for a limited period, but are not curative, as the underlying molecular causes of neurodegeneration are unknown. Several causative PD mutations have been identified and could provide insight into the defective molecular pathways in PD. Multiplication or missense mutation of the SNCA gene leads to autosomal dominant PD. Alpha-synuclein, encoded by the SNCA gene, is a defining component of proteinaceous deposits found in surviving neurons in PD and a central protein in PD aetiology. Induced pluripotent stem cells (iPSCs) self-renew indefinitely and generate all germ layer lineages. Human iPSCs derived from an individual with a genetic variant known to cause disease, provide a platform to investigate the molecular basis of disease. However, genetic variation between iPSC lines can lead to functional disparities, masking or accentuating disease-specific phenotypes. Genome engineering facilitates the generation of iPSCs which differ exclusively at the locus of interest, providing a genetically stable cellular model. iPSCs from an individual with a SNCA missense mutation, G51D, and an unaffected relative were characterised, demonstrating ex vivo pluripotency was established and dopaminergic neurons could be derived. The clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 system was exploited to introduce the G51D mutation into control iPSCs. Changes in dopamine turnover and protein metabolism were detected after differentiation of CRISPR-Cas9 generated iPSCs, now harbouring the heterozygote G51D mutation. A CRISPR-Cas9 G51D homozygote iPSC clone was generated and a reduction in the number of dopaminergic neurons produced observed. This study demonstrates human iPSCs can be used to detect phenotypic differences in specialised cells, despite the latency of PD, and before overt neurodegeneration.

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MUTTI, VERONICA. "IPSC-derived neurons and astrocytes: a novel patient-specific model to study the pre-degenerative molecular alteration in Parkinson's Disease." Doctoral thesis, Università degli studi di Brescia, 2021. http://hdl.handle.net/11379/544657.

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IPSC-derived neurons and astrocytes: a novel patient-specific model to study the pre-degenerative molecular alteration in Parkinson's Disease
IPSC-derived neurons and astrocytes: a novel patient-specific model to study the pre-degenerative molecular alteration in Parkinson's Disease

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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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Книги з теми "IPSC-derived neurons"

Phenotyping of Human iPSC-derived Neurons. Elsevier, 2023. http://dx.doi.org/10.1016/c2019-0-04202-1.

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Buttermore, Elizabeth D. Phenotyping of Human IPSC-Derived Neurons: Patient-Driven Research. Elsevier Science & Technology, 2022.

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Buttermore, Elizabeth D. Phenotyping of Human IPSC-Derived Neurons: Patient-Driven Research. Elsevier Science & Technology Books, 2022.

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Wainger, Brian J. Amyotrophic Lateral Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0028.

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Mouse and cellular models of ALS including stem cells have revealed tremendous insight into the molecular processes that lead to ALS. Models of ALS and other neurodegenerative diseases have led to emergent molecular themes that span several diseases. Future models must account for neuronal subtype specificity of different neurodegenerative diseases, particularly between tightly related diseases such as FTD and ALS. Human iPSC-derived motor neurons offer promise both with regard to the use of human cells and in particular the ability to model sporadic disease, which is critically important given the overwhelming abundance of sporadic disease in ALS and other neurodegenerative diseases.

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Частини книг з теми "IPSC-derived neurons"

Little, Daniel, Christin Luft, Olukunbi Mosaku, Robin Ketteler, Michael J. Devine, and Paul Gissen. "High-Content Autophagy Analysis in iPSC-Derived Neurons Using Immunofluorescence." In Methods in Molecular Biology, 165–74. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9477-9_15.

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Little, Daniel, Christin Luft, Olukunbi Mosaku, Robin Ketteler, Michael J. Devine, and Paul Gissen. "High-Content Analysis of Mitochondrial Function in iPSC-Derived Neurons." In Methods in Molecular Biology, 175–84. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9477-9_16.

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Pandya, Nikhil J., David Avila, Tom Dunkley, Ravi Jagasia, and Manuel Tzouros. "TMT-MS3-Enabled Proteomic Quantification of Human IPSC-Derived Neurons." In Neuromethods, 103–17. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9662-9_10.

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Roy-Choudhury, Gourav, and Marcel M. Daadi. "Assay for Assessing Mitochondrial Function in iPSC-Derived Neural Stem Cells and Dopaminergic Neurons." In Methods in Molecular Biology, 161–73. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9007-8_12.

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Harasta, Anne E., and Lars M. Ittner. "Alzheimer’s Disease: Insights from Genetic Mouse Models and Current Advances in Human IPSC-Derived Neurons." In Advances in Neurobiology, 3–29. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57193-5_1.

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Kizner, Valeria, Sandra Fischer, and Maximilian Naujock. "Multielectrode Array (MEA)-Based Detection of Spontaneous Network Activity in Human iPSC-Derived Cortical Neurons." In Methods in Molecular Biology, 209–16. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9477-9_19.

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Clark, Alex J. "Establishing Myelinating Cocultures Using Human iPSC-Derived Sensory Neurons to Investigate Axonal Degeneration and Demyelination." In Methods in Molecular Biology, 111–29. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0585-1_9.

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Liu, Lumei, Youngmi Koo, Teal Russell, and Yeoheung Yun. "A Three-Dimensional Brain-on-a-Chip Using Human iPSC-Derived GABAergic Neurons and Astrocytes." In Methods in Molecular Biology, 117–28. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2289-6_6.

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Turkalj, Luka, Monal Mehta, Paul Matteson, Smrithi Prem, Madeline Williams, Robert J. Connacher, Emanuel DiCicco-Bloom, and James H. Millonig. "Using iPSC-Based Models to Understand the Signaling and Cellular Phenotypes in Idiopathic Autism and 16p11.2 Derived Neurons." In Advances in Neurobiology, 79–107. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-45493-7_4.

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Tukker, Anke M., Fiona M. J. Wijnolts, Aart de Groot, Richard W. Wubbolts, and Remco H. S. Westerink. "In Vitro Techniques for Assessing Neurotoxicity Using Human iPSC-Derived Neuronal Models." In Neuromethods, 17–35. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9228-7_2.

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Тези доповідей конференцій з теми "IPSC-derived neurons"

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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Анотація:

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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Puppo, Francesca, Sanaz Sadegh, Cleber A. Trujillo, Martin Thunemann, Evan Campbell, Matthieu Vandenberghe, Evan W. Miller, et al. "All-Optical Electrophysiology in iPSC-Derived Neurons with Synthetic NIR Voltage Reporter." In Clinical and Translational Biophotonics. Washington, D.C.: OSA, 2020. http://dx.doi.org/10.1364/translational.2020.jth2a.30.

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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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Bunting, Emma, Jasmine Donaldson, Jessica Olive, Holly Kordasiewicz, Frank Bennett, Sarah A. Cumming, Darren G. Monckton, Michael Flower, and Sarah J. Tabrizi. "I01 Msh3-targeting antisense oligonucleotides halt CAG repeat expansions in Huntington’s disease IPSC-derived neurons." In EHDN 2022 Plenary Meeting, Bologna, Italy, Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jnnp-2022-ehdn.227.

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Badin, Romina Aron, Aurore Bugi, Susannah Williams, Marta Vadori, Marie Michael, Caroline Jan, Alberto Nassi, et al. "I24 MHC matching fails to prevent long-term rejection of ipsc-derived neurons in non-human primate." In EHDN 2018 Plenary Meeting, Vienna, Austria, Programme and Abstracts. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/jnnp-2018-ehdn.260.

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Carleo, Giusy, Yi-Shin Lee, Agnese Secondo, Francesco Miceli, and Maurizio Taglialatela. "Multi-electrode array (MEASs) to investigate pathogenetic disease mechanisms and pharmacological properties in iPSC-derived neurons modelling neuropsychiatric diseases." In 2022 IEEE International Conference on Metrology for Extended Reality, Artificial Intelligence and Neural Engineering (MetroXRAINE). IEEE, 2022. http://dx.doi.org/10.1109/metroxraine54828.2022.9967629.

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Ferguson, Ross, Michael Flower, and Sarah J. Tabrizi. "C07 A CRISPRI platform to assess the role of HD risk modifiers in CAG repeat expansion in iPSC derived striatal neurons." In EHDN 2022 Plenary Meeting, Bologna, Italy, Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jnnp-2022-ehdn.51.

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Wood-Kaczmar, Alison, Ralph Andre, Sahar Farag, Aneesa P. Ali, and Sarah J. Tabrizi. "B14 Development of a high content imaging platform for hd therapeutic screening using human medium spiny neurons derived from an hd family ipsc series." In EHDN 2018 Plenary Meeting, Vienna, Austria, Programme and Abstracts. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/jnnp-2018-ehdn.66.

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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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Schmieder, Felix, Rouhollah Habibey, Lars Büttner, Jürgen W. Czarske, and Volker Busskamp. "Optogenetic investigation of in vitro human iPSC-derived neuronal networks (Conference Presentation)." In Optogenetics and Optical Manipulation 2019, edited by Samarendra K. Mohanty and E. Duco Jansen. SPIE, 2019. http://dx.doi.org/10.1117/12.2507855.

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