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neuron reprogramming

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https://www.readbyqxmd.com/read/29130506/animal-models-of-acquired-epilepsy-insights-into-mechanisms-of-human-epileptogenesis
#1
Albert J Becker
In many patients who suffer from epilepsies, recurrent epileptic seizures do not start at birth but develop later in life. This holds particularly true for epilepsies with a focal seizure origin including focal cortical dysplasias (FCDs) and temporal lobe epilepsy (TLE). TLE most frequently has its seizure onset in the hippocampal formation. Hippocampal biopsies of pharmacoresistant TLE patients undergoing epilepsy surgery for seizure control most frequently reveal the damage pattern of hippocampal sclerosis, i...
November 12, 2017: Neuropathology and Applied Neurobiology
https://www.readbyqxmd.com/read/29116664/unraveling-the-biology-of-bipolar-disorder-using-induced-pluripotent-stem-derived-neurons
#2
REVIEW
Nathaniel D Miller, John R Kelsoe
OBJECTIVES: Bipolar disorder has been studied from numerous angles, from pathological studies to large-scale genomic studies, overall making moderate gains toward an understanding of the disorder. With the advancement of induced pluripotent stem (iPS) cell technology, in vitro models based on patient samples are now available that inherently incorporate the complex genetic variants that largely are the basis for this disorder. A number of groups are starting to apply iPS technology to the study of bipolar disorder...
November 8, 2017: Bipolar Disorders
https://www.readbyqxmd.com/read/29079884/modeling-neurological-diseases-using-ipsc-derived-neural-cells-ipsc-modeling-of-neurological-diseases
#3
REVIEW
Li Li, Jianfei Chao, Yanhong Shi
Developing efficient models for neurological diseases enables us to uncover disease mechanisms and develop therapeutic strategies to treat them. Discovery of reprogramming somatic cells to induced pluripotent stem cells (iPSCs) has revolutionized the way of modeling human diseases, especially neurological diseases. Currently almost all types of neural cells, including but not limited to neural stem cells, neurons, astrocytes, oligodendrocytes and microglia, can be derived from iPSCs following developmental principles...
October 28, 2017: Cell and Tissue Research
https://www.readbyqxmd.com/read/29044560/regulating-the-transcriptomes-that-mediate-the-conversion-of-fibroblasts-to-various-nervous-system-neural-cell-types
#4
Niusha Khazaei, Shima Rastegar-Pouyani, Nicholas O'Toole, Ping Wee, Abdulshakour Mohammadnia, Moein Yaqubi
Our understanding of the mechanism of cell fate transition during the direct reprogramming of fibroblasts into various central nervous system (CNS) neural cell types has been limited by the lack of a comprehensive analysis on generated cells, independently and in comparison with other CNS neural cell types. Here, we applied an integrative approach on 18 independent high throughput expression data sets to gain insight into the regulation of the transcriptome during the conversion of fibroblasts into induced neural stem cells, induced neurons, induced astrocytes, and induced oligodendrocyte progenitor cells...
October 17, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/29034884/generation-of-six-multiple-sclerosis-patient-derived-induced-pluripotent-stem-cell-lines
#5
L Miquel-Serra, A Duarri, Y Muñoz, B Kuebler, B Aran, C Costa, M Martí, M Comabella, S Malhotra, X Montalban, A Veiga, A Raya
Multiple sclerosis (MS) is considered a chronic autoimmune disease of the central nervous system that leads to gliosis, demyelination, axonal damage and neuronal death. The MS disease aetiology is unknown, though a polymorphism of the TNFRSF1A gene, rs1800693, is known to confer an increased risk for MS. Using retroviral delivery of reprogramming transgenes, we generated six MS patient-specific iPSC lines with two distinct genotypes, CC or TT, of the polymorphism rs1800693. iPSC lines had normal karyotype, expressed pluripotency genes and differentiated into the three germ layers...
October 2017: Stem Cell Research
https://www.readbyqxmd.com/read/29033781/direct-neuronal-reprogramming-for-disease-modeling-studies-using-patient-derived-neurons-what-have-we-learned
#6
REVIEW
Janelle Drouin-Ouellet, Karolina Pircs, Roger A Barker, Johan Jakobsson, Malin Parmar
Direct neuronal reprogramming, by which a neuron is formed via direct conversion from a somatic cell without going through a pluripotent intermediate stage, allows for the possibility of generating patient-derived neurons. A unique feature of these so-called induced neurons (iNs) is the potential to maintain aging and epigenetic signatures of the donor, which is critical given that many diseases of the CNS are age related. Here, we review the published literature on the work that has been undertaken using iNs to model human brain disorders...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/29030949/microrna-expression-in-the-neural-retina-focus-on-m%C3%A3-ller-glia
#7
REVIEW
Heberto Quintero, Mónica Lamas
The neural retina hosts a unique specialized type of macroglial cell that not only preserves retinal homeostasis, function, and integrity but also may serve as a source of new neurons during regenerative processes: the Müller cell. Precise microRNA-driven mechanisms of gene regulation impel and direct the processes of Müller glia lineage acquisition from retinal progenitors during development, the triggering of their response to retinal degeneration and, in some cases, Müller cell reprogramming and regenerative events...
October 14, 2017: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/29025968/activation-of-ampk-mtorc1-mediated-autophagy-by-metformin-reverses-clk1-deficiency-sensitized-dopaminergic-neuronal-death
#8
Qiuting Yan, Chaojun Han, Guanghui Wang, John L Waddington, Longtai Zheng, Xuechu Zhen
The autophagy-lysosome pathway (ALP) plays a critical role in the pathology of Parkinson's disease (PD). Clk1 (coq7) is a mitochondrial hydroxylase that is essential for Coenzyme Q (ubiquinone) biosynthesis. We have reported previously that Clk1 regulates microglia activation via modulating microglia metabolic reprogramming, which contributes to dopaminergic neuronal survival. This study explored the direct effect of Clk1 on dopaminergic neuronal survival. We demonstrated that Clk1 deficiency inhibited dopaminergic neuronal autophagy in cultured MN9D dopaminergic neurons and in SNc of Clk+/- mutant mice and consequently sensitized dopaminergic neuron damage and behavioral defects...
October 12, 2017: Molecular Pharmacology
https://www.readbyqxmd.com/read/28987284/lentivirus-carrying-the-neurod1-gene-promotes-the-conversion-from-glial-cells-into-neurons-in-a-spinal-cord-injury-model
#9
Wenhao Chen, Baoquan Zhang, Shuxia Xu, Ren Lin, Wei Wang
In this study, we aimed to reprogram reactive glial cells into neural stem cells and neurons in vivo, by up-regulating NeuroD1. 60 rats were randomly divided into three groups with equal numbers. All rats received a spinal cord injury. Group A received only normal saline injection. Group B received unloaded lentivirus injection. Group C received NeuroD1 recombinant lentivirus injection. The BBB scores of the animals were documented at 3, 7, 14, 21days after SCI. 5 random rats of each group were removed at those timings after SCI and sacrificed...
October 5, 2017: Brain Research Bulletin
https://www.readbyqxmd.com/read/28981879/activation-of-a-cryptic-5-splice-site-reverses-the-impact-of-pathogenic-splice-site-mutations-in-the-spinal-muscular-atrophy-gene
#10
Natalia N Singh, José Bruno Del Rio-Malewski, Diou Luo, Eric W Ottesen, Matthew D Howell, Ravindra N Singh
Spinal muscular atrophy (SMA) is caused by deletions or mutations of the Survival Motor Neuron 1 (SMN1) gene coupled with predominant skipping of SMN2 exon 7. The only approved SMA treatment is an antisense oligonucleotide that targets the intronic splicing silencer N1 (ISS-N1), located downstream of the 5' splice site (5'ss) of exon 7. Here, we describe a novel approach to exon 7 splicing modulation through activation of a cryptic 5'ss (Cr1). We discovered the activation of Cr1 in transcripts derived from SMN1 that carries a pathogenic G-to-C mutation at the first position (G1C) of intron 7...
September 15, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/28978921/sensitive-and-long-term-monitoring-of-intracellular-micrornas-using-a-non-integrating-cytoplasmic-rna-vector
#11
Masayuki Sano, Manami Ohtaka, Minoru Iijima, Asako Nakasu, Yoshio Kato, Mahito Nakanishi
MicroRNAs (miRNAs) are small noncoding RNAs that modulate gene expression at the post-transcriptional level. Different types of cells express unique sets of miRNAs that can be exploited as potential molecular markers to identify specific cell types. Among the variety of miRNA detection methods, a fluorescence-based imaging system that utilises a fluorescent-reporter gene regulated by a target miRNA offers a major advantage for long-term tracking of the miRNA in living cells. In this study, we developed a novel fluorescence-based miRNA-monitoring system using a non-integrating cytoplasmic RNA vector based on a replication-defective and persistent Sendai virus (SeVdp)...
October 4, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28975140/patient-derived-hipsc-neurons-with-heterozygous-cntnap2-deletions-display-altered-neuronal-gene-expression-and-network-activity
#12
Erin Flaherty, Rania M Deranieh, Elena Artimovich, Inkyu S Lee, Arthur J Siegel, Deborah L Levy, Michael W Nestor, Kristen J Brennand
Variants in CNTNAP2, a member of the neurexin family of genes that function as cell adhesion molecules, have been associated with multiple neuropsychiatric conditions such as schizophrenia, autism spectrum disorder and intellectual disability; animal studies indicate a role for CNTNAP2 in axon guidance, dendritic arborization and synaptogenesis. We previously reprogrammed fibroblasts from a family trio consisting of two carriers of heterozygous intragenic CNTNAP2 deletions into human induced pluripotent stem cells (hiPSCs) and described decreased migration in the neural progenitor cells (NPCs) differentiated from the affected CNTNAP2 carrier in this trio...
2017: NPJ Schizophrenia
https://www.readbyqxmd.com/read/28970473/patient-derived-hipsc-neurons-with-heterozygous-cntnap2-deletions-display-altered-neuronal-gene-expression-and-network-activity
#13
Erin Flaherty, Rania M Deranieh, Elena Artimovich, Inkyu S Lee, Arthur J Siegel, Deborah L Levy, Michael W Nestor, Kristen J Brennand
Variants in CNTNAP2, a member of the neurexin family of genes that function as cell adhesion molecules, have been associated with multiple neuropsychiatric conditions such as schizophrenia, autism spectrum disorder and intellectual disability; animal studies indicate a role for CNTNAP2 in axon guidance, dendritic arborization and synaptogenesis. We previously reprogrammed fibroblasts from a family trio consisting of two carriers of heterozygous intragenic CNTNAP2 deletions into human induced pluripotent stem cells (hiPSCs) and described decreased migration in the neural progenitor cells (NPCs) differentiated from the affected CNTNAP2 carrier in this trio...
October 2, 2017: NPJ Schizophrenia
https://www.readbyqxmd.com/read/28966629/live-cell-imaging-new-avenues-to-investigate-retinal-regeneration
#14
REVIEW
Manuela Lahne, David R Hyde
Sensing and responding to our environment requires functional neurons that act in concert. Neuronal cell loss resulting from degenerative diseases cannot be replaced in humans, causing a functional impairment to integrate and/or respond to sensory cues. In contrast, zebrafish (Danio rerio) possess an endogenous capacity to regenerate lost neurons. Here, we will focus on the processes that lead to neuronal regeneration in the zebrafish retina. Dying retinal neurons release a damage signal, tumor necrosis factor α, which induces the resident radial glia, the Müller glia, to reprogram and re-enter the cell cycle...
August 2017: Neural Regeneration Research
https://www.readbyqxmd.com/read/28954238/rapid-chromatin-switch-in-the-direct-reprogramming-of-fibroblasts-to-neurons
#15
Orly L Wapinski, Qian Yi Lee, Albert C Chen, Rui Li, M Ryan Corces, Cheen Euong Ang, Barbara Treutlein, Chaomei Xiang, Valérie Baubet, Fabian Patrik Suchy, Venkat Sankar, Sopheak Sim, Stephen R Quake, Nadia Dahmane, Marius Wernig, Howard Y Chang
How transcription factors (TFs) reprogram one cell lineage to another remains unclear. Here, we define chromatin accessibility changes induced by the proneural TF Ascl1 throughout conversion of fibroblasts into induced neuronal (iN) cells. Thousands of genomic loci are affected as early as 12 hr after Ascl1 induction. Surprisingly, over 80% of the accessibility changes occur between days 2 and 5 of the 3-week reprogramming process. This chromatin switch coincides with robust activation of endogenous neuronal TFs and nucleosome phasing of neuronal promoters and enhancers...
September 26, 2017: Cell Reports
https://www.readbyqxmd.com/read/28946615/use-of-human-neurons-derived-via-cellular-reprogramming-methods-to-study-host-parasite-interactions-of-toxoplasma-gondii-in-neurons
#16
REVIEW
Sandra K Halonen
Toxoplasma gondii is an intracellular protozoan parasite, with approximately one-third of the worlds' population chronically infected. In chronically infected individuals, the parasite resides in tissue cysts in neurons in the brain. The chronic infection in immunocompetant individuals has traditionally been considered to be asymptomatic, but increasing evidence indicates that chronic infection is associated with diverse neurological disorders such as schizophrenia, cryptogenic epilepsy, and Parkinson's Disease...
September 23, 2017: Cells
https://www.readbyqxmd.com/read/28916331/depressive-like-phenotype-induced-by-prenatal-dexamethasone-in-mice-is-reversed-by-desipramine
#17
Mirko Conti, Stefan Spulber, Marilena Raciti, Sandra Ceccatelli
Exposure to prenatal insults has been associated with an increased risk for neuropsychiatric disorders, including depression, but the mechanisms are still poorly understood. Persistent alterations of the HPA axis feedback mechanism as well as adult impaired neurogenesis are believed to play a relevant role in the etiology of depression. In addition, growing evidence points at epigenetic reprogramming as a key factor. We have previously shown that prenatal exposure to the synthetic glucocorticoid dexamethasone (DEX) impairs neurogenesis and leads to late onset of depression-like behavior that does not respond to the SSRI antidepressant fluoxetine (FLX)...
September 13, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28915325/brown-and-beige-adipose-tissues-in-health-and-disease
#18
Liangyou Rui
Brown and beige adipocytes arise from distinct developmental origins. Brown adipose tissue (BAT) develops embryonically from precursors that also give to skeletal muscle. Beige fat develops postnatally and is highly inducible. Beige fat recruitment is mediated by multiple mechanisms, including de novo beige adipogenesis and white-to-brown adipocyte transdifferentiaiton. Beige precursors reside around vasculatures, and proliferate and differentiate into beige adipocytes. PDGFRα+Ebf2+ precursors are restricted to beige lineage cells, while another PDGFRα+ subset gives rise to beige adipocytes, white adipocytes, or fibrogenic cells...
September 12, 2017: Comprehensive Physiology
https://www.readbyqxmd.com/read/28899812/the-starving-brain-overfed-meets-undernourished-in-the-pathology-of-mild-cognitive-impairment-mci-and-alzheimer-s-disease-ad
#19
REVIEW
Kelly J Gibas
Type II Diabetes affects 400 million people worldwide (IDF, 2013). The pathology is paradoxical: internal starvation activated by overfeeding. Hyperinsulinemic impairments of glucose homeostasis are treated with anti-hyperglycemics exacerbating cell starvation, inducing hypoglycemia and raising respiratory quotient. Reductions in hyperglycemia are achieved at the expense of glucose dependency and metabolic inflexibility (Gibas & Gibas, 2017). The brain is not immune from these cycles of starvation. The bioenergetic model characterizes propagation of late-onset, sporadic Alzheimer's disease as loss of molecular fidelity and compromised energy originating in brain networks with highest metabolic demand...
November 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28886366/micrornas-induce-a-permissive-chromatin-environment-that-enables-neuronal-subtype-specific-reprogramming-of-adult-human-fibroblasts
#20
Daniel G Abernathy, Woo Kyung Kim, Matthew J McCoy, Allison M Lake, Rebecca Ouwenga, Seong Won Lee, Xiaoyun Xing, Daofeng Li, Hyung Joo Lee, Robert O Heuckeroth, Joseph D Dougherty, Ting Wang, Andrew S Yoo
Directed reprogramming of human fibroblasts into fully differentiated neurons requires massive changes in epigenetic and transcriptional states. Induction of a chromatin environment permissive for acquiring neuronal subtype identity is therefore a major barrier to fate conversion. Here we show that the brain-enriched miRNAs miR-9/9(∗) and miR-124 (miR-9/9(∗)-124) trigger reconfiguration of chromatin accessibility, DNA methylation, and mRNA expression to induce a default neuronal state. miR-9/9(∗)-124-induced neurons (miNs) are functionally excitable and uncommitted toward specific subtypes but possess open chromatin at neuronal subtype-specific loci, suggesting that such identity can be imparted by additional lineage-specific transcription factors...
September 7, 2017: Cell Stem Cell
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