Listing 1 - 7 of 7 |
Sort by
|
Choose an application
Demyelination disorders are among the most frequent neurological conditions. Types of these disorders include multiple sclerosis, Guillain Barré syndrome, diabetic peripheral neuropathy, entrapment neuropathies, and others, all of which can result in serious physical incapacity and diminished quality of life. This book examines various aspects of demyelination from clinical, diagnostic, and therapeutic points of view. Chapters address different types of demyelination diseases, their associated mechanisms, and pharmacologic and nonpharmacologic treatment approaches, among other topics.
Myelin sheath --- Demyelination. --- Diseases.
Choose an application
Demyelinating disorders are chronic autoimmune disorders characterized by inflammation, demyelination, axonal degeneration, and neuronal loss. They have complex pathophysiology and diverse clinical presentations. The etiology of these disorders lies in the interaction between genetic and environmental factors. Due to the complexity in pathophysiology and presentation, diagnosis and treatment can be challenging. Advanced technology, including modern imaging techniques, as well as optical coherence tomography (OCT), enrich our understanding of the disease process, improve diagnostic accuracy, and may guide treatment decisions.
Demyelination. --- Myelin sheath --- Myelination --- Nervous system --- Diseases
Choose an application
If you are engaged in the treatment of patients with MS (pwMS), this e-book’s aim is to offer novel insights to improve on an understanding of one of the major problems of pwMS: fatigue. Although there is increasing research into fatigue and its impact on MS, this collection of ten articles supports a better understanding of fatigue in MS patients. It explores pathophysiological concepts, provoking mechanisms, objective measurements, personality interactions, pharmacological and non-pharmacological interventions and summarizes clinical management. It is written by neurologists, psychologists, scientists and therapists and addresses this group of people, who deal with pwMS in private, clinical, rehabilitation or scientific settings. Its aim is to communicate high-quality information, knowledge and experience on MS to healthcare professionals, while providing global support for the international MS community.
Multiple sclerosis. --- MS (Disease) --- Sclerosis, Multiple --- Demyelination --- Myelin sheath --- Virus diseases --- Diseases --- Multiple Sclerosis --- cognitive fatigue --- motor fatigue --- Fatigue --- Depression --- Cognition --- Personality --- Rehabilitation --- gait analysis --- natalizumab
Choose an application
Plasticity occurs at multiple levels in multiple sclerosis (MS), from cells to synapses, from myelin to axons, from individual regions to large-scale brain networks. A growing body of evidence supports the notion that the course of MS and its extremely heterogeneous clinical manifestations might be the net result of disease burden and compensatory capacity. As a consequence, identifying what can be considered as "positive" plasticity and what, on the contrary, is a maladaptive reorganization is a very attractive goal which might help to develop therapeutic strategies able to promote the individual adaptive capacity. The aim of this Research Topic forum is to provide a state of the art update on the diversity of available data in humans with MS, derived from the many studies performed using different research tools, including immunological, neurophysiological and neuroimaging techniques which have addressed neuroplasticity at multiple system level, from motor, to visual, and cognitive. Synopsis of recent advances of plasticity research in MS aims to broaden the view across systems and techniques and to stimulate further studies on this emerging topic.
Neuroplasticity. --- Multiple sclerosis --- Research. --- Multiple Sclerosis --- motor --- cognitive --- Compensation --- Neurophysiological --- plasticity --- adaptation --- visual --- reorganization --- functional magnetic resonance imaging --- MS (Disease) --- Sclerosis, Multiple --- Demyelination --- Myelin sheath --- Virus diseases --- Nervous system plasticity --- Neural adaptation --- Neural plasticity --- Neuronal adaptation --- Neuronal plasticity --- Plasticity, Nervous system --- Soft-wired nervous system --- Synaptic plasticity --- Adaptation (Physiology) --- Neurophysiology --- Developmental neurobiology --- Diseases
Choose an application
Multiple sclerosis (MS) is one of the most common neurological disorders in young adults. The etiology of MS is not known, but it is generally accepted that it is autoimmune in nature. Our knowledge of the pathogenesis of MS has increased tremendously in the past decade through clinical studies and the use of experimental autoimmune encephalomyelitis (EAE), a model that has been widely used for MS research. Major advances in the field, such as understanding the roles of pathogenic Th17 cells, myeloid cells, and B cells in MS/EAE, as well as cytokine and chemokine signaling that controls neuroinflammation, have led to the development of potential and clinically approved disease-modifying agents (DMAs). There are many aspects related to the initiation, relapse and remission, and progression of MS that are yet to be elucidated. For instance, what are the genetic and environmental risk factors that promote the initiation of MS, and how do these factors impact the immune system? What factors drive the progression of MS, and what are the roles of peripheral immune cells in disease progression? How do the CNS-infiltrated immune cells interact with the CNS-resident glial cells when the disease progresses? What is the role of microbiome in MS? Can we develop animal models that better represent subcategories of MS? Understanding the cellular and molecular mechanisms that govern the pathogenesis of MS will help to develop novel and more specific therapeutic strategies that will ultimately improve clinical outcomes of the treatments. This Special Issue of Cells has published original research articles, a retrospective clinical report, and review articles that investigate the cellular and molecular basis of MS.
neutrophils --- lymphocytes --- NLR --- multiple sclerosis --- disease activity --- inside-out --- outside-in --- oligodendrocytosis --- demyelination --- gliosis --- histology --- top-down proteomics --- bioinformatics --- mitochondria --- CD4+ T cells --- memory T cells --- autoimmune disease --- effector memory T cell --- central memory T cell --- tissue-resident T cell --- experimental autoimmune encephalomyelitis --- monocytes --- granulocyte-macrophage colony-stimulating factor --- S100B --- relapsing–remitting experimental autoimmune encephalomyelitis --- pentamidine --- NG2-glia --- progenitors --- lineage --- in utero electroporation --- morphometric analyses --- clonal analyses --- lesioned brain --- sphingosine-1-phosphate receptors --- glutamate synaptic dysfunction --- microglia --- T lymphocytes --- experimental autoimmune encephalomyelitis (EAE) --- pro-inflammatory cytokines --- neuroinflammation --- ozanimod --- AUY954 --- A971432 --- S1P1 --- S1P5 --- kynurenine pathway --- kynurenic acid --- oxidative stress --- quinolinic acid --- N-acetylserotonin --- IDO --- NAD+, multiple sclerosis --- laquinimod --- n/a --- relapsing-remitting experimental autoimmune encephalomyelitis
Choose an application
The adult vertebrate central nervous system mainly consists of neurons, astrocytes, microglia cells, and oligodendrocytes. Oligodendrocytes, the myelin-forming cells of the CNS, are subjected to cell stress and subsequent death in a number of metabolic or inflammatory disorders, among which multiple sclerosis (MS) is included. This disease is associated with the development of large demyelinated plaques, oligodendrocyte destruction, and axonal degeneration, paralleled by the activation of astrocytes and microglia as well as the recruitment of peripheral immune cells to the site of tissue injury. Of note, viable oligodendrocytes and an intact myelin sheath are indispensable for neuronal health. For example, it has been shown that oligodendrocytes provide nutritional support to neurons, fast axonal transport depends on proper oligodendrocyte function, and mice deficient in mature myelin proteins eventually display severe neurodegeneration. This Special Issue contains a collection of highly relevant primary research articles as well as review articles focusing on the development, physiology, and pathology of the oligodendrocyte–axon–myelin unit.
plasma membrane proteins --- liquid chromatography-mass spectrometry --- murine acute brain slices --- reproducibility --- rat cerebellum --- Nsun5 --- Williams-Beuren syndrome (WBS) --- corpus callosum (CC) --- oligodendrocyte (OL) --- myelination --- remyelination --- EGFR inhibitor --- smoothened agonist --- microfibers --- drug screening --- multiple sclerosis --- cuprizone --- atrophy --- design-based stereology --- 18F-FDG --- macromolecular proton fraction --- MPF --- myelin --- magnetic resonance imaging --- cuprizone model --- demyelination --- oligodendrocyte precursors --- oligodendrocytes --- immunohistochemistry --- oligodendrocyte --- epigenetics --- neurodegeneration --- laquinimod --- energy drinks --- caffeine --- taurine --- neuron --- OPC --- oligodendrocyte progenitor cells --- screening --- nanofibers --- DigiGait™ --- experimental autoimmune encephalomyelitis --- gait analysis --- schizophrenia --- interneuron --- pluripotent stem cells --- cognition --- treatment --- cre-recombinase --- experimental autoimmune encephalomyelitis (EAE) --- glial progenitor cells --- tamoxifen --- down syndrome --- white matter --- glial fate --- transient receptor potential ankyrin 1 --- astrocyte --- conditional knockout --- astrocytes --- white matter disease --- cross-talk --- CNS --- glial cells. --- age --- microglia --- n/a
Choose an application
A Special Issue in memory of Randall J. Cohrs, Ph.D. Topics include original research reports on a variety of viruses as well as reviews and commentaries on Randy’s contributions to many investigations.
Research & information: general --- Biology, life sciences --- varicella-zoster virus --- Oka strain --- human herpesvirus 6 --- human herpesvirus 7 --- corticosteroids --- serious adverse event --- herpes zoster --- IL-6 --- IL-10 --- innate immunity --- VLT --- VLT-ORF63 --- CRISPR/Cas9 --- BAC mutagenesis --- flavivirus --- SARS-CoV-2 --- pandemic preparedness --- host–virus interactions --- prion --- vaccines --- interferon lambda --- virus --- herpes simplex virus type 1 --- herpes simplex virus type 2 --- neonatal herpesvirus infection --- HSV UL6 --- herpesvirus encephalitis --- herpesvirus hepatitis --- acyclovir --- HerpeSelect test --- viral sequencing --- HELLP syndrome --- lipids --- dengue virus --- acyl-CoA --- acyl-CoA thioesterase --- fatty acids --- membranes --- rheostat --- fatty acyl-CoA --- Marek’s disease virus --- live-cell genome visualization --- lytic replication --- T cells --- latency --- genome integration --- TetO/TetR system --- varicella zoster virus --- reactivation --- genome cleavage --- AAV --- antiviral therapies --- HSV-1 --- cornea --- trigeminal ganglia --- interferon-γ --- interferon stimulatory genes --- TRIM21 --- HSV --- EBV --- KSHV --- MHV68 --- PIC --- transcription --- productive elongation --- mRNA --- rRNA --- tRNA --- herpes --- viral reactivation --- spaceflight --- dermatitis --- stress --- immune depression --- antiviral drugs --- bacterial artificial chromosome --- luciferase --- bioluminescence imaging --- skin organ culture --- humanized mice --- β-Coronavirus --- mouse hepatitis virus-A59/MHV-A59 --- mouse hepatitis virus-2/MHV2 spike protein --- fusion peptide/FP --- cell-to-cell fusion (fusogenicity) --- neuropathogenesis --- hepatitis --- demyelination --- structural rigidity --- simian varicella virus --- herpesvirus --- varicella --- VZV --- neuro-attenuated --- ORF7 --- vaccine --- n/a --- antiviral --- COVID-19 --- drug discovery --- coronavirus --- spike protein --- Mpro --- RdRp --- PLpro --- skin --- epidermis --- keratinocytes --- epidermal differentiation --- cutaneous blistering lesions --- keratins --- autophagy --- immunity --- human neuron culture --- non-coding RNA --- CD8 T cell --- T-cell epitope --- NK cell --- KIR3DL1 --- HLA-B*57:01 --- herpes simplex virus --- zoster --- skin pathogenesis --- HSV-2 --- neurons --- cell culture --- varicella-zoster --- gene expression --- ganglion --- autopsy --- saliva --- salivary VZV DNA --- dengue viruses --- Aedes aegypti --- adaptive mutation --- host-virus interactions --- Marek's disease virus
Listing 1 - 7 of 7 |
Sort by
|