The spectrum of primary demyelinating diseases of the CNS is composed of a variety of pathologic entities. MS, the most common form, is classically defined by a relapsing-remitting or progressive clinical course; the pathologic findings demonstrate multiple well-circumscribed lesions that lack mass effect or edema and that occur in characteristic locations such as the periventricular white matter (25). A subset of patients with demyelinating disease present with large solitary lesions with prominent edema and mass effect that produce clinical symptoms suggestive of a mass lesion (1-6). Most patients with these TDLs have single acute clinical attacks, and these generally do not progress to MS (26).. The MR imaging presentation of TDLs can mimic that of a high-grade glial neoplasm, resulting in a diagnostic dilemma (2-8). Both TDLs and high-grade gliomas can demonstrate ill-defined borders, extensive perilesional edema and mass effect, and the appearance of necrosis or cystic degeneration. ...
Tumefactive lesions are an uncommon manifestation of demyelinating disease and can pose a diagnostic challenge in patients without a pre-existing diagnosis of multiple sclerosis. Choosing when to biopsy a tumefactive lesion to exclude alternative pathology can be difficult. Other questions include how best to treat an acute attack as well as the optimal timing of therapy to prevent relapse. This article aims to review the available literature for tumefactive demyelination and to propose an approach to diagnosis and management. We argue that disease modifying therapy should be considered for acute tumefactive demyelinating lesions only once criteria of dissemination in time and space are fulfilled and the diagnosis of multiple sclerosis is confirmed.. ...
We report the course of a 16-year-old girl who presented with near complete visual loss associated with chiasmal neuritis and a biopsy proven tumefactive demyelinating lesion on magnetic resonance imaging (MRI) in association with a recent immunization against human papilloma virus. She had received her second vaccination against human papilloma virus 10 days prior to her presentation. Larger epidemiologic studies will be needed to confirm a role of the human papilloma virus immunization and demyelinating disease. September 19, 2008 - CNS demyelination and quadrivalent HPV vaccination. - journal article (Multiple Sclerosis) - We report five patients who presented with multifocal or atypical demyelinating syndromes within 21 days of immunization with the quadrivalent human papilloma virus (HPV) vaccine, Gardasil((R)). Although the target population for vaccination, young females, has an inherently high risk for MS, the temporal association with demyelinating events in these cases may be ...
Inflammatory demyelinating diseases (IDDs), sometimes called Idiopathic (IIDDs) because the unknown etiology of some of them, and sometimes known as borderline forms of multiple sclerosis, is a collection of multiple sclerosis variants, sometimes considered different diseases, but considered by others to form a spectrum differing only in terms of chronicity, severity, and clinical course. Multiple Sclerosis for some people is a syndrome more than a single disease. It can be considered among the acquired demyelinating syndromes with a multiphasic instead of monophasic behaviour. Multiple sclerosis also has a prodromal stage in which an unknown underlying condition, able to damage the brain, is present, but no lesion has still developed. The list of these diseases depends of the author, but usually are included: multiple sclerosis, normally defined by the dissemination in time and space of demyelinating lesions, with two (or sometimes three) clinical presentations: Relapsing-Onset multiple ...
The pathogenesis of murine hepatitis virus, strain JHM, was studied in 6- and 12-week-old C57iBL mice. There was 100% mortality in the 6-week-old mice after intracerebral inoculation. The lesions were characterized by necrotizing encephalomyelitis, without demyelination. Intracerebral inoculation of 12-week-old animals, however, resulted in no morbidity or mortality. The 12-week-old animals showed transient virus replication in the brain, spinal cord, and liver, which was cleared by day 14. Histologic examination showed evidence of ongoing demyelination, concomitant remyelination, and hydrocephalus ex vacuo. Although viral antigen was demonstrated by immunofluorescence in the central nervous system of these animals, no infectious virus was recovered, and immunosuppression regimens did not potentiate the disease.. ...
TY - PAT. T1 - Treatment of Demyelinating Disorders with Soluble Lymphotoxin-Beta-Receptor. AU - Browning,Jeffrey L.. AU - Ting,Jenny P-Y. N1 - Status: published applicationnumber: 12/446,041 usclass: 514/19.2 ; 514/1.1; 530/351 applicationnumber: 12/446,041. PY - 1800. Y1 - 1800. N2 - Methods of treating a demyelinating disorder using inhibitors of the lymphotoxin pathway.. AB - Methods of treating a demyelinating disorder using inhibitors of the lymphotoxin pathway.. M3 - Patent. M1 - 8067375. ER - ...
Increased risk of non-multiple sclerosis demyelinating syndromes in patients with preexisting septicaemia: a nationwide retrospective cohort study ...
Grinkers myelinopathy, also known as anoxic leukoencephalopathy and delayed post-hypoxic leukoencephalopathy (DPHL), is a rare disease of the central nervous system. Grinkers myelinopathy was originally characterized by Roy R. Grinker in 1925 or 1926, depending on the source. The disease is characterized by a delayed leukoencephalopathy after an hypoxic episode. It is typically, though not necessarily, related to carbon monoxide poisoning or heroin overdose. It occurs in roughly 2.8% of those who experience an acute hypoxic/anoxic episode. Because of the wide range of symptoms and the delay in onset, it is often misdiagnosed as other neuropathologies. Following an apparent rehabilitation from a severe episode of prolonged cerebral oxygen deprivation, patients with Grinkers myelinopathy begin to experience massive white matter death that leads to a wide range of neurological dysfunctions ranging from confusion and apathy to Parkinson-like symptoms. The symptoms have been known to include ...
Inflammatory demyelinating diseases (DD) affecting the central nervous system (CNS) are increasingly recognized in children. During the past decade significant advances have been made in this field. Pediatric DD are important not just because 3-5% of MS cases are diagnosed in childhood, but also because their pathogenesis may provide unique insights into the earliest events and triggers of acquired CNS DD. The purpose of this article is to offer an update into pediatric DD for the general pediatrician and child neurologist. Current evidence on epidemiology, pathology, diagnosis, management and prognosis are reviewed for both monophasic (ADEM and CIS) and polyphasic/chronic DD (MS and NMO). We also review new research advances including novel biomarkers and treatments from the latest literature.. ...
A growing number of CNS-reactive autoantibodies are emerging as useful diagnostic markers in the context of CNS inflammatory diseases, including pediatric demyelinating disorders. The method used to measure the CNS-autoreactive antibodies is an important consideration. For autoantibodies that bind to the extracellular domains of proteins such as AQP4 (in NMO14) and MOG,32 CBAs have emerged as the preferred approach, as these present the antigen in its conformational state at the cell surface, which is likely to be more representative of the in vivo interaction.33 In contrast, antibody assays that alter proteins (by unraveling them) or expose antigens or linear epitopes that are not present at the cell surface are less likely to measure antibodies that are pathophysiologically relevant in vivo. It remains unknown whether antibodies are primary contributors to pediatric CNS demyelinating disease immunopathogenesis, modify pathogenesis, or merely represent secondary epiphenomenon of immune ...
Experimental allergic encephalomyelitis (EAE) is the commonest, readily induced, organspecific, autoimmune disorder of laboratory animals of its kind. It is an artificial disorder brought about by the immunization of susceptible animals with brain antigens in complete Freunds adjuvant (CFA). Variations can be induced by altering the nature of the antigen and the conditions involving immunization. Whilst it is often described as a demyelinating disease, in strict terms it is not, since the primary pathologic process is not demyelination but rather an encephalomyelitis that is immunologically induced. Rather, the prototype demyelinating disease is multiple sclerosis and its variants. In this paper, the central question we ask is whether the data gleaned from the EAE model contributes to our understanding of the pathological events in MS. Towards answering this, we describe the historical development of EAE and its hyperacute form, and discuss the findings studied extensively in the non-human ...
The pathological basis of multiple sclerosis involves damage to both myelin sheaths and axons. Demyelination and axonal transection are considered to cause reversible and irreversible neurological deficits respectively, gradually destroying the neuronal circuitry of the CNS. In order to analyse the individual effects of the pathological hallmarks of multiple sclerosis on neurons, the pontocerebellar pathway was targeted with either lysolecithin-induced chemical demyelination or complete pathway transection. Transcriptional changes in the pontocerebellar neuronal nuclei were investigated with microarrays at days 4, 10 and 37 post-intervention to identify underlying molecular responses. A common as well as unique set of injury response genes was identified in the transection and the demyelination conditions. The increased expression of activating transcription factor 3 (Atf3) and thyrotropin-releasing hormone (Trh) in both injury paradigms was validated by immunohistochemistry. Expression of Atf3 in a
Sorensen, O; Dugre, R; Percy, D; and Dales, S, "In vivo and in vitro models of demyelinating disease: endogen- ous factors influencing demyelinating disease caused by mouse hepatitis virus in rats and mice." (1982). Subject Strain Bibliography 1982. 4405 ...
Definition of Demyelinating disease with photos and pictures, translations, sample usage, and additional links for more information.
There is much evidence to support the goal of remyelination as a means to prevent axon degeneration and slow deficit progression in neurologic disease [14]. In the year 2000, we reported the identification of a natural human IgM that promoted robust spinal cord remyelination in both the TMEV-IDD and lysolecithin-induced demyelination models [15, 16]. A recombinant form of this human IgM, termed rHIgM22, was expressed in a F3B6 cell line with the assembled IgM containing a mouse J chain [17]. rHIgM22 binds to myelin and the surface of oligodendrocytes (OL) and in pre-clinical studies is effective in vivo at very low doses. A single 0.025 mg/kg intraperitoneal injection of rHIgM22 given to TMEV-IDD mice with demyelination promoted significant remyelination 5 weeks later [18] and increased brainstem NAA concentrations [13], indicating a preservation of axon health [19]. In a recently concluded dose escalation clinical trial in humans with MS, rHIgM22 was tested at doses ranging from 0.025 up to 2 ...
Free Essay: Multiple Sclerosis (MS) is an autoimmune demyelinating disorder it is characterized by inflammation and destruction of CNS myelin. It affects...
Multiple Sclerosis (MS) is an inflammatory disease which causes areas of demyelination in the Central Nervous System (CNS) and affects only humans. Current therapies for MS are focused on anti-inflammatory treatment, which reduce the occurrence and clinical relapses of the disease. However, progressive disability of the disease is related to axonal degeneration. After demyelination, remyelination occurs, which helps repair the demyelinated lesions and protects axons from degeneration. However, this endogenous remyelination is inefficient, and currently there are no therapies available to enhance remyelination. The aim of this thesis was to first characterize a fast and reliable model to study CNS remyelination in vitro, and second to investigate the role of semaphorin 3a (Sema3A) and semaphorin 3f (Sema3F) signaling in CNS remyelination. Various in vivo models have been developed to investigate the pathology of multiple sclerosis, and can be used to test remyelination therapies. However, in vivo ...
The February 2007 issue of the American Journal of Neuroradiology reported the findings of A. Ciafoni et al.1 In this article, the authors reported the approach of examining glutamate/glutamine peaks in 1H-MR (proton) spectroscopy to increase the specificity in differentiating tumefactive demyelinating processes from neoplasms. The thought of using MR spectroscopy in this situation is attractive because the current clinical approach may warrant a lumbar puncture and even biopsy. Although we commend the authors enthusiasm for this technique, the paper lacks statistical significance and contains much bias to support the authors claim that MR spectroscopy "can be helpful in the noninvasive diagnosis of acute demyelinating diseases"1 when elevated glutamate/glutamine peaks are identified. We believe that this article should be represented as an idea backed by case reports and not be considered as original research.. First, the authors never fully give the inclusion or exclusion criteria for how ...
Demyelinating diseases, such as multiple sclerosis and leukodystrophy, are characterized by damage to the protective myelin sheath that surrounds the axons of neurons. This demyelination can be caused by an autoimmune response or impaired myelin production by oligodendrocytes.. A new report in JCI Insight from Arjun Saha and colleagues at Duke University demonstrates that a cell therapy product called DUOC-01 can accelerate remyelination of axons in mice treated with a demyelinating chemical agent. DUOC-01 cells, which are derived from banked umbilical cord blood, were transplanted into mice following toxic demyelination. DUOC-01 treatment resulted in faster remyelination and promoted the differentiation of oligodendrocyte progenitor cells. These results suggest that a cord blood-derived cell product can promote neuronal repair and remyelination. Future clinical studies will be needed to determine if DUOC-01 cell therapy benefits patients with demyelinating diseases.. ...
SUPERVISORS: OLE DIDRIK LÆRUM, ØYSTEIN BRUSERUD 2000 DR.MED. PEER KÅRE LILLENG. TUMOUR CELLS IN THE AXILLARY NODES IN PATIENTS WITH BREAST CANCER. SUPERVISORS: FLORA HARTVEIT, BJØRN MÆHLE.. 1999 DR.MED. HANS KRISTIAN HAUGLAND. MODULATION OF INVASIVE BEHAVIOR IN CULTURED HUMAN GLIOMA CELLS. SUPERVISOR: OLE DIDRIK LÆRUM. 1998 DR.MED. LARS BØ. MULTIPLE SCLEROSIS. IMMUNOPATHOLOGICAL STUDIES OF INFLAMMATORY CENTRAL NERVOUS SYSTEM DEMYELINATION. SUPERVISOR: SVERRE MØRK. 1999 DR.MED. LARS FJELLBIRKELAND. THREE-DIMENSIONAL CULTURE OF HUMAN BRONCHIAL MUCOSA AND LUNG CANCER TISSUE. SUPERVISORS: OLE DIDRIK LÆRUM, ROLF BJERKVIG. 1998 DR.MED. JOHANNA OLWEUS. EARLY EVENTS IN HUMAN MYELOPOIESIS. SUPERVISORS: OLE DIDRIK LÆRUM, FRIDTJOF LUND-JOHANSEN. 1998 DR.MED. SVEIN JACOB TJOFLAAT NYGAARD. DYNAMIC DETERMINATION AND MODULATION OF GLIOMA CELL INVASION IN VITRO. SUPERVISORS: OLE DIDRIK LÆRUM, OLE BJØRN TYSNES. 1998 DR.MED. KARIN COLLETT. OPERABLE BREAST CANCER. SUPERVISORS: BJØRN MÆHLE, ROLV ...
Other Primary Demyelinating Diseases - Learn about the causes, symptoms, diagnosis & treatment from the Merck Manuals - Medical Consumer Version.
Question - Done with brain MRI. Diagnosis of demyelinating disease. Suggestion?. Ask a Doctor about when and why MRI is advised, Ask a Neurologist
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Case Reports in Neurological Medicine is a peer-reviewed, Open Access journal that publishes case reports focusing on diseases of the nervous system, as well as abnormal neurological function.
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This category includes those diseases which predominantly affect the myelin (the structure that coats nerves). Examples include the leukodystrophies (in which the myelin in the brain is affected), demyelinating neuropathies (in which the myelin of peripheral nerves is affected) and multiple sclerosis.
The role of prolonged cortical myelination in human evolution has been implicated as a contributing factor in some cases of demyelinating disease. Unlike other primates, humans exhibit a unique pattern of postpubertal myelination, which may contribute to the development of psychiatric disorders and neurodegenerative diseases that present in early adulthood and beyond. The extended period of cortical myelination in humans may allow greater opportunity for disruption in myelination, resulting in the onset of demyelinating disease. Furthermore, it has been noted that humans have significantly greater prefrontal white matter volume than other primate species, which implies greater myelin density. Increased myelin density in humans as a result of a prolonged myelination may therefore structure risk for myelin degeneration and dysfunction. Evolutionary considerations for the role of prolonged cortical myelination as a risk factor for demyelinating disease are particularly pertinent given that genetics ...
Hi, I found this newsgroup via alt.epilepsy and thought this may be the appropriate place for this request. We have a friend who has been diagnosed as having multifocal motor sensory demyelinating neuropathy. We have tried to find information, but not too successful. From what we have been told, this is very rare, and does not have a great prognosis. If anyone has information about this disorder, we would appreciate it if you could pass it along. TIA Ray ...
RefSeq Summary (NM_206814): The product of this gene is a membrane protein expressed on the oligodendrocyte cell surface and the outermost surface of myelin sheaths. Due to this localization, it is a primary target antigen involved in immune-mediated demyelination. This protein may be involved in completion and maintenance of the myelin sheath and in cell-cell communication. Alternatively spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq, Jul 2008 ...
Free full text: http://onlinelibrary.wiley.com/doi/10.1111/cei.12077/full Early-life hygiene-related factors affect risk of central nervous system...
The symptoms of multiple sclerosis (MS), an immune-mediated, degenerative disease of the central nervous system (CNS), are thought to be due to demyelination and axonal damage leading to impairment of neurotransmission. In a mouse model of MS, chronic relapsing experimental allergic encephalomyelitis (CREAE), cannabinoid compounds have been shown to protect axons and improve disease severity. In this study, CREAE and rotation-mediated CNS aggregate cell cultures were used to examine the role of cannabinoid receptor 1 (CB1R) in endocannabinoid-mediated modulation of demyelination and neurodegeneration. The aggregate cell culture system was developed and characterised in mouse to exploit CB1R knockout (CB1R-KO) animals. CREAE was induced in CB1R-KO mice and wildtype counterparts, and CNS aggregate cell cultures derived from the same mouse strains were demyelinated with interferon gamma. CREAE animals were assessed for functional deficit by clinical scoring and in an open field activity chamber. ...
One of the main roles of myelin in the central nervous system seems to be related to maintaining a low ionic conductivity around axons (1) and a modification of its composition, intermodular...
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\ref{239014}BACKGROUND:Multiple sclerosis (MS) as an auto-immunedisease is an inflammatory demyelinating disease of the central nervoussystem. Certain genes have shown to be involved in the initiation of MS but thespecific role of some of them e.g. I
Although dysregulation of iron has been associated with neurodegeneration and demyelination in MS, the inability to assess its dynamics in relation to mechanisms of tissue damage in vivo has impeded our understanding of its true role in disease pathogenesis. The fact that iron is essential for CNS myelinogenesis during development (2-4) raises the possibility that it may facilitate remyelination, even though most prior work in MS has focused on inflammation and neurodegeneration (5-9). MRI sequences, such as T2*w imaging, can be used in MS, especially at ultra-high magnetic field (7 tesla), to characterize the spatiotemporal distribution of intralesional iron deposition; however, MRI can only provide limited pathobiological and temporal information in practical clinical studies. By using the marmoset EAE model, serial in vivo MRI, and histopathological analyses, we were able to assess the spatiotemporal dynamics of intralesional iron deposition, as well as the cellular and molecular composition ...
Chemokines mediate repair in the adult CNS. Following demyelination, CXCL12 and its receptors, CXCR4 and CXCR7, are upregulated on astrocytes and endothelial ce
Voltage-independent K+ currents and Na+ currents did not change in white matter OPCs following demyelination. (A-C) Capacitance, K+ and Na+ current densities
Question - Imaging states chronic microvascular ischemic change or demyelinating plaques. Meaning?. Ask a Doctor about when and why MRI is advised, Ask a Neurologist
Ith VIP, which also has a vasodilator chonocapillaris, the capillar bed of the choroid action (Miller ct a!. Demyelinating Diseases See pp.
Fingerprint Explore the research topics touched on by this project. These labels are generated based on the underlying awards/grants. Together they form a unique fingerprint. ...
Valery, Patricia C., Lucas, Robyn M., Williams, David B., Pender, Michael P., Chapman, Caron, Coulthard, Alan, Dear, Keith, Dwyer, Terence, Kilpatrick, Trevor. J., McMichael, Anthony J., van, der Mei, Ingrid, Taylor, Bruce and Ponsonby, Anne-Louise (2013). Occupational Exposure and Risk of Central Nervous System Demyelination. American Journal of Epidemiology,177(9):954-961. ...
Demyelinating Autoimmune Diseases, CNS; Autoimmune Demyelinating Diseases, Central Nervous System; Spinal Cord Demyelinating Autoimmune Diseases. On-line free medical diagnosis assistant. Ranked list of possible diseases from either several symptoms or a full patient history. A similarity measure between symptoms and diseases is provided.
I noticed some similarities between wumedicals anecdotal SCI neural stem cell treatment case, Asterias prelim cervical AST-OPC1 reports and reports about use of 4-AP (4-Aminopyridine), a potassium channel blocker. They all appear to target demyelinated axons with poor conduction, a consequence of SCI. Asteria even mentions the target of their AST-OPC1 stem cells is demyelinated axons. So I got 4-AP compounded and tested it at 10mg x 4 times a day dose (later went down to 5mg 4x a day
I noticed some similarities between wumedicals anecdotal SCI neural stem cell treatment case, Asterias prelim cervical AST-OPC1 reports and reports about use of 4-AP (4-Aminopyridine), a potassium channel blocker. They all appear to target demyelinated axons with poor conduction, a consequence of SCI. Asteria even mentions the target of their AST-OPC1 stem cells is demyelinated axons. So I got 4-AP compounded and tested it at 10mg x 4 times a day dose (later went down to 5mg 4x a day
However, French Secretary of State for Health Dr Bernard Kouchner took the decision to ban the jab in light of evidence that the vaccine could cause multiple sclerosis or other forms of central nervous system demyelination. Studies in both France and Britain have shown that, in school aged children, the risk of demyelinating reactions in the central nervous system increases during the two months after vaccination (BMJ, 1998; 317: 1034 ...
Previous studies have clearly demonstrated the indispensable role of IL-17 in the induction and pathogenesis of EAE, which resembles the pattern I and II MS lesions driven by T cell-mediated autoimmune inflammatory response. In this study, we show for the first time that IL-17-mediated signaling plays a critical role in cuprizone-induced demyelination, which shares similarities with pattern III MS lesions associated with apoptosis of myelin-forming oligodendrocytes and pronounced loss of oligodendrocytes. Interestingly, mice deficient in IL-17A, IL-17RC, and adaptor protein Act1 (of IL-17R) displayed diminished demyelination, microglial accumulation, and leukocyte infiltration compared with that in wild-type mice in response to cuprizone. Importantly, astrocytes are highly responsive to IL-17 in vitro, and selective deletion of Act1 in astrocytes ameliorated cuprizone-induced demyelination. Together, these results suggest that IL-17-mediated signaling in astrocytes contributes to the ...
In this study, we investigate the basis of T cell recognition of myelin that governs the progression from acute symptoms into disease remission, relapse, and chronic progression in a secondary progressive model of demyelinating disease. Until now, the frequency and affinity of myelin-reactive CD4 T cells that elicit relapsing-remitting disease have not been quantified. The micropipette adhesion frequency assay was used to obtain a sensitive and physiologically relevant two-dimensional measurement of frequency and TCR affinity for myelin, as the inherent low affinity does not allow the use of specific peptide:MHC-II tetramers for this purpose. We found the highest affinity and frequency of polyclonal myelin oligodendrocyte glycoprotein-reactive cells infiltrate the CNS during acute disease, whereas affinities during remission, relapse, and chronic disease are not significantly different from each other. Frequency analysis revealed that the vast majority of CNS-infiltrating CD4 T cells are myelin ...
T.I. KHAYBULLIN1, 2, F.A. KHABIROV1,2, L.A.AVERIANOVA1, 2, G.M. AKHMEDOVA1, N.N. BABICHEVA2, E.V. GRANATOV2 1 Kazan State Medical Academy, 11 Mushtary St., Kazan, Russian Federation, 420012 2 Republican Clinical Diagnostic Center for Demyelinating Diseases of the Ministry of Healthcare of the Republic of Tatarstan, 13 Vatutina St., Kazan, Russian Federation, 420021 Khaybullin T.I. - PhD (Medicine), Associate Professor of the Department of Neurology and Manual Therapy, tel. (843) 278-88-29, e-mail: [email protected],2 Khabirov […]. ...
... is a chapter in the book, Neurology, containing the following 2 pages: Multiple Sclerosis, Guillain Barre Syndrome.
Central nervous system (CNS) myelination is important for proper nervous system function in vertebrates. In demyelinating diseases such as multiple sclerosis, autoimmune-mediated myelin destruction results in neurological impairment; and although remyelination does occur spontaneously, it is poorly understood and insufficient in humans. Zebrafish (Danio rerio) are known to harbour tremendous regenerative capacity of various CNS tissues; however, there is presently only little knowledge of their myelin repair efficiency. An experimental model of myelin injury in zebrafish would permit study of the mechanisms involved in successful remyelination and could potentially guide the development of novel therapeutic agents for mammalian remyelination. This doctoral thesis describes the characterisation of the novel myelin protein Claudin k in zebrafish, demonstrates the establishment of adult zebrafish as an experimental model for CNS de- and remyelination and explores some mechanisms underlying myelin ...