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11:00, 01 March 2018

Bench to Bedside: Myelination 1 – Myelination, Remyelination and Multiple Sclerosis – Mikael Simons


Improving our understanding of nerve cell (may refer to) myelination (is a fatty white substance that surrounds the axon of some nerve cells, forming an electrically insulating layer) and remyelination in both animal models and humans may to improve treatment for demyelinating diseases such as multiple sclerosis.   Part 1: Myelination, Remyelination and Multiple Sclerosis (is a hardening of tissue and other anatomical features; it may refer to: Sclerosis (medicine), a hardening of tissue in zoology, a process which hardens forms sclerites, a hardened exoskeleton in): During multiple sclerosis, the myelin sheath around axons is destroyed and nerve function is lost.  Yet sometimes a few lesions undergo remyelination.  Why? And how can this be improved?   Part 2: Neuropathology of Multiple Sclerosis: Better understanding of the brain (brain is an organ that serves as the center of the nervous system in all vertebrate and most invertebrate animals) pathology that correlates with the progression of multiple sclerosis may improve diagnosis and treatment. https://www.ibiology.org/ibioeducation/myelination-remyelination-multiple-sclerosis.html Talk Overview: Multiple (may refer to) sclerosis (MS) is a debilitating autoimmune disease in which immune cells infiltrate the central nervous system and attack the myelin sheath surrounding axons.  Dr. Simons explains that myelin is necessary for signal conduction by nerve cells and for the metabolic support of axons (axon (from Greek ἄξων áxōn, axis) or nerve fiber, is a long, slender projection of a nerve cell, or neuron, that typically conducts electrical impulses known as action potentials, away from the). Demyelination results in axonal loss and formation of lesions in the brain. A small percentage of MS lesions are capable of remyelination following steps similar to axonal myelination during normal development.  Since lesion remyelination (is the process of propagating oligodendrocyte precursor cells to form oligodendrocytes to create new myelin sheaths on demyelinated axons in the CNS) correlates with reduced neurodegeneration, Simons and his colleagues strive to understand why remyelination occurs in only a small number of MS patients and to identify drugs that may promote it.    MS begins as a disease of intermittent episodes with (or WITH may refer to: Carl Johannes With (1877–1923), Danish doctor and arachnologist With (character), a character in D. N. Angel With (novel), a novel by Donald Harrington With (album),) recovery in between. With time, however, MS changes to a progressive disease with increasing disability.  In her talk, Dr. Stadelmann explains that studies of MS brain lesions (lesion is any abnormal damage or change in the tissue of an organism, usually caused by disease or trauma) have identified specific changes that occur with disease progression (may refer to: In mathematics: Arithmetic progression, sequence of numbers such that the difference of any two successive members of the sequence is a constant Geometric progression, sequence of). For example, chronic MS lesions contain many fewer oligodendrocytes than do early lesions.  Since oligodendrocytes produce the myelin (is a fatty white substance that surrounds the axon of some nerve cells, forming an electrically insulating layer) sheath that surrounds axons, drugs that stimulate the migration and establishment of oligodendrocytes in lesions may increase axonal remyelination and improve the prognosis of MS patients. Stadelmann also explains that brain lesions can be caused by conditions other than MS, such as neuromyelitis optica.  Improved studies will help to correctly diagnose and treat these distinct diseases.   About Mikael Simons: Dr. Simons’ research focuses on developing new ways to promote remyelination of damaged axons in demyelinating diseases (disease is a particular abnormal condition that affects part or all of an organism not caused by external force (see ‘injury’) and that consists of a disorder of a structure or function, usually) such as multiple sclerosis (MS). To reach this goal, his lab strives to better understand the cellular processes underlying myelin formation in normal development.   Simons received his MD from the University (university (Latin: universitas, “a whole”) is an institution of higher (or tertiary) education and research which awards academic degrees in various academic disciplines) of Heidelberg and did his residency in neurology at the University of Tübingen. He joined the University of Göttingen in 2004 and, in 2016, he moved to Munich to become Director of the Institute of Neuronal Cell Biology at the Technical University, and the German Center for Neurodegenerative Diseases. Learn more about Dr. Simons (may refer to)’ research here: http://www.neuroscience.med.tum.de/index.php?id=5 About Christine Stadelmann: Dr. Stadelmann is a Professor and Deputy Director of the Institute for Neuropathology at the University of Göttingen Medical Center.  Her studies focus on inflammatory diseases of the central nervous system including multiple sclerosis and neuromyelitis optica. She is particularly interested in understanding which pathological events correlate (statistics, dependence or association is any statistical relationship, whether causal or not, between two random variables or bivariate data) with disease progression. Learn more about Dr. Stadelmann’s research here: http://www.neuropathologie.med.uni-goettingen.de/deutsch/forschung/ag-c.stadelmann.htmFrom: iBiology

Source: https://www.youtube.com/watch?v=hEFdVPkQfJk


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