subject:(Cuprizone)

Victoria University of Wellington

1. Templeton, Nicola. The effect of clozapine and MIS416 on demyelination, remyelination and immunomodulation in the murine cuprizone model.

Degree: 2017, Victoria University of Wellington

URL: http://hdl.handle.net/10063/6439

► Multiple Sclerosis (MS) is a disorder of the central nervous system that affects approximately 2.5 million people worldwide. Due to the heterogeneous nature of the… (more)

▼ Multiple Sclerosis (MS) is a disorder of the central nervous system that affects approximately 2.5 million people worldwide. Due to the heterogeneous nature of the disease, and the want of an identified cause, treatment of MS remains difficult. Treatments are available, however these are limited in efficacy and are not suitable for all forms of MS. Disease pathology is characterised by the formation of demyelinating lesions in the central nervous system (CNS) which lead to cognitive and motor impairments associated with the disease. These CNS lesions can be classified as those with immune cell involvement or those without immune cell infiltrate, which are more commonly seen in progressive forms of MS, and currently, there are no treatments available for progressive MS. Due to the limited options available for treating progressive MS, this thesis aims to identify the therapeutic effect provided by the immunomodulatory compounds, MIS416 and clozapine, in a non-immune mediated model of MS, which is believed to more closely resemble progressive disease. Both of these compounds have been shown previously to reduce disease burden in an immune-driven animal model of MS. To investigate the effect of immune-modulating therapies on lesions without immune cell infiltrate, the cuprizone model of non-immune demyelination was used. In summary, the work presented in this thesis found that treatment with MIS416 and clozapine led to improved performance on behavioural assays, although neither agent inhibited cuprizone-induced demyelination or enhanced remyelination. The cellular mechanism behind the observed behavioural improvement is yet to be confirmed. MIS416 was able to maintain its previously identified immunomodulatory properties when administered in this novel setting. Moreover, novel changes to serum growth factors were identified that could provide unexpected benefit to MS patients administered MIS416. In addition to reversing cuprizone-induced behavioural deficits, clozapine reduced LPS-driven inflammatory cytokine production by microglia, indicating that clozapine has the ability to directly reduce inflammation, which may benefit progressive MS patients. Protective effects provided by either of these compounds could aid in the development of unique combination therapies to target both the inflammatory immune component and the cellular components seen at different stages of MS. MIS416 induced changes to serum cytokines and growth factors in the periphery could be harnessed to treat not just MS but other auto-immune diseases characterised by a similar cytokine profile. Advisors/Committee Members: La Flamme, Anne, Kivell, Bronwyn.

Subjects/Keywords: Multiple sclerosis; Cuprizone; Clozapine; Myelin

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APA (6^th Edition):

Templeton, N. (2017). The effect of clozapine and MIS416 on demyelination, remyelination and immunomodulation in the murine cuprizone model. (Doctoral Dissertation). Victoria University of Wellington. Retrieved from http://hdl.handle.net/10063/6439

Chicago Manual of Style (16^th Edition):

Templeton, Nicola. “The effect of clozapine and MIS416 on demyelination, remyelination and immunomodulation in the murine cuprizone model.” 2017. Doctoral Dissertation, Victoria University of Wellington. Accessed February 28, 2021. http://hdl.handle.net/10063/6439.

MLA Handbook (7^th Edition):

Templeton, Nicola. “The effect of clozapine and MIS416 on demyelination, remyelination and immunomodulation in the murine cuprizone model.” 2017. Web. 28 Feb 2021.

Vancouver:

Templeton N. The effect of clozapine and MIS416 on demyelination, remyelination and immunomodulation in the murine cuprizone model. [Internet] [Doctoral dissertation]. Victoria University of Wellington; 2017. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/10063/6439.

Council of Science Editors:

Templeton N. The effect of clozapine and MIS416 on demyelination, remyelination and immunomodulation in the murine cuprizone model. [Doctoral Dissertation]. Victoria University of Wellington; 2017. Available from: http://hdl.handle.net/10063/6439

University of Rochester

2. Szymaniak, Brittany M. Loss of ATM Induces Glial Cell Dysfunction in a Novel Murine Model of Ataxia-telangiectasia.

Degree: PhD, 2016, University of Rochester

URL: http://hdl.handle.net/1802/31655

► Ataxia-telangiectasia (A-T) is a rare, recessive, pediatric disorder that is primarily characterized by cerebellar degeneration of Purkinje neurons and results from mutations in the Ataxia-telangiectasia… (more)

▼ Ataxia-telangiectasia (A-T) is a rare, recessive, pediatric disorder that is primarily characterized by cerebellar degeneration of Purkinje neurons and results from mutations in the Ataxia-telangiectasia Mutated (ATM) gene. Patients exhibit extreme sensitivity to ionizing radiation, immunodeficiency, an increased risk for malignancy, and increased oxidative stress. In order to study the effects of true loss of ATM, our lab has generated an inducible A-T mouse model, AtmMmpl, with a novel N-terminal mutation. The mutant mice show decreased levels of peripheral T and B cell populations, have a low incidence of thymic lymphoma, and do not show evidence of increased oxidative stress. Our analyses of these phenotypes in two different strains of AtmAwb mice indicate that the background genetics may play a role in modulating the disease manifestation. Despite a mild motor phenotype, the development and morphology of the cerebellum is normal, with no overt change in Purkinje cell number or morphology. Analysis of other critical cell types within the cerebellum also did not reveal any significant changes. Preliminary RNAseq analysis suggests that there may be compensatory mechanisms employed by our mice that protect against the consequences of loss of ATM. However, we found evidence of a cortical white matter defect in our year old mice, which is reminiscent of reports in A-T patients. In order to test if the loss of ATM results in an underlying defect that would be exacerbated upon an insult, we exposed our murine model to cuprizone, a common model for studying demyelination. We hypothesized that the loss of ATM in the glial cell populations, such as the oligodendrocytes and oligodendrocyte precursor cells, would make them more vulnerable and less capable of responding to a neurotoxic insult. We found that the A-T mutant mice are more sensitive to cuprizone-induced demyelination, showing increased oligodendrocyte cell death, and have an increased inflammatory environment following treatment, but are capable of repair. These data demonstrate that there is a novel glial cell dysfunction that is induced by the loss of ATM.

Subjects/Keywords: ATM; Mouse model; Ataxia-telangiectasia; Cuprizone

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APA (6^th Edition):

Szymaniak, B. M. (2016). Loss of ATM Induces Glial Cell Dysfunction in a Novel Murine Model of Ataxia-telangiectasia. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/31655

Chicago Manual of Style (16^th Edition):

Szymaniak, Brittany M. “Loss of ATM Induces Glial Cell Dysfunction in a Novel Murine Model of Ataxia-telangiectasia.” 2016. Doctoral Dissertation, University of Rochester. Accessed February 28, 2021. http://hdl.handle.net/1802/31655.

MLA Handbook (7^th Edition):

Szymaniak, Brittany M. “Loss of ATM Induces Glial Cell Dysfunction in a Novel Murine Model of Ataxia-telangiectasia.” 2016. Web. 28 Feb 2021.

Vancouver:

Szymaniak BM. Loss of ATM Induces Glial Cell Dysfunction in a Novel Murine Model of Ataxia-telangiectasia. [Internet] [Doctoral dissertation]. University of Rochester; 2016. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1802/31655.

Council of Science Editors:

Szymaniak BM. Loss of ATM Induces Glial Cell Dysfunction in a Novel Murine Model of Ataxia-telangiectasia. [Doctoral Dissertation]. University of Rochester; 2016. Available from: http://hdl.handle.net/1802/31655

University of Saskatchewan

3. Mooshekhian, Ali 1979-. Effects of Low Field Magnetic Stimulation on.

Degree: 2019, University of Saskatchewan

URL: http://hdl.handle.net/10388/13084

► Cognitive impairment (CI) is a leading cause of disability in patients with Multiple Sclerosis (MS). Although CI has catastrophic effects on patients’ quality of life,… (more)

▼ Cognitive impairment (CI) is a leading cause of disability in patients with Multiple Sclerosis (MS). Although CI has catastrophic effects on patients’ quality of life, there is no approved treatment for it. Low Field Magnetic Stimulation (LFMS) is a novel non-invasive brain stimulation technique that has promising benefits in improving mood and cognitive function in animal studies of traumatic brain injury, major depressive disorder and Alzheimer’s disease, suggesting a transtherapeutic cognitive benefit among different neuropsychiatric disorders. In this study, we hypothesized that LFMS can alleviate demyelination-related cognitive deficits in a cuprizone (CPZ) mouse model of MS. CPZ is a copper chelator widely used to generate brain demyelination. Feeding CPZ to young adult mice for six weeks generates diffuse demyelinating lesions in both gray matter and white matter areas, predominantly in the prefrontal cortex, hippocampus and corpus callosum. One-hundred and twenty mice were divided into four groups (30 mice/group) and received CPZ (no, yes) and LFMS (no, yes) for up to 6 weeks, respectively. Behavioral tests including open-field test (OFT), Y-maze test and forced swim test (FST) were done after 3 and 6 weeks of treatment. Half of the mice from each group were euthanized at each time point, followed by brain immunobiology and Western blots. The study showed that CPZ treatment caused significant working memory, short term memory and learning deficits, which were prevented with LFMS co-administration. The OFT and Y-maze test did not reveal motor function impairment in demyelinated mice. LFMS treatment also decreased the severity of demyelination in both frontal cortex and hippocampus. LFMS may exert its protective effects through modulating the expression of Transforming ii i Growth Factor Beta-1 (TGF-β1), a target for an investigational intervention under clinical trials for MS. TGF-β1 is a critical cytokine for neurogenesis and inflammation. The results suggest the therapeutic potential of LFMS for cognitive remediation in MS patients. In addition, it provides a non-invasive and affordable approach to increase TGF-β1 in the brain for neuroprotection and neurogenesis. Advisors/Committee Members: Zhang, Yanbo, Cayabyab, Francisco, Taghibiglou, Changiz, Levin, Michael.

Subjects/Keywords: Demyelination; Multiple Sclerosis; Cuprizone; Cognitive deficit

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APA (6^th Edition):

Mooshekhian, A. 1. (2019). Effects of Low Field Magnetic Stimulation on. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/13084

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Mooshekhian, Ali 1979-. “Effects of Low Field Magnetic Stimulation on.” 2019. Thesis, University of Saskatchewan. Accessed February 28, 2021. http://hdl.handle.net/10388/13084.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Mooshekhian, Ali 1979-. “Effects of Low Field Magnetic Stimulation on.” 2019. Web. 28 Feb 2021.

Vancouver:

Mooshekhian A1. Effects of Low Field Magnetic Stimulation on. [Internet] [Thesis]. University of Saskatchewan; 2019. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/10388/13084.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Mooshekhian A1. Effects of Low Field Magnetic Stimulation on. [Thesis]. University of Saskatchewan; 2019. Available from: http://hdl.handle.net/10388/13084

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Manitoba

4. Palmer, Vanessa Leanne. Understanding white matter pathology through correlating longitudinal and quantitative MRI metrics weekly in the cuprizone mouse model of demyelination.

Degree: Biomedical Engineering, 2016, University of Manitoba

URL: http://hdl.handle.net/1993/31207

► Magnetic resonance imaging (MRI) methods thought to assess myelin and axon integrity are improving the understanding of white matter diseases like multiple sclerosis (MS). This… (more)

Subjects/Keywords: MRI; Electron Microscopy; Cuprizone mouse model; White matter

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APA (6^th Edition):

Palmer, V. L. (2016). Understanding white matter pathology through correlating longitudinal and quantitative MRI metrics weekly in the cuprizone mouse model of demyelination. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/31207

Chicago Manual of Style (16^th Edition):

Palmer, Vanessa Leanne. “Understanding white matter pathology through correlating longitudinal and quantitative MRI metrics weekly in the cuprizone mouse model of demyelination.” 2016. Masters Thesis, University of Manitoba. Accessed February 28, 2021. http://hdl.handle.net/1993/31207.

MLA Handbook (7^th Edition):

Palmer, Vanessa Leanne. “Understanding white matter pathology through correlating longitudinal and quantitative MRI metrics weekly in the cuprizone mouse model of demyelination.” 2016. Web. 28 Feb 2021.

Vancouver:

Palmer VL. Understanding white matter pathology through correlating longitudinal and quantitative MRI metrics weekly in the cuprizone mouse model of demyelination. [Internet] [Masters thesis]. University of Manitoba; 2016. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1993/31207.

Council of Science Editors:

Palmer VL. Understanding white matter pathology through correlating longitudinal and quantitative MRI metrics weekly in the cuprizone mouse model of demyelination. [Masters Thesis]. University of Manitoba; 2016. Available from: http://hdl.handle.net/1993/31207

University of Melbourne

5. Xing, Yao Lulu. Investigation of the relative contribution of neural precursor cells and oligodendrocyte progenitor cells to myelin repair.

Degree: 2015, University of Melbourne

URL: http://hdl.handle.net/11343/59457

► Remyelination following demyelination of the central nervous system is mediated via the generation of new myelin-forming oligodendrocytes. It has been demonstrated that both parenchymal oligodendrocyte… (more)

▼ Remyelination following demyelination of the central nervous system is mediated via the generation of new myelin-forming oligodendrocytes. It has been demonstrated that both parenchymal oligodendrocyte progenitor cells (OPCs) and neural precursor cells (NPCs) that reside in the adult subventricular zone (SVZ) contribute to oligodendrocyte regeneration. However, the relative contribution of each progenitor cell population to oligodendrogenesis and remyelination of demyelinated lesions remains unknown. I have used an in vivo genetic fate-mapping approach to assess the spatiotemporal dynamics of oligodendrogenesis and remyelination by OPCs and NPCs within the corpus callosi (CC) of mice subjected to cuprizone-induced demyelination. Nestin-CreERT2 and Pdgfra-CreERT2 mice were crossed with fluorescent Cre reporter strains to map the fate of NPCs and OPCs, respectively. In cuprizone-challenged mice, substantial numbers of NPCs migrated into the demyelinated CC and the vast majority of cells differentiated into mature oligodendrocytes. This capacity was most prominent in the rostral regions adjacent to the SVZ where NPC-derived oligodendrocytes outnumbered those generated from OPCs. OPC-derived oligodendrocytes at recovery were distributed in a converse manner to NPC-derived cells. Sixty-two percent of all nodes of Ranvier adjacent to the SVZ were flanked by at least one paranode myelinated by an NPC-derived oligodendrocyte, which contributed to the formation of nodal clusters of Nav1.6 channels despite diffused localisation of paranodal Caspr proteins. An extended analysis of morphological characteristics of the newly-synthesised myelin generated by each progenitor cell population has demonstrated that NPC-derived oligodendrocytes elaborated many more, shorter myelin internodes than OPC-derived counterparts. Compared to unchallenged controls, g-ratios of myelinated fibers in regions adjacent to the SVZ were equivalent. Importantly, fate-mapping followed by immunoelectron microscopy provided definitive evidence that NPC-derived myelin was substantially thicker than that generated by parenchymal OPCs and was indistinguishable from normal healthy myelin. Immunohistochemical analysis also revealed that NPC-mediated oligodendrogenesis was associated with a higher proportion of immature oligodendrocytes exhibiting phospho-Erk1/2 and phospho-Akt signalling activity, which are known to positively regulate myelin thickness during postnatal development. This finding raises the possibility that enhanced Erk1/2 and Akt signaling in oligodendrogenic NPCs could endow these cells with the capacity to regenerate myelin of normal thickness. In addition, I have developed a novel transgenic mouse model of conditional OPC ablation for future studies of NPC function after demyelination. To achieve this, I crossed Pdgfra-CreERT2 mice with a Cre-conditional cell ablation line called Sox10-lox-GFP-STOP-lox-DTA (denoted Sox10-DTA). Administration of tamoxifen to double heterozygous mice induced the expression of diphtheria toxin fragment A…

Subjects/Keywords: neural precursor cells; oligodendrocyte progenitor cells; remyelination; multiple sclerosis; cuprizone

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Xing, Y. L. (2015). Investigation of the relative contribution of neural precursor cells and oligodendrocyte progenitor cells to myelin repair. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/59457

Chicago Manual of Style (16^th Edition):

Xing, Yao Lulu. “Investigation of the relative contribution of neural precursor cells and oligodendrocyte progenitor cells to myelin repair.” 2015. Doctoral Dissertation, University of Melbourne. Accessed February 28, 2021. http://hdl.handle.net/11343/59457.

MLA Handbook (7^th Edition):

Xing, Yao Lulu. “Investigation of the relative contribution of neural precursor cells and oligodendrocyte progenitor cells to myelin repair.” 2015. Web. 28 Feb 2021.

Vancouver:

Xing YL. Investigation of the relative contribution of neural precursor cells and oligodendrocyte progenitor cells to myelin repair. [Internet] [Doctoral dissertation]. University of Melbourne; 2015. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/11343/59457.

Council of Science Editors:

Xing YL. Investigation of the relative contribution of neural precursor cells and oligodendrocyte progenitor cells to myelin repair. [Doctoral Dissertation]. University of Melbourne; 2015. Available from: http://hdl.handle.net/11343/59457

Kent State University

6. Shelestak, John Wesley. EVALUATION OF BLOOD-BRAIN BARRIER INTEGRITY UNDER CUPRIZONE ADMINISTRATION.

Degree: PhD, College of Arts and Sciences / School of Biomedical Sciences, 2019, Kent State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=kent1574351981114558

► The blood-brain barrier is an extremely important protective mechanism for the central nervous system. The blood-brain barrier is often damaged in neurodegenerative diseases and understanding… (more)

▼ The blood-brain barrier is an extremely important protective mechanism for the central nervous system. The blood-brain barrier is often damaged in neurodegenerative diseases and understanding how the damage occurs is vital to understanding disease progression and for the development of new therapies. The cuprizone model of toxic demyelination is a common animal model used to study the effects of demyelination and remyelination in mice. It is a useful model because the demyelination is not caused by autoimmune assault, as is the case in many models. However, historically, the cuprizone model was believed to demyelination the brain without damage to the blood-brain barrier. This study sought to examine blood-brain barrier integrity throughout the administration of cuprizone to determine if blood-brain barrier disintegration occurs and at what time during administration. Mice were fed a 0.3% diet of cuprizone and timepoints across six weeks were analyzed for changes in blood-brain barrier permeability, changes in blood-brain barrier proteins, and immune activation of cell populations known to affect blood-brain barrier permeability. Blood-brain barrier hyperpermeability was observed to be highest early under cuprizone administration three days after beginning treatment. This permeability coincided with changes to tight junction protein expression as well as mast cell activation. It preceded, however, immune activation of CNS astrocytes and microglia as well as measurable changes in myelination. These findings indicate that the blood-brain barrier is affected by cuprizone administration and the timing of this effect coincides with mast cell activation and degranulation. This provides new timepoints at which to investigate early changes during cuprizone administration as well as new targets for treatment to prevent not only blood-brain barrier alterations, but also potentially the progression of the demyelination seen under cuprizone administration. Advisors/Committee Members: Clements, Robert (Advisor).

Subjects/Keywords: Biology; Biomedical Research; Neurobiology; Blood-Brain Barrier; Cuprizone; Demyelination; Neurodegeneration; Neuroimmunology

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APA (6^th Edition):

Shelestak, J. W. (2019). EVALUATION OF BLOOD-BRAIN BARRIER INTEGRITY UNDER CUPRIZONE ADMINISTRATION. (Doctoral Dissertation). Kent State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=kent1574351981114558

Chicago Manual of Style (16^th Edition):

Shelestak, John Wesley. “EVALUATION OF BLOOD-BRAIN BARRIER INTEGRITY UNDER CUPRIZONE ADMINISTRATION.” 2019. Doctoral Dissertation, Kent State University. Accessed February 28, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=kent1574351981114558.

MLA Handbook (7^th Edition):

Shelestak, John Wesley. “EVALUATION OF BLOOD-BRAIN BARRIER INTEGRITY UNDER CUPRIZONE ADMINISTRATION.” 2019. Web. 28 Feb 2021.

Vancouver:

Shelestak JW. EVALUATION OF BLOOD-BRAIN BARRIER INTEGRITY UNDER CUPRIZONE ADMINISTRATION. [Internet] [Doctoral dissertation]. Kent State University; 2019. [cited 2021 Feb 28]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=kent1574351981114558.

Council of Science Editors:

Shelestak JW. EVALUATION OF BLOOD-BRAIN BARRIER INTEGRITY UNDER CUPRIZONE ADMINISTRATION. [Doctoral Dissertation]. Kent State University; 2019. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=kent1574351981114558

7. Prevost, Valentin. Validation du transfert d'aimantation inhomogène (ihMT) comme nouveau biomarqueur IRM de la myéline : Validation of inhomogeneous magnetization transfer (ihMT) as a new MRI myelin biomarker.

Degree: Docteur es, Neurosciences, 2018, Aix Marseille Université

URL: http://www.theses.fr/2018AIXM0037

►

L’imagerie par résonance magnétique (IRM) est une technique d’imagerie médicale largement utilisée pour son caractère non-invasif et pour sa capacité à explorer les tissus mous.… (more)

▼

L’imagerie par résonance magnétique (IRM) est une technique d’imagerie médicale largement utilisée pour son caractère non-invasif et pour sa capacité à explorer les tissus mous. Des techniques IRM avancées et innovantes ont été développées de manière à améliorer la spécificité du signal des techniques conventionnelles et ainsi accéder à de nouvelles informations. Un axe de recherche particulièrement important en IRM concerne la possibilité d’accéder in vivo à des informations sur la myéline. Cette dernière est un constituant majeur du système nerveux central qui assure la bonne conduction nerveuse. Sa dégradation est l’une des caractéristiques de la sclérose en plaques, qui est la première cause de handicap sévère non traumatique chez le jeune adulte. Imager la myéline par IRM demeure néanmoins un challenge du fait du temps de relaxation T2 très court des protons la constituant. Le transfert d’aimantation inhomogène (ihMT) est une technique récemment découverte qui permet d’isoler le signal de composantes macromoléculaires grâce à leurs propriétés de relaxation dipolaire, caractérisées par la constante T1D. L’objectif de ce travail de thèse a concerné la validation de la technique ihMT comme biomarqueur de la myéline et l’évaluation de la spécificité du signal pour la myéline, sur des modèles murins (souris).

Magnetic resonance imaging (MRI) is a non-invasive medical imaging technique, widely used to explore soft tissues. Advanced and innovated MRI techniques have been developed to improve the specificity of conventional MR sequences thus allowing accessing new information. A particularly important research topic concerns the ability to in vivo access myelin information. Myelin is a major component of the central nervous system responsible for a good nerve conduction. Myelin alteration occurs in multiple sclerosis, one of the main cause for young adult permanent disability. However, myelin MRI is challenged by the very short relaxation time, T2, of myelin protons. Inhomogeneous magnetization transfer (ihMT) is a recent technique, which allows assessing macromolecular tissue component by exploiting their dipolar order relaxation properties, characterized by the time constant T1D. The objective of this thesis concerned the validation of ihMT as a myelin biomarker and the evaluation of the specificity of ihMT for myelin on mouse models.

Advisors/Committee Members: Duhamel, Guillaume (thesis director), Alsop, David (thesis director).

Subjects/Keywords: Imagerie; Irm; Myéline; IhMT; Transfert d'aimantation; Inhomogène; Modèle; Cuprizone; Validation; Biomarqueur; Imaging; Mri; Myelin; IhMT; Magnetization transfer; Inhomogeneous; Model; Cuprizone; Validation; Biomarker

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Prevost, V. (2018). Validation du transfert d'aimantation inhomogène (ihMT) comme nouveau biomarqueur IRM de la myéline : Validation of inhomogeneous magnetization transfer (ihMT) as a new MRI myelin biomarker. (Doctoral Dissertation). Aix Marseille Université. Retrieved from http://www.theses.fr/2018AIXM0037

Chicago Manual of Style (16^th Edition):

Prevost, Valentin. “Validation du transfert d'aimantation inhomogène (ihMT) comme nouveau biomarqueur IRM de la myéline : Validation of inhomogeneous magnetization transfer (ihMT) as a new MRI myelin biomarker.” 2018. Doctoral Dissertation, Aix Marseille Université. Accessed February 28, 2021. http://www.theses.fr/2018AIXM0037.

MLA Handbook (7^th Edition):

Prevost, Valentin. “Validation du transfert d'aimantation inhomogène (ihMT) comme nouveau biomarqueur IRM de la myéline : Validation of inhomogeneous magnetization transfer (ihMT) as a new MRI myelin biomarker.” 2018. Web. 28 Feb 2021.

Vancouver:

Prevost V. Validation du transfert d'aimantation inhomogène (ihMT) comme nouveau biomarqueur IRM de la myéline : Validation of inhomogeneous magnetization transfer (ihMT) as a new MRI myelin biomarker. [Internet] [Doctoral dissertation]. Aix Marseille Université 2018. [cited 2021 Feb 28]. Available from: http://www.theses.fr/2018AIXM0037.

Council of Science Editors:

Prevost V. Validation du transfert d'aimantation inhomogène (ihMT) comme nouveau biomarqueur IRM de la myéline : Validation of inhomogeneous magnetization transfer (ihMT) as a new MRI myelin biomarker. [Doctoral Dissertation]. Aix Marseille Université 2018. Available from: http://www.theses.fr/2018AIXM0037

8. Becquet, Laurine. Evaluation des effets thérapeutiques de neuropeptides contre la sclérose en plaques : les orexines, le vasoactive intestinal peptide, le pituitary adenylate cyclase-activating polypeptide et leurs analogues : Therapeutic effects of VIP, PACAP, orexins and their analogs in experimental models of multiple sclerosis.

Degree: Docteur es, Sciences de la vie et de la sante, 2018, Normandie

URL: http://www.theses.fr/2018NORMR071

► La sclérose en plaques (SEP) est une maladie autoimmune inflammatoire et neurodégénérative du système nerveux central (SNC) chez le jeune adulte résultant d’une altération ciblée… (more)

▼ La sclérose en plaques (SEP) est une maladie autoimmune inflammatoire et neurodégénérative du système nerveux central (SNC) chez le jeune adulte résultant d’une altération ciblée de la myéline. Les premiers symptômes de la SEP sont une détérioration cognitive, des vertiges, des douleurs, de la fatigue et une perte de la vision. En condition physiologique, les axones des neurones sont entourés par une gaine de myéline synthétisée par les oligodendrocytes permettant d’accélérer la vitesse de conduction des influx nerveux et de prévenir la mort neuronale. Le modèle expérimental le plus utilisé dans l’étude des mécanismes de la SEP est le modèle de l’encéphalomyélite autoimmune expérimentale (EAE). Après une immunisation contre la glycoprotéine oligodendrocytaire de la myéline 35-55 (MOG35-55), les lymphocytes T Cluster of differentiation (CD)4+ helper (Th)1 et Th17 auto-réactifs induisent une réponse inflammatoire aiguë à la périphérie puis migrent dans le SNC. Ils provoquent alors une réponse inflammatoire dirigée contre la myéline, avec l’intervention descellules myéloïdes. Cela aboutit à la destruction des gaines de myéline diminuant la vitesse de conduction des influx nerveux et une perte axonale, responsables des symptômes mentionnés précédemment. A l’heure actuelle, les traitements contre la SEP peuvent ralentir la progression de la paralysie et diminuer la sévérité ainsi que l’incidence des symptômes diminuant l’inflammation. En revanche, ils n’ont pas d’effets sur les formes progressives de la maladie au cours desquellesles processus neurodégénératifs s’amplifient et dominent ceux de l’inflammation. Il est donc nécessaire de trouver de nouvelles thérapies qui pourront à la fois bloquer l’inflammation et promouvoir la remyélinisation et la neurorégénération. Dans cette optique, de nouvelles cibles thérapeutiques ont émergé pour traiter la SEP : le Vasoactive Intestinal Peptide (VIP), le Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP), l’orexine A, leurs récepteurs ainsi queleurs analogues. En effet, ces neuropeptides présentent des activités anti-inflammatoires et neuroprotectrices. Mes travaux de thèse ont porté sur l’étude des effets d’un agoniste de VPAC2, l’un des récepteurs de VIP et PACAP, et de l’orexine A sur les processus inflammatoires et neurodégénératifs dans le modèle d’EAE ainsi que dans le modèle toxique de la cuprizone (CPZ), induisant la mort des oligodendrocytes matures et la démyélinisation indépendamment des lymphocytes T. Après une immunisation contre la MOG35-55, un traitement systémique de court durée avec BAY55-9837, un agoniste de VPAC2, diminue la sévérité de l’EAE chronique en diminuant la réponse inflammatoire à la périphérie avec une baisse de l’activation lymphocytaire, de l’activité de présentation antigénique des cellules dendritiques et des monocytes ainsi qu’une modulation de la population des lymphocytes T régulateurs. Au niveau de la moelle épinière, l’infiltration descellules immunitaires est moindre et la proportion en microglie/macrophages est plus élevée après… Advisors/Committee Members: Tan, Yossan-Var (thesis director), Boyer, Olivier (thesis director).

Subjects/Keywords: Agoniste de VPAC2; Cuprizone; Encéphalomyélite autoimmune expérimentale; Orexine A; Sclérose en plaques; Neuropeptides; Cuprizone; Experimental autoimmune encephalomyelitis; Orexin A; Multiple sclerosis; Neuropeptides; VPAC2 agonist; 615.78

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Becquet, L. (2018). Evaluation des effets thérapeutiques de neuropeptides contre la sclérose en plaques : les orexines, le vasoactive intestinal peptide, le pituitary adenylate cyclase-activating polypeptide et leurs analogues : Therapeutic effects of VIP, PACAP, orexins and their analogs in experimental models of multiple sclerosis. (Doctoral Dissertation). Normandie. Retrieved from http://www.theses.fr/2018NORMR071

Chicago Manual of Style (16^th Edition):

Becquet, Laurine. “Evaluation des effets thérapeutiques de neuropeptides contre la sclérose en plaques : les orexines, le vasoactive intestinal peptide, le pituitary adenylate cyclase-activating polypeptide et leurs analogues : Therapeutic effects of VIP, PACAP, orexins and their analogs in experimental models of multiple sclerosis.” 2018. Doctoral Dissertation, Normandie. Accessed February 28, 2021. http://www.theses.fr/2018NORMR071.

MLA Handbook (7^th Edition):

Becquet, Laurine. “Evaluation des effets thérapeutiques de neuropeptides contre la sclérose en plaques : les orexines, le vasoactive intestinal peptide, le pituitary adenylate cyclase-activating polypeptide et leurs analogues : Therapeutic effects of VIP, PACAP, orexins and their analogs in experimental models of multiple sclerosis.” 2018. Web. 28 Feb 2021.

Vancouver:

Becquet L. Evaluation des effets thérapeutiques de neuropeptides contre la sclérose en plaques : les orexines, le vasoactive intestinal peptide, le pituitary adenylate cyclase-activating polypeptide et leurs analogues : Therapeutic effects of VIP, PACAP, orexins and their analogs in experimental models of multiple sclerosis. [Internet] [Doctoral dissertation]. Normandie; 2018. [cited 2021 Feb 28]. Available from: http://www.theses.fr/2018NORMR071.

Council of Science Editors:

Becquet L. Evaluation des effets thérapeutiques de neuropeptides contre la sclérose en plaques : les orexines, le vasoactive intestinal peptide, le pituitary adenylate cyclase-activating polypeptide et leurs analogues : Therapeutic effects of VIP, PACAP, orexins and their analogs in experimental models of multiple sclerosis. [Doctoral Dissertation]. Normandie; 2018. Available from: http://www.theses.fr/2018NORMR071

UCLA

9. Kim, Youn-Jung Roy. Mechanisms of Neuroprotection and Remyelination in Demyelinating Disease Models of Multiple Sclerosis: A Lesson From Estrogen Receptor Specific Ligands.

Degree: Molec, Cell, & Integ Physiology, 2018, UCLA

URL: http://www.escholarship.org/uc/item/09j2798f

► Currently, available drugs for multiple sclerosis (MS) are predominantly immune-modulatory. They are effective in reducing relapses, but not in slowing down or stopping progressive disease… (more)

▼ Currently, available drugs for multiple sclerosis (MS) are predominantly immune-modulatory. They are effective in reducing relapses, but not in slowing down or stopping progressive disease course. Therefore, there is a need to develop treatment strategies that will provide neuroprotection and halt disability progression. Pregnancy is neuroprotective in patients with MS. A pregnancy hormone and a moderate estrogen receptor beta (ERβ)-ligand, estriol, has been reported to have beneficial effects on reducing relapses and improving cognition when treated in MS patients. Although, the mechanisms of ERβ-ligand mediated treatment effects on neuroprotection remains poorly understood. Here I hypothesized that ERβ signaling on CD11c+ immune cells and Olig1+ oligodendrocytes plays an essential role in providing neuroprotection and enhancing remyelination. To test the hypothesis, I created conditional knockout mice (CKO) with ERβ deleted from each cell type using the Cre-LoxP recombinase system and investigated neuroprotective effects of ERβ-ligand treatment in experimental autoimmune encephalomyelitis (EAE) and cuprizone diet-induced demyelinating disease models. Also, I used RiboTag mice to determine oligodendrocyte specific gene expression to understand the molecular mechanisms of remyelination. Subsequently, I studied the mechanisms of ERβ-ligand treatment effects in oligodendrocytes during remyelination. The results revealed that ERβ-ligand treatment reduced pro-inflammatory responses through ERβ on CD11c+ myeloid DC/MΦ and increased oligodendrocyte maturation through ERβ on Olig1+ oligodendrocytes during EAE. The use of CKO mice proved that both were necessary as one without the other was not sufficient. Mechanistic insights on remyelination using the RiboTag mice revealed that oligodendrocytes upregulate de novo cholesterol biosynthesis during remyelination after chronic demyelination. Furthermore, when compared to vehicle treated naturally remyelinating mice, ERβ-ligand treated mice showed enhanced remyelination by increasing oligodendrocyte maturation, increasing cholesterol synthesis pathway genes, increasing oligodendrocyte progenitor cells (OPCs), and increasing Sox2 expression in OPCs during remyelination. I extended our investigation of ERβ-ligand treatment in the cuprizone model to the EAE model, to discover that ERβ-ligand treated mice showed neuroprotection by increasing oligodendrocyte maturation, and increasing cholesterol synthesis pathway genes, but not by increasing OPC Sox2 expression. This comprehensive approach using two different demyelinating disease models of MS and two transgenic mouse models provided critical insights regarding treatment effects of ERβ-ligand on neuroprotection and remyelination in vivo.

Subjects/Keywords: Neurosciences; Physiology; Cuprizone; Estrogen Receptor Beta Ligand; Experimental Autoimmune Encephalomyelitis; Multiple Sclerosis; Myeloid cells; Oligodendrocytes

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kim, Y. R. (2018). Mechanisms of Neuroprotection and Remyelination in Demyelinating Disease Models of Multiple Sclerosis: A Lesson From Estrogen Receptor Specific Ligands. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/09j2798f

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kim, Youn-Jung Roy. “Mechanisms of Neuroprotection and Remyelination in Demyelinating Disease Models of Multiple Sclerosis: A Lesson From Estrogen Receptor Specific Ligands.” 2018. Thesis, UCLA. Accessed February 28, 2021. http://www.escholarship.org/uc/item/09j2798f.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kim, Youn-Jung Roy. “Mechanisms of Neuroprotection and Remyelination in Demyelinating Disease Models of Multiple Sclerosis: A Lesson From Estrogen Receptor Specific Ligands.” 2018. Web. 28 Feb 2021.

Vancouver:

Kim YR. Mechanisms of Neuroprotection and Remyelination in Demyelinating Disease Models of Multiple Sclerosis: A Lesson From Estrogen Receptor Specific Ligands. [Internet] [Thesis]. UCLA; 2018. [cited 2021 Feb 28]. Available from: http://www.escholarship.org/uc/item/09j2798f.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kim YR. Mechanisms of Neuroprotection and Remyelination in Demyelinating Disease Models of Multiple Sclerosis: A Lesson From Estrogen Receptor Specific Ligands. [Thesis]. UCLA; 2018. Available from: http://www.escholarship.org/uc/item/09j2798f

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

McMaster University

10. Moldovan, Nataliya. MEASUREMENT OF TRANSITION METALS IN THE RODENT BRAIN USING X-RAY FLUORESCENCE AND NEUTRON ACTIVATION ANALYSIS.

Degree: MSc, 2012, McMaster University

URL: http://hdl.handle.net/11375/12372

►

Transition metals, such as iron, manganese, and copper are essential in the development and function of biological systems. However, disrupted levels of transition metals… (more)

Subjects/Keywords: transition metal homeostasis; cuprizone; manganese enhanced MRI; manganese overexposure; demyelination; x-ray fluorescence; neutron activation analysis; Medical Biophysics; Medical Biophysics

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APA (6^th Edition):

Moldovan, N. (2012). MEASUREMENT OF TRANSITION METALS IN THE RODENT BRAIN USING X-RAY FLUORESCENCE AND NEUTRON ACTIVATION ANALYSIS. (Masters Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/12372

Chicago Manual of Style (16^th Edition):

Moldovan, Nataliya. “MEASUREMENT OF TRANSITION METALS IN THE RODENT BRAIN USING X-RAY FLUORESCENCE AND NEUTRON ACTIVATION ANALYSIS.” 2012. Masters Thesis, McMaster University. Accessed February 28, 2021. http://hdl.handle.net/11375/12372.

MLA Handbook (7^th Edition):

Moldovan, Nataliya. “MEASUREMENT OF TRANSITION METALS IN THE RODENT BRAIN USING X-RAY FLUORESCENCE AND NEUTRON ACTIVATION ANALYSIS.” 2012. Web. 28 Feb 2021.

Vancouver:

Moldovan N. MEASUREMENT OF TRANSITION METALS IN THE RODENT BRAIN USING X-RAY FLUORESCENCE AND NEUTRON ACTIVATION ANALYSIS. [Internet] [Masters thesis]. McMaster University; 2012. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/11375/12372.

Council of Science Editors:

Moldovan N. MEASUREMENT OF TRANSITION METALS IN THE RODENT BRAIN USING X-RAY FLUORESCENCE AND NEUTRON ACTIVATION ANALYSIS. [Masters Thesis]. McMaster University; 2012. Available from: http://hdl.handle.net/11375/12372

11. Zhang, Lin. The effect of galanin alone and combined with estrogen in a cuprizone-induced demyelination mouse model of multiple sclerosis.

Degree: Human Anatomy and Cell Science, 2011, University of Manitoba

URL: http://hdl.handle.net/1993/4749

► Multiple Sclerosis (MS) is an autoimmune demyelination disease of the central nervous system (CNS). The traditional immunotherapies so far have not been able to stop… (more)

Subjects/Keywords: Multiple sclerosis; galanin; estrogen; cuprizone; demyelination; remyelination

…Abbreviations 12wCPZ twelve-week cuprizone (challenge) 12wCPZ+3wR twelve-week cuprizone… …x28;challenge) plus three-week recovery 6wCPZ six-week cuprizone (challenge)… …6wCPZ+3wR six-week cuprizone (challenge) plus three-week recovery aco anterior… …callosum cing cingulum bundle CNS central nervous system CP caudoputamen CPZ cuprizone…

10 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Zhang, L. (2011). The effect of galanin alone and combined with estrogen in a cuprizone-induced demyelination mouse model of multiple sclerosis. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/4749

Chicago Manual of Style (16^th Edition):

Zhang, Lin. “The effect of galanin alone and combined with estrogen in a cuprizone-induced demyelination mouse model of multiple sclerosis.” 2011. Masters Thesis, University of Manitoba. Accessed February 28, 2021. http://hdl.handle.net/1993/4749.

MLA Handbook (7^th Edition):

Zhang, Lin. “The effect of galanin alone and combined with estrogen in a cuprizone-induced demyelination mouse model of multiple sclerosis.” 2011. Web. 28 Feb 2021.

Vancouver:

Zhang L. The effect of galanin alone and combined with estrogen in a cuprizone-induced demyelination mouse model of multiple sclerosis. [Internet] [Masters thesis]. University of Manitoba; 2011. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1993/4749.

Council of Science Editors:

Zhang L. The effect of galanin alone and combined with estrogen in a cuprizone-induced demyelination mouse model of multiple sclerosis. [Masters Thesis]. University of Manitoba; 2011. Available from: http://hdl.handle.net/1993/4749

University of Akron

12. Ray, Lucille Alexandria. Live single cell fluorescence microscopy; from antibiotic resistance detection to mitochondrial dysfunction.

Degree: PhD, Chemistry, 2020, University of Akron

URL: http://rave.ohiolink.edu/etdc/view?acc_num=akron1597342775751888

► Single-cell fluorescence microscopy is a powerful tool which can be used to investigate the nature of cellular responses to external stimuli. The application of single-cell… (more)

▼ Single-cell fluorescence microscopy is a powerful tool which can be used to investigate the nature of cellular responses to external stimuli. The application of single-cell fluorescence microscopy to the growing problem of antimicrobial susceptibility detection stands to improve and refine our ability to address bacterial resistance in human infections. In cases of severe bacterial infection, determining the correct antibiotic to use to combat an infection is a race against the patient’s dwindling lifespan. By combining the RedoxSensor™ Green fluorescent dye with live single-cell imaging, we have developed a method for antimicrobial susceptibility testing which can identify susceptibility to a given antibiotic within 100 minutes of treatment. We show that this method is reproducible and can identify susceptibility to several bacterial cell wall targets and bacterial cell membrane targeted antibiotics. Our methodology has considerable applicability within the sphere of rational antibiotic drug design as well in its ability to identify antibiotic efficacy as a function of time instead of antibiotic concentration. We use our method to compare the efficacy of 4 recently synthesized polyurethane antimicrobials. Our work lays the framework for expansion upon our method into microfluidics systems and use in screening candidate antimicrobial drugs.Mitochondrial morphological analysis within living eukaryotic cells represents another challenge which requires careful application of single-cell fluorescence microscopy. The cuprizone mouse treatment model for multiple sclerosis is known to generate enlarged mitochondria within oligodendrocytes, but much remains unknown about the dynamics of their formation. Cultured MO3.13 oligodendrocyte cells treated with cuprizone are shown to undergo mitochondrial enlargement within 8 hours of direct cuprizone exposure via single-cell mitochondrial size determination with MitoTracker Red fluorescent dye. Cuprizone treatment is also shown to increase oxygen consumption rapidly following oligodendrocyte exposure using porphyrin-based fluorescence lifetime oxygen consumption measurement. Advisors/Committee Members: Konopka, Michael (Advisor).

Subjects/Keywords: Biochemistry; Chemistry; Microbiology; microscopy; single-cell; antibiotic resistance; fluorescence; mitochondria; cuprizone; antibacterial susceptibility testing; antimicrobial polymer

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APA (6^th Edition):

Ray, L. A. (2020). Live single cell fluorescence microscopy; from antibiotic resistance detection to mitochondrial dysfunction. (Doctoral Dissertation). University of Akron. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=akron1597342775751888

Chicago Manual of Style (16^th Edition):

Ray, Lucille Alexandria. “Live single cell fluorescence microscopy; from antibiotic resistance detection to mitochondrial dysfunction.” 2020. Doctoral Dissertation, University of Akron. Accessed February 28, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=akron1597342775751888.

MLA Handbook (7^th Edition):

Ray, Lucille Alexandria. “Live single cell fluorescence microscopy; from antibiotic resistance detection to mitochondrial dysfunction.” 2020. Web. 28 Feb 2021.

Vancouver:

Ray LA. Live single cell fluorescence microscopy; from antibiotic resistance detection to mitochondrial dysfunction. [Internet] [Doctoral dissertation]. University of Akron; 2020. [cited 2021 Feb 28]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=akron1597342775751888.

Council of Science Editors:

Ray LA. Live single cell fluorescence microscopy; from antibiotic resistance detection to mitochondrial dysfunction. [Doctoral Dissertation]. University of Akron; 2020. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=akron1597342775751888

13. Taraboletti, Alexandra Anna. Chemical and Metabolomic Analyses of Cuprizone-Induced Demyelination and Remyelination.

Degree: PhD, Chemistry, 2017, University of Akron

URL: http://rave.ohiolink.edu/etdc/view?acc_num=akron1498535047689141

► The cuprizone intoxication model of demyelination and remyelination has long been used to test myelin regenerative therapies for neurodegenerative diseases such as multiple sclerosis. Mice… (more)

Subjects/Keywords: Biochemistry; Bioinformatics; Cellular Biology; Chemistry; metabolomics; cuprizone; multiple sclerosis; copper; transcriptomics; neurodegenerative; oligodendrocytes; myelin; rapamycin; mTOR; BCAA; TDO; demyelination; remyelination

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Taraboletti, A. A. (2017). Chemical and Metabolomic Analyses of Cuprizone-Induced Demyelination and Remyelination. (Doctoral Dissertation). University of Akron. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=akron1498535047689141

Chicago Manual of Style (16^th Edition):

Taraboletti, Alexandra Anna. “Chemical and Metabolomic Analyses of Cuprizone-Induced Demyelination and Remyelination.” 2017. Doctoral Dissertation, University of Akron. Accessed February 28, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=akron1498535047689141.

MLA Handbook (7^th Edition):

Taraboletti, Alexandra Anna. “Chemical and Metabolomic Analyses of Cuprizone-Induced Demyelination and Remyelination.” 2017. Web. 28 Feb 2021.

Vancouver:

Taraboletti AA. Chemical and Metabolomic Analyses of Cuprizone-Induced Demyelination and Remyelination. [Internet] [Doctoral dissertation]. University of Akron; 2017. [cited 2021 Feb 28]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=akron1498535047689141.

Council of Science Editors:

Taraboletti AA. Chemical and Metabolomic Analyses of Cuprizone-Induced Demyelination and Remyelination. [Doctoral Dissertation]. University of Akron; 2017. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=akron1498535047689141

14. Sen, Monokesh. An investigation of the effect of cuprizone-induced demyelination using histological, behavioural, proteomics and immunological approaches.

Degree: 2019, Western Sydney University

URL: http://hdl.handle.net/1959.7/uws:58405

► Feeding cuprizone (CPZ) to animals has been long known to lead to regional degeneration of oligodendrocytes (OLG) and has been used to model the demyelinating… (more)

Subjects/Keywords: multiple sclerosis; demyelination; diseases; causes and theories of causation; proteomics; bioinformatics; mitochondria; cuprizone; Thesis (Ph.D.) – Western Sydney University, 2019

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sen, M. (2019). An investigation of the effect of cuprizone-induced demyelination using histological, behavioural, proteomics and immunological approaches. (Thesis). Western Sydney University. Retrieved from http://hdl.handle.net/1959.7/uws:58405

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Sen, Monokesh. “An investigation of the effect of cuprizone-induced demyelination using histological, behavioural, proteomics and immunological approaches.” 2019. Thesis, Western Sydney University. Accessed February 28, 2021. http://hdl.handle.net/1959.7/uws:58405.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Sen, Monokesh. “An investigation of the effect of cuprizone-induced demyelination using histological, behavioural, proteomics and immunological approaches.” 2019. Web. 28 Feb 2021.

Vancouver:

Sen M. An investigation of the effect of cuprizone-induced demyelination using histological, behavioural, proteomics and immunological approaches. [Internet] [Thesis]. Western Sydney University; 2019. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1959.7/uws:58405.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Sen M. An investigation of the effect of cuprizone-induced demyelination using histological, behavioural, proteomics and immunological approaches. [Thesis]. Western Sydney University; 2019. Available from: http://hdl.handle.net/1959.7/uws:58405

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

15. Papazian, Irini. Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ.

Degree: 2019, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/45595

► TNF is a member of a large family of cytokines and has multiple roles in the CNS. Regulated TNF production is necessary for successful host… (more)

▼ TNF is a member of a large family of cytokines and has multiple roles in the CNS. Regulated TNF production is necessary for successful host defense responses against infection and for tissue repair mechanisms. On the other hand, deregulation of TNF production and molecular signaling leads to chronic inflammation and immune activation, which can lead to autoimmunity. Increased TNF levels have been associated with inflammatory autoimmune diseases, including neurodegenerative CNS disorders such as multiple sclerosis (MS). However, while TNF inhibitors are blockbuster drugs for chronic immune diseases in the periphery, such as rheumatoid arthritis, they exacerbate disease in MS patients, induce de novo demyelination in patients treated for other diseases, and even cause MS. These clinical data clearly show that TNF has overall beneficial effects in the CNS. In experimental models for MS, TNF receptor 1 (TNFR1) mediates the detrimental pro- inflammatory effects of soluble TNF (solTNF), whereas TNFR2 and transmembrane TNF (tmTNF) are essential for beneficial effects, mainly in myelin maintenance and repair. This mechanistic framework supports the use of novel selective inhibitors of solTNF and/or TNFR1, or TNFR2 agonists, for safer therapy of chronic inflammatory diseases including those of the CNS. A potential obstacle to such an approach is substantial evidence that TNF has neuroprotective effects against a wide variety of oxidative and excitotoxic stimuli when used to pretreat cultured neurons, and that protection involves both TNFR1 and TNFR2. However, the relevance of these effects for CNS protection in vivo have yet to be proven and is this subject of this thesis. In a separate line of investigation, previous studies in our lab show that, similar to TNF, conditioned medium from MSC has neuroprotective effects against glutamate excitotoxicity when used to pretreat cultured neurons. MSC provide therapeutic effects in experimental CNS disease models and therefore show promise as cell-based therapies for humans. However, their modes of action, and whether TNF is secreted and involved in their neuroprotection, need to be elucidated. To address the questions described above, we used a genetic approach, combining mice with conventionally and conditionally targeted genes for TNF and its receptors, with an in vitro of glutamate excitotoxicity and in vivo models for multiple sclerosis. Glutamate, and specifically NMDA excitotoxicity, was used because it is directly relevant for neuronal death in a wide variety of neurodegenerative disorders including MS. The NMDA, AMPA and kainate receptors belong to the family of ionotropic glutamate receptors and bind glutamate, which is the major excitatory neurotransmitter in the mammalian CNS. Under certain conditions, dysregulated glutamate function can lead to pathology. High levels of glutamate are toxic for neurons and induce so-called excitotoxic death resulting from increased calcium influx into the cell via the NMDA receptors. First the neuroprotective function of TNF against…

Subjects/Keywords: TNF υποδοχείς; TNF; Νευροεκφυλισμός; Νευροπροστασία; Σκλήρυνση κατά πλάκας; Γλουταμινικοί υποδοχείς; Απομυελίνωση απο κουπριζόνη; Πειραματική αυτοάνοση εγκεφαλομυελίτιδα; TNF receptors; TNF; Neurodegeneration; Neuroprotection; Multiple sclerosis; Glutamate receptors; Cuprizone model; Experimental autoimmune encephalomyelitis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Papazian, I. (2019). Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/45595

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Papazian, Irini. “Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ.” 2019. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed February 28, 2021. http://hdl.handle.net/10442/hedi/45595.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Papazian, Irini. “Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ.” 2019. Web. 28 Feb 2021.

Vancouver:

Papazian I. Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2019. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/10442/hedi/45595.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Papazian I. Μελέτη του ρόλου του διαλυτού και διαμεμβρανικού TNF κατά την παθολογία του ΚΝΣ. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2019. Available from: http://hdl.handle.net/10442/hedi/45595

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Virginia Commonwealth University

16. Moffatt, David. INVESTIGATING THE RESPONSE OF OLIGODENDROCYTE PROGENITOR CELLS TO THE CUPRIZONE MODEL OF DEMYELINATION.

Degree: MS, Anatomy & Neurobiology, 2009, Virginia Commonwealth University

URL: https://doi.org/10.25772/FBVA-G038 ; https://scholarscompass.vcu.edu/etd/1850

► Multiple sclerosis and other myelin diseases affect the quality of life many people. In the United States alone, multiple sclerosis afflicts as many as 400,000… (more)

Subjects/Keywords: oligodendrocyte progenitor cell; SVZ; cuprizone; demyelination; Anatomy; Medicine and Health Sciences; Nervous System

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Moffatt, D. (2009). INVESTIGATING THE RESPONSE OF OLIGODENDROCYTE PROGENITOR CELLS TO THE CUPRIZONE MODEL OF DEMYELINATION. (Thesis). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/FBVA-G038 ; https://scholarscompass.vcu.edu/etd/1850

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Moffatt, David. “INVESTIGATING THE RESPONSE OF OLIGODENDROCYTE PROGENITOR CELLS TO THE CUPRIZONE MODEL OF DEMYELINATION.” 2009. Thesis, Virginia Commonwealth University. Accessed February 28, 2021. https://doi.org/10.25772/FBVA-G038 ; https://scholarscompass.vcu.edu/etd/1850.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Moffatt, David. “INVESTIGATING THE RESPONSE OF OLIGODENDROCYTE PROGENITOR CELLS TO THE CUPRIZONE MODEL OF DEMYELINATION.” 2009. Web. 28 Feb 2021.

Vancouver:

Moffatt D. INVESTIGATING THE RESPONSE OF OLIGODENDROCYTE PROGENITOR CELLS TO THE CUPRIZONE MODEL OF DEMYELINATION. [Internet] [Thesis]. Virginia Commonwealth University; 2009. [cited 2021 Feb 28]. Available from: https://doi.org/10.25772/FBVA-G038 ; https://scholarscompass.vcu.edu/etd/1850.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Moffatt D. INVESTIGATING THE RESPONSE OF OLIGODENDROCYTE PROGENITOR CELLS TO THE CUPRIZONE MODEL OF DEMYELINATION. [Thesis]. Virginia Commonwealth University; 2009. Available from: https://doi.org/10.25772/FBVA-G038 ; https://scholarscompass.vcu.edu/etd/1850

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

17. Millet, Violeta. Dinámica celular en respuesta a la desmielinización inducida por intoxicación con cuprizona en diferentes condiciones experimentales.

Degree: Farmacia y Bioquímica, 2016, Universidad de Buenos Aires

URL: http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgrauba&cl=CL1&d=HWA_1752 ; http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgrauba/index/assoc/HWA_1752.dir/1752.PDF

►

Demyelination models have proven useful tools in the assessment of new therapies to target demyelinating disorders. Among these models, cuprizone (CPZ) intoxication is simple and… (more)

▼

Demyelination models have proven useful tools in the assessment of new therapies to target demyelinating disorders. Among these models, cuprizone (CPZ) intoxication is simple and highly reproducible and renders low mortality levels. The aim of the present study was to use the CPZ model to analyze the mechanisms underlying oligodendrocyte (OLG) viability and differentiation and leading to demyelination. Results show that CPZ-induced demyelination and mature OLG death are mediated by microglial production of pro-inflammatory cytokines, a dysfunction in the mithochondrial respiratory chain and the generation of reactive oxygen species (ROS). Therefore, transgenic animals expressing EGFP under the CNPase promoter exhibit basal hypomyelination and greater susceptibility to CPZ-induced demyelination, as high EGFP expression leads to oxidative stress and mature OLG apoptotic death. As a consequence, partial inhibition of proteasome activity enhances remyelination, reduces microglial recruitment and NF?B activation, thus producing a recovery in the mitochondrial respiratory chain. Finally, our results also show Gal-3 to be secreted by microglia, to induce OLG differentiation and to modulate myelination and the response to demyelination. It may be therefore concluded that OLG viability and differentiation are affected by the production of free radicals and the presence of microglia-secreted factors.

Fil: Millet, Violeta. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Buenos Aires, Argentina

Los modelos desmielinización son herramientas útiles en el estudio de nuevas terapias aplicables a enfermedades desmielinizantes. El modelo inducido por intoxicación con CPZ es altamente reproducible, simple y de baja mortalidad. Nos propusimos estudiar los mecanismos que controlan la viabilidad y la diferenciación oligodendroglial, y que conducen a la desmielinización utilizando este modelo. Nuestros resultados muestran que la desmielinización y muerte de OLGs maduros inducida por CPZ es mediada por la producción de citoquinas pro-inflamatorias desde la microglia, con disfunción de la cadena respiratoria mitocondrial y generación de EROs. Así, animales transgénicos expresando EGFP bajo el promotor de CNPasa presentan una hipomielinización basal y una mayor susceptibilidad a la desmielinización con CPZ debida a la alta expresión de EGFP que lleva al estrés oxidativo y la apoptosis de los OLGs maduros. En concordancia, la inhibición parcial de la actividad del proteasoma mejora la remielinización, disminuye en el reclutamiento de microglia y la activación de NF?B recuperando la actividad de la cadena respiratoria mitocondrial. Finalmente, nuestros resultados muestran a Gal-3 como una nueva molécula secretada desde la microglia, capaz de inducir diferenciación oligodendroglial y de modular la mielinización y la respuesta a la desmielinización. En conclusión, podemos afirmar que la viabilidad y la diferenciación oligodendroglial dependen de la producción de radicales libres así como de la presencia de mediadores…

Advisors/Committee Members: Pasquini, Laura A., Lores Arnaiz, Silvia, De Nicola, Alejandro, Correale, Jorge.

Subjects/Keywords: Cuprizona; Mielinización; Proteasoma; Galectinas 1y3; Microglia; Ratones CNP::EGFPasa; Oligodendrocitos; Desmielinización; Remielinización; Especies reactivas del oxígeno; Citoquinas pro-inflamatorias; Oligodendrocytes; Microglia; Myelination; Demyelination; Remyelination; Reactive oxygen species; Pro-inflammatory cytokines; Proteasome; Cuprizone; Galectins 1 and 3; EGFP::CNPase mice; Ciencia de la vida

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Millet, V. (2016). Dinámica celular en respuesta a la desmielinización inducida por intoxicación con cuprizona en diferentes condiciones experimentales. (Thesis). Universidad de Buenos Aires. Retrieved from http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgrauba&cl=CL1&d=HWA_1752 ; http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgrauba/index/assoc/HWA_1752.dir/1752.PDF

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Millet, Violeta. “Dinámica celular en respuesta a la desmielinización inducida por intoxicación con cuprizona en diferentes condiciones experimentales.” 2016. Thesis, Universidad de Buenos Aires. Accessed February 28, 2021. http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgrauba&cl=CL1&d=HWA_1752 ; http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgrauba/index/assoc/HWA_1752.dir/1752.PDF.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Millet, Violeta. “Dinámica celular en respuesta a la desmielinización inducida por intoxicación con cuprizona en diferentes condiciones experimentales.” 2016. Web. 28 Feb 2021.

Vancouver:

Millet V. Dinámica celular en respuesta a la desmielinización inducida por intoxicación con cuprizona en diferentes condiciones experimentales. [Internet] [Thesis]. Universidad de Buenos Aires; 2016. [cited 2021 Feb 28]. Available from: http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgrauba&cl=CL1&d=HWA_1752 ; http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgrauba/index/assoc/HWA_1752.dir/1752.PDF.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Millet V. Dinámica celular en respuesta a la desmielinización inducida por intoxicación con cuprizona en diferentes condiciones experimentales. [Thesis]. Universidad de Buenos Aires; 2016. Available from: http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgrauba&cl=CL1&d=HWA_1752 ; http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgrauba/index/assoc/HWA_1752.dir/1752.PDF

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

18. Kuypers, Nicholas John. Functional implications of demyelination and the molecular control of remyelination in the adult mouse.

Degree: PhD, 2014, University of Louisville

URL: 10.18297/etd/786 ; https://ir.library.louisville.edu/etd/786

► Oligodendrocyte (OL) loss contributes to the functional deficits underlying diseases with a demyelinating component (Gajjar et al., 1997; Miller et al., 2002). Remyelination can… (more)

Subjects/Keywords: MicroRNA; Cuprizone; Demyelination; Remyelination; Oligodendrocyte; Ethidium bromide; Anatomy; Neuroscience and Neurobiology

…adult mice with the vii copper chelator cuprizone demyelinates specific brain… …regions which remyelinate following cuprizone cessation (Torkildsen et al., 2008)… …Therefore, Chapter 4 focuses on the role of oligodendroglial-specific miRNAs in cuprizone-induced… …facilitates the quantification of cuprizone-induced de- and re-myelination. 115 10. FACS-based… …miRNAs are significantly decreased at 6 weeks on cuprizone compared to no cuprizone miRNA…

11 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kuypers, N. J. (2014). Functional implications of demyelination and the molecular control of remyelination in the adult mouse. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/786 ; https://ir.library.louisville.edu/etd/786

Chicago Manual of Style (16^th Edition):

Kuypers, Nicholas John. “Functional implications of demyelination and the molecular control of remyelination in the adult mouse.” 2014. Doctoral Dissertation, University of Louisville. Accessed February 28, 2021. 10.18297/etd/786 ; https://ir.library.louisville.edu/etd/786.

MLA Handbook (7^th Edition):

Kuypers, Nicholas John. “Functional implications of demyelination and the molecular control of remyelination in the adult mouse.” 2014. Web. 28 Feb 2021.

Vancouver:

Kuypers NJ. Functional implications of demyelination and the molecular control of remyelination in the adult mouse. [Internet] [Doctoral dissertation]. University of Louisville; 2014. [cited 2021 Feb 28]. Available from: 10.18297/etd/786 ; https://ir.library.louisville.edu/etd/786.

Council of Science Editors:

Kuypers NJ. Functional implications of demyelination and the molecular control of remyelination in the adult mouse. [Doctoral Dissertation]. University of Louisville; 2014. Available from: 10.18297/etd/786 ; https://ir.library.louisville.edu/etd/786

Kyoto University

19. Fukudome, Daisuke. Translocator protein (TSPO) and stress cascades in mouse models of psychosis with inflammatory disturbances .

Degree: 2020, Kyoto University

URL: http://hdl.handle.net/2433/259710

Subjects/Keywords: Cuprizone short-term exposure (CSE); Maternal immune activation (MIA); Inflammatory disturbances; Translocator protein 18 kDa (TSPO); Stress cascades; Psychosis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fukudome, D. (2020). Translocator protein (TSPO) and stress cascades in mouse models of psychosis with inflammatory disturbances . (Thesis). Kyoto University. Retrieved from http://hdl.handle.net/2433/259710

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Fukudome, Daisuke. “Translocator protein (TSPO) and stress cascades in mouse models of psychosis with inflammatory disturbances .” 2020. Thesis, Kyoto University. Accessed February 28, 2021. http://hdl.handle.net/2433/259710.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Fukudome, Daisuke. “Translocator protein (TSPO) and stress cascades in mouse models of psychosis with inflammatory disturbances .” 2020. Web. 28 Feb 2021.

Vancouver:

Fukudome D. Translocator protein (TSPO) and stress cascades in mouse models of psychosis with inflammatory disturbances . [Internet] [Thesis]. Kyoto University; 2020. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/2433/259710.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Fukudome D. Translocator protein (TSPO) and stress cascades in mouse models of psychosis with inflammatory disturbances . [Thesis]. Kyoto University; 2020. Available from: http://hdl.handle.net/2433/259710

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

20. 山本, 梓司. Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果.

Degree: 博士(医学), 2018, Saitama Medical University / 埼玉医科大学

URL: http://id.nii.ac.jp/1386/00000615/

►

Multiple sclerosis is a neuroinflammatory demyelinating and neurodegenerative disease of the central nervous system characterized by recurrent and progressive demyelination/remyelination cycles, neuroinflammation, oligodendrocyte loss, demyelination,… (more)

▼

Multiple sclerosis is a neuroinflammatory demyelinating and neurodegenerative disease of the central nervous system characterized by recurrent and progressive demyelination/remyelination cycles, neuroinflammation, oligodendrocyte loss, demyelination, and axonal degeneration. Cyclic phosphatidic acid (cPA) is a natural phospholipid mediator with a unique cyclic phosphate ring structure at the sn-2 and sn-3 positions of the glycerol backbone. We reported earlier that cPA elicits a neurotrophin-like action and protects hippocampal neurons from ischemia-induced delayed neuronal death. We designed, chemically synthesized, and metabolically stabilized derivatives of cPA: 2-carba-cPA (2ccPA), a synthesized compound in which one of the phosphate oxygen molecules is replaced with a methylene group at the sn-2 position. In the present study, we investigated whether 2ccPA exerts protective effects in oligodendrocytes and suppresses pathology in the two most common mouse models of multiple sclerosis.

To evaluate whether 2ccPA has potential beneficial effects on the pathology of multiple sclerosis, we investigated the effects of 2ccPA on oligodendrocyte cell death in vitro and administrated 2ccPA to mouse models of experimental autoimmune encephalomyelitis (EAE) and cuprizone-induced demyelination.

We demonstrated that 2ccPA suppressed the CoCl

-induced increase in the Bax/Bcl-2 protein expression ratio and phosphorylation levels of p38MAPK and JNK protein. 2ccPA treatment reduced cuprizone-induced demyelination, microglial activation, NLRP3 inflammasome, and motor dysfunction. Furthermore, 2ccPA treatment reduced autoreactive T cells and macrophages, spinal cord injury, and pathological scores in EAE, the autoimmune multiple sclerosis mouse model.

We demonstrated that 2ccPA protected oligodendrocytes via suppression of the mitochondrial apoptosis pathway. Also, we found beneficial effects of 2ccPA in the multiperiod of cuprizone-induced demyelination and the pathology of EAE. These data indicate that 2ccPA may be a promising compound for the development of new drugs to treat demyelinating disease and ameliorate the symptoms of multiple sclerosis.

平成29年度

Subjects/Keywords: Animals; Anti-Inflammatory Agents; Apoptosis; Cell Differentiation; Cell Line, Transformed; Cuprizone; Demyelinating Diseases; Disease Models, Animal; Female; Gene Expression Regulation; Humans; MAP Kinase Signaling System; Male; Mice; Mice, Inbred C57BL; Monoamine Oxidase Inhibitors; Myelin Sheath; NLR Family, Pyrin Domain-Containing 3 Protein; Phosphatidic Acids; Proto-Oncogene Proteins c-bcl-2; p38 Mitogen-Activated Protein Kinases

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

山本, �. (2018). Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果. (Thesis). Saitama Medical University / 埼玉医科大学. Retrieved from http://id.nii.ac.jp/1386/00000615/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

山本, 梓司. “Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果.” 2018. Thesis, Saitama Medical University / 埼玉医科大学. Accessed February 28, 2021. http://id.nii.ac.jp/1386/00000615/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

山本, 梓司. “Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果.” 2018. Web. 28 Feb 2021.

Vancouver:

山本 �. Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果. [Internet] [Thesis]. Saitama Medical University / 埼玉医科大学; 2018. [cited 2021 Feb 28]. Available from: http://id.nii.ac.jp/1386/00000615/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

山本 �. Protective and therapeutic role of 2-carba-cyclic phosphatidic acid in demyelinating disease. : 脱髄性疾患における環状ホスファチジン酸誘導体の脱髄抑制及び治療効果. [Thesis]. Saitama Medical University / 埼玉医科大学; 2018. Available from: http://id.nii.ac.jp/1386/00000615/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

21. Thiessen, Jonathan. Development and application of quantitative MRI methods for assessing white matter integrity in the mouse brain.

Degree: Physics and Astronomy, 2012, University of Manitoba

URL: http://hdl.handle.net/1993/9221

► Healthy white matter in the brain and spinal cord is composed primarily of myelinated axons and glial cells. Myelinated axons transfer information between the peripheral… (more)

▼ Healthy white matter in the brain and spinal cord is composed primarily of myelinated axons and glial cells. Myelinated axons transfer information between the peripheral nervous system and the central nervous system (CNS) as well as between centres within the CNS. Demyelination, a hallmark of neurodegenerative autoimmune diseases such as multiple sclerosis (MS), can cause nerve damage and degrade signal propagation. Magnetic resonance imaging (MRI) methods thought to assess myelin integrity and the structural integrity of axons are improving both the diagnosis and understanding of white matter diseases such as MS. Current methods, however, are sensitive to many different pathologies, making the interpretation of individual MRI results difficult. For this dissertation, several quantitative MRI methods were developed and compared, including single component T1 and T2 relaxometry, multicomponent T2 relaxometry, diffusion tensor imaging (DTI), and quantitative magnetization transfer imaging (qMTI). These methods were tested on agarose gels, fixed rat spinal cords, healthy control mice, and the cuprizone mouse model of demyelination. Quantitative MRI measurements were correlated to ultrastructural measurements of white matter to determine the influence myelin content and axonal structure have on different MRI methods. Cellular distributions measured in electron micrographs of the corpus callosum correlated strongly to several different quantitative MRI metrics. The largest Spearman correlation coefficient varied depending on cellular type: longitudinal relaxation rates (RA/T1) vs. the myelinated axon fraction ( r = 0.90/-0.90), the qMTI-derived bound pool fraction (f) vs. the myelin sheath fraction ( r = 0.93), and the DTI-derived axial diffusivity vs. the non-myelinated cell fraction (r = 0.92). Using Pearson’s correlation coefficient, f was strongly correlated to the myelin sheath fraction (r = 0.98) with a linear equation predicting myelin content (5.37f −0.25). Of the calculated MRI metrics, f was the strongest indicator of myelin content while longitudinal relaxation rates and diffusivity measurements were the strongest indicators of changes in tissue structure. Multiparametric MRI measurements of relaxation, diffusion, and magnetization transfer give a more complete picture of white matter integrity. Advisors/Committee Members: Martin, Melanie (Physics and Astronomy) (supervisor), Gericke, Michael (Physics and Astronomy) King, Scott (Physics and Astronomy) Gough, Kathy (Chemistry) Kozlowski, Piotr (Physics and Astronomy, University of British Columbia) (examiningcommittee).

Subjects/Keywords: magnetic resonance imaging; diffusion tensor imaging; magnetization transfer imaging; relaxometry; demyelination; cuprizone; corpus callosum; myelin; electron microscopy; multiple sclerosis; white matter; image processing

…Discussion . . . . . . . . . . . . . . . . . . . . . 4.3 Cuprizone Mouse Model of Demyelination… …Cuprizone 105 . . . . . . 106 . . . . . . 106 . . . . . . 106 . . . . . . 107 . . . . . . 112… …157 5 Quantitative MRI and Ultrastructural Examination of the Cuprizone Model of… …163 5.2.1 Cuprizone Mouse Model . . . . . . . . . . . . . . . . . . . . . . . . . 163 5.2.2… …166 5.3.1 Cuprizone Diet . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 166…

10 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Thiessen, J. (2012). Development and application of quantitative MRI methods for assessing white matter integrity in the mouse brain. (Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/9221

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Thiessen, Jonathan. “Development and application of quantitative MRI methods for assessing white matter integrity in the mouse brain.” 2012. Thesis, University of Manitoba. Accessed February 28, 2021. http://hdl.handle.net/1993/9221.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Thiessen, Jonathan. “Development and application of quantitative MRI methods for assessing white matter integrity in the mouse brain.” 2012. Web. 28 Feb 2021.

Vancouver:

Thiessen J. Development and application of quantitative MRI methods for assessing white matter integrity in the mouse brain. [Internet] [Thesis]. University of Manitoba; 2012. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1993/9221.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Thiessen J. Development and application of quantitative MRI methods for assessing white matter integrity in the mouse brain. [Thesis]. University of Manitoba; 2012. Available from: http://hdl.handle.net/1993/9221

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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Open Access Theses and Dissertations