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Cuprizone

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https://www.readbyqxmd.com/read/29775986/effects-of-two-training-programs-on-transcriptional-levels-of-neurotrophins-and-glial-cells-population-in-hippocampus-of-experimental-multiple-sclerosis
#1
Maryam Naghibzadeh, Rouhollah Ranjbar, Mohammad Reza Tabandeh, Abdolhamid Habibi
The aim of the present study was to investigate the effects of high-intensity interval training (HIIT) versus low-intensity continuous training (LICT) on transcriptional levels of neurotrophic factors and oligodendrocyte/microglia cell loss in a cuprizone (CP) induced animal model of demyelination. Male C57BL/6 mice were assigned to six groups: control (C), cuprizone-induced demyelination (CP), interval training (IT), continuous training (CT), IT plus CP (ITCP), and CT plus CP (CTCP). Training programs on the treadmill were performed for four weeks, and then demyelination was induced by feeding mice a diet containing 0...
May 18, 2018: International Journal of Sports Medicine
https://www.readbyqxmd.com/read/29775564/the-antibody-rhigm22-facilitates-hippocampal-remyelination-and-ameliorates-memory-deficits-in-the-cuprizone-mouse-model-of-demyelination
#2
Charlene Cui, Jing Wang, Ariana P Mullin, Anthony O Caggiano, Tom J Parry, Raymond W Colburn, Elias Pavlopoulos
Multiple sclerosis (MS) is a chronic, inflammatory demyelinating disease of the CNS. In addition to motor, sensory and visual deficits, MS is also characterized by hippocampal demyelination and memory impairment. We recently demonstrated that a recombinant human-derived monoclonal IgM antibody, which is designated rHIgM22 and currently in clinical development for people with MS, accelerates remyelination of the corpus callosum in the brains of cuprizone-treated mice. Here, we investigated the effects of rHIgM22 in the hippocampus and on hippocampal-dependent learning and memory in the same mouse model of cuprizone-induced demyelination and spontaneous remyelination...
May 15, 2018: Brain Research
https://www.readbyqxmd.com/read/29761559/conditional-depletion-of-gsk3b-protects-oligodendrocytes-from-apoptosis-and-lessens-demyelination-in-the-acute-cuprizone-model
#3
Bin Xing, Lauren E Brink, Kelly Maers, Mara L Sullivan, Richard J Bodnar, Donna B Stolz, Franca Cambi
Apoptosis is recognized as the main mechanism of oligodendrocyte loss in Multiple Sclerosis caused either by immune mediated injury (Barnett & Prineas, ) or a direct degenerative process (oligodendrogliapathy; Lucchinetti et al., ). Cuprizone induced demyelination is the result of non-immune mediated apoptosis of oligodendrocytes (OL) and represents a model of oligodendrogliapathy (Simmons, Pierson, Lee, & Goverman, ). Glycogen Synthase Kinase (GSK) 3b has been shown to be pro-apoptotic for cells other than OL...
May 15, 2018: Glia
https://www.readbyqxmd.com/read/29759134/behavioural-alterations-and-morphological-changes-are-attenuated-by-the-lack-of-trpa1-receptors-in-the-cuprizone-induced-demyelination-model-in-mice
#4
Kata Bölcskei, Gábor Kriszta, Éva Sághy, Maja Payrits, Éva Sipos, Anett Vranesics, Zoltán Berente, Hajnalka Ábrahám, Péter Ács, Sámuel Komoly, Erika Pintér
We have recently reported that the Transient Receptor Potential Ankyrin 1 (TRPA1) receptor deficiency significantly attenuated cuprizone-induced demyelination by reducing the apoptosis of mature oligodendrocytes. The aim of the present study was to gather additional data on the role of TRPA1 by investigating the time course of behavioural alterations and morphological changes in cuprizone-treated TRPA1 receptor gene-deficient mice. Demyelination was induced by feeding male wild-type (WT) and TRPA1 gene-deleted (TRPA1 KO) mice with 0...
July 15, 2018: Journal of Neuroimmunology
https://www.readbyqxmd.com/read/29744572/protective-potential-of-dimethyl-fumarate-in-a-mouse-model-of-thalamocortical-demyelination
#5
Manuela Cerina, Venu Narayanan, Anna Delank, Patrick Meuth, Stephanie Graebenitz, Kerstin Göbel, Alexander M Herrmann, Stefanie Albrecht, Thiemo Daldrup, Thomas Seidenbecher, Ali Gorji, Tanja Kuhlmann, Heinz Wiendl, Christoph Kleinschnitz, Erwin J Speckmann, Hans-Christian Pape, Sven G Meuth, Thomas Budde
Alterations in cortical cellular organization, network functionality, as well as cognitive and locomotor deficits were recently suggested to be pathological hallmarks in multiple sclerosis and corresponding animal models as they might occur following demyelination. To investigate functional changes following demyelination in a well-defined, topographically organized neuronal network, in vitro and in vivo, we focused on the primary auditory cortex (A1) of mice in the cuprizone model of general de- and remyelination...
May 9, 2018: Brain Structure & Function
https://www.readbyqxmd.com/read/29730092/kolaviron-protects-the-brain-in-cuprizone-induced-model-of-experimental-multiple-sclerosis-via-enhancement-of-intrinsic-antioxidant-mechanisms-possible-therapeutic-applications
#6
Gabriel Olaiya Omotoso, Ileje Inelo Ukwubile, Leviticus Arietarhire, Fatima Sulaimon, Ismail Temitayo Gbadamosi
Multiple sclerosis is a demyelinating condition of the central nervous system which commonly affects young adults. Kolaviron, a biflavonoid isolate of Garcinia kola, has been used in experimental studies which explored its anti-oxidative, anti-inflammatory and anti-genotoxic properties. This work was aimed at unraveling the possible ameliorative effect of kolaviron on cuprizone-induced demyelination in the prefrontal cortices of Wistar rats. A total of 28 adult male Wistar rats were divided into four groups A-D...
April 27, 2018: Pathophysiology: the Official Journal of the International Society for Pathophysiology
https://www.readbyqxmd.com/read/29728463/biochemically-altered-myelin-triggers-autoimmune-demyelination
#7
Andrew V Caprariello, James A Rogers, Megan L Morgan, Vahid Hoghooghi, Jason R Plemel, Adam Koebel, Shigeki Tsutsui, Jeffrey F Dunn, Lakshmi P Kotra, Shalina S Ousman, V Wee Yong, Peter K Stys
Although immune attack against central nervous system (CNS) myelin is a central feature of multiple sclerosis (MS), its root cause is unresolved. In this report, we provide direct evidence that subtle biochemical modifications to brain myelin elicit pathological immune responses with radiological and histological properties similar to MS lesions. A subtle myelinopathy induced by abbreviated cuprizone treatment, coupled with subsequent immune stimulation, resulted in lesions of inflammatory demyelination. The degree of myelin injury dictated the resulting immune response; biochemical damage that was too limited or too extensive failed to trigger overt pathology...
May 4, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29697861/microglial-mhc-class-ii-is-dispensable-for-experimental-autoimmune-encephalomyelitis-and-cuprizone-induced-demyelination
#8
Yochai Wolf, Anat Shemer, Liron Levy-Efrati, Mor Gross, Jung-Seok Kim, Adrien Engel, Eyal David, Louise Chappell-Maor, Jonathan Grozovski, Ron Rotkopf, Inbal Biton, Raya Eilam-Altstadter, Steffen Jung
Microglia are resident immune cells in the central nervous system (CNS), strategically positioned to clear dead cells and debris, and orchestrate CNS inflammation and immune defense. In steady state, these macrophages lack major histocompatibility complex class II (MHCII) expression, but microglia activation can be associated with MHCII induction. Whether microglial MHCII serves antigen presentation for critical local T cell re-stimulation in CNS auto-immune disorders or modulates microglial signaling output remains under debate...
April 26, 2018: European Journal of Immunology
https://www.readbyqxmd.com/read/29681799/correction-disinhibition-of-cathepsin-c-caused-by-cystatin-f-deficiency-aggravates-the-demyelination-in-a-cuprizone-model
#9
Junjie Liang, Ning Li, Yanli Zhang, Changyi Hou, Xiaohan Yang, Takahiro Shimizu, Xiaoyu Wang, Kazuhiro Ikenaka, Kai Fan, Jianmei Ma
[This corrects the article on p. 152 in vol. 9, PMID: 28066178.].
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29627579/genetic-detection-of-sonic-hedgehog-shh-expression-and-cellular-response-in-the-progression-of-acute-through-chronic-demyelination-and-remyelination
#10
Maria A Sanchez, Genevieve M Sullivan, Regina C Armstrong
Multiple sclerosis is a demyelinating disease in which neurological deficits result from damage to myelin, axons, and neuron cell bodies. Prolonged or repeated episodes of demyelination impair remyelination. We hypothesized that augmenting Sonic hedgehog (Shh) signaling in chronically demyelinated lesions could enhance oligodendrogenesis and remyelination. Shh regulates oligodendrocyte development during postnatal myelination, and maintains adult neural stem cells. We used genetic approaches to detect Shh expression and Shh responding cells in vivo...
April 6, 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/29627379/the-antipsychotic-drug-quetiapine-stimulates-oligodendrocyte-differentiation-by-modulating-the-cell-cycle
#11
Guiyun Mi, Yituo Wang, Enmao Ye, Yunyun Gao, Qiaowei Liu, Pinhong Chen, Yuyang Zhu, Hongju Yang, Zheng Yang
Recent studies have revealed that oligodendrocyte differentiation deficits and de-myelination occur in the brains of schizophrenic patients. Cell cycle proteins play a critical role in modulating oligodendrocyte proliferation and differentiation. In our previous studies, we found that cuprizone, a copper chelant, induces oligodendrocyte loss and demyelination, and this effect can be alleviated by using the atypical antipsychotic drug quetiapine. To explore the mechanisms of quetiapine in oligodendrocyte development, we examined the effects of quetiapine on cell cycle progression...
April 5, 2018: Neurochemistry International
https://www.readbyqxmd.com/read/29623914/heterozygous-carriers-of-galactocerebrosidase-mutations-that-cause-krabbe-disease-have-impaired-microglial-function-and-defective-repair-of-myelin-damage
#12
REVIEW
Nicole J Scott-Hewitt, Christopher J Folts, Mark D Noble
This review addresses two puzzling findings related to mutations in galactocerebrosidase (GALC) that cause Krabbe disease (KD), a severe lysosomal storage disorder characterized by extensive myelin damage in children with mutations in both GALC alleles. First, heterozygous carriers of KD-causing mutations, which include the biological parents of children with KD, exhibit increased risk for developing other diseases. Second, variants in the GALC locus increase the risk of developing multiple sclerosis (MS), another disease characterized by extensive myelin damage...
March 2018: Neural Regeneration Research
https://www.readbyqxmd.com/read/29606615/promoting-myelin-repair-through-in-vivo-neuroblast-reprogramming
#13
Bilal El Waly, Myriam Cayre, Pascale Durbec
Demyelination is frequently observed in a variety of CNS insults and neurodegenerative diseases. In rodents, adult neural stem cells can generate oligodendrocytes and participate to myelin repair. However, these cells mainly produce migratory neuroblasts that differentiate in the olfactory bulb. Here, we show that, in the demyelination context, a small subset of these neuroblasts can spontaneously convert into myelinating oligodendrocytes. Furthermore, we demonstrate that the contribution of neuroblasts to myelin repair can be improved by in vivo forced expression of two transcription factors: OLIG2 and SOX10...
March 27, 2018: Stem Cell Reports
https://www.readbyqxmd.com/read/29593734/experimental-demyelination-and-axonal-loss-are-reduced-in-microrna-146a-deficient-mice
#14
Nellie A Martin, Viktor Molnar, Gabor T Szilagyi, Maria L Elkjaer, Arkadiusz Nawrocki, Justyna Okarmus, Agnieszka Wlodarczyk, Eva K Thygesen, Miklos Palkovits, Ferenc Gallyas, Martin R Larsen, Hans Lassmann, Eirikur Benedikz, Trevor Owens, Asa F Svenningsen, Zsolt Illes
Background: The cuprizone (CPZ) model of multiple sclerosis (MS) was used to identify microRNAs (miRNAs) related to in vivo de- and remyelination. We further investigated the role of miR-146a in miR-146a-deficient (KO) mice: this miRNA is differentially expressed in MS lesions and promotes differentiation of oligodendrocyte precursor cells (OPCs) during remyelination, but its role has not been examined during demyelination. Methods: MicroRNAs were examined by Agilent Mouse miRNA Microarray in the corpus callosum during CPZ-induced demyelination and remyelination...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29574981/phosphatidylcholine-36-1-concentration-decreases-along-with-demyelination-in-the-cuprizone-animal-model-and-post-mortem-of-multiple-sclerosis-brain-tissue
#15
Marc-Olivier Trépanier, Kayla D Hildebrand, Stella D Nyamoya, Sandra Amor, Richard P Bazinet, Markus Kipp
Multiple sclerosis (MS) is a demyelinating and inflammatory disease. Myelin is enriched in lipids, and more specifically, oleic acid. The goal of this study was to evaluate the concentration of oleic acid following demyelination and remyelination in the cuprizone model, test if these changes occurred in specific lipid species, and whether differences in the cuprizone model correlate with changes observed in post-mortem human brains. Eight-week-old C57Bl/6 mice were fed a 0.2% cuprizone diet for 5 weeks and some animals allowed to recover for 11 days...
March 25, 2018: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29498007/erythropoietin-upregulates-brain-hemoglobin-expression-and-supports-neuronal-mitochondrial-activity
#16
N K Singhal, K Alkhayer, J Shelestak, R Clements, E Freeman, J McDonough
Multiple sclerosis (MS) is a neuro-inflammatory and demyelinating disease. Downregulation of neuronal mitochondrial gene expression and activity have been reported in several studies of MS. We have previously shown that hemoglobin-β (Hbb) signals to the nucleus of neurons and upregulates H3K4me3, a histone mark involved in regulating cellular metabolism and differentiation. The present study was undertaken to evaluate the effect of erythropoietin (EPO) on the upregulation of hemoglobin and mitochondrial-associated neuroprotection...
March 1, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29464444/cuprizone-administration-alters-the-iron-metabolism-in-the-mouse-model-of-multiple-sclerosis
#17
E Varga, E Pandur, H Abrahám, A Horváth, P Ács, S Komoly, A Miseta, K Sipos
Cuprizone (CZ) is a widely used copper chelating agent to develop non-autoimmune animal model of multiple sclerosis, characterized by demyelination of the corpus callosum (CC) and other brain regions. The exact mechanisms of CZ action are still arguable, but it seems that the only affected cells are the mature oligodendrocytes, possibly via metabolic disturbances caused by copper deficiency. During the pathogenesis of multiple sclerosis, high amount of deposited iron can be found throughout the demyelinated areas of the brain in the form of extracellular iron deposits and intracellularly accumulated iron in microglia...
February 20, 2018: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/29460173/changes-in-the-axo-glial-junctions-of-the-optic-nerves-of-cuprizone-treated-mice
#18
Wataru Kojima, Kensuke Hayashi
Demyelination induced by cuprizone in mice has served a useful model system for the study of demyelinating diseases, such as multiple sclerosis. Severity of demyelination by cuprizone, however, varies across different regions of the central nervous system; the corpus callosum is sensitive, while the optic nerves are resistant. Here, we investigated the effects of cuprizone on optic nerves, focusing on the axo-glial junctions. Immunostaining for sodium channels, contactin-associated protein, neurofascins, and potassium channels revealed that there were no massive changes in the density and morphology of the axo-glial junctions in cuprizone-treated optic nerves...
February 19, 2018: Histochemistry and Cell Biology
https://www.readbyqxmd.com/read/29448957/brain-region-specific-enhancement-of-remyelination-and-prevention-of-demyelination-by-the-csf1r-kinase-inhibitor-blz945
#19
Nicolau Beckmann, Elisa Giorgetti, Anna Neuhaus, Stefan Zurbruegg, Nathalie Accart, Paul Smith, Julien Perdoux, Ludovic Perrot, Mark Nash, Sandrine Desrayaud, Peter Wipfli, Wilfried Frieauff, Derya R Shimshek
Multiple sclerosis (MS) is a chronic inflammatory disease affecting the central nervous system (CNS). While multiple effective immunomodulatory therapies for MS exist today, they lack the scope of promoting CNS repair, in particular remyelination. Microglia play a pivotal role in regulating myelination processes, and the colony-stimulating factor 1 (CSF-1) pathway is a key regulator for microglia differentiation and survival. Here, we investigated the effects of the CSF-1 receptor kinase inhibitor, BLZ945, on central myelination processes in the 5-week murine cuprizone model by non-invasive and longitudinal magnetic resonance imaging (MRI) and histology...
February 15, 2018: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/29424466/differential-local-tissue-permissiveness-influences-the-final-fate-of-gpr17-expressing-oligodendrocyte-precursors-in-two-distinct-models-of-demyelination
#20
Giusy T Coppolino, Davide Marangon, Camilla Negri, Gianluca Menichetti, Marta Fumagalli, Paolo Gelosa, Leda Dimou, Roberto Furlan, Davide Lecca, Maria P Abbracchio
Promoting remyelination is recognized as a novel strategy to foster repair in neurodegenerative demyelinating diseases, such as multiple sclerosis. In this respect, the receptor GPR17, recently emerged as a new target for remyelination, is expressed by early oligodendrocyte precursors (OPCs) and after a certain differentiation stage it has to be downregulated to allow progression to mature myelinating oligodendrocytes. Here, we took advantage of the first inducible GPR17 reporter mouse line (GPR17-iCreERT2 xCAG-eGFP mice) allowing to follow the final fate of GPR17+ cells by tamoxifen-induced GFP-labeling to unveil the destiny of these cells in two demyelination models: experimental autoimmune encephalomyelitis (EAE), characterized by marked immune cell activation and inflammation, and cuprizone induced demyelination, where myelin dysfunction is achieved by a toxic insult...
May 2018: Glia
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