BACKGROUND: Traumatic injury to axons produces breakdown of axons and myelin at the site of the lesion and then further distal to this where Wallerian degeneration develops. The rapid removal of degenerated myelin by phagocytosis is advantageous for repair since molecules in myelin impede regeneration of severed axons. Thus, revealing mechanisms that regulate myelin phagocytosis by macrophages and microglia is important. We hypothesize that myelin regulates its own phagocytosis by simultaneous activation and down-regulation of microglial and macrophage responses. Activation follows myelin binding to receptors that mediate its phagocytosis (e.g. complement receptor-3), which has been previously studied. Down-regulation, which we test here, follows binding of myelin CD47 to the immune inhibitory receptor SIRPalpha (signal regulatory protein-alpha) on macrophages and microglia.. METHODS: CD47 and SIRPalpha expression was studied by confocal immunofluorescence microscopy, and myelin phagocytosis by ...
The thickness of the myelin sheath that insulates axons is fitted for optimal nerve conduction velocity. Here, we show that, in Schwann cells, mammalian disks large homolog 1 (Dlg1) interacts with PTEN (phosphatase and tensin homolog deleted on chromosome 10) to inhibit axonal stimulation of myelination. This mechanism limits myelin sheath thickness and prevents overmyelination in mouse sciatic nerves. Removing this brake results also in myelin outfoldings and demyelination, characteristics of some peripheral neuropathies. Indeed, the Dlg1 brake is no longer functional in a mouse model of Charcot-Marie-Tooth disease. Therefore, negative regulation of myelination appears to be essential for optimization of nerve conduction velocity and myelin maintenance.. ...
The myelin sheath is found surrounding axons of the both the central and peripheral nervous system. Axons may be myelinated or unmyelinated. In myelinated axons the sheath is arranged with small gaps known as the nodes of Ranvier, this is where the action potentials are generated as this is where the majority of the axons ion channels are located. This article shall discuss the myelin sheath, its affect on transmission of signals in the nervous system and relevant clinical conditions.
We show here that β1 integrins are required for the myelination of axonal tracts in the CNS and we establish a link between β1 integrins and AKT in oligodendrocyte function. Myelin thickness was reduced in the spinal cord, cerebellum and optic nerve of Itgb1-CNSko mice without a reduction in oligodendrocyte numbers. These findings suggest that the myelination defects in mutant mice were caused by perturbations in the formation of myelin membrane sheaths. Consistent with this finding, myelin outgrowth was substantially impaired in cultured β1-deficient oligodendrocytes. Myelination was also affected in the spinal cord of Itgb1-OL-ko mice, providing additional evidence that β1 integrins act, at least in part, cell-autonomously in oligodendrocytes to regulate myelination. Interestingly, activation of AKT signaling was affected in cultured β1-deficient oligodendrocytes. Furthermore, myelin membrane sheet formation in the β1-mutant cultured cells was restored by inhibiting PTEN or by ...
We report a large family with a multigenerational pedigree of HMSN with focally folded myelin sheaths. The family studied allowed us to uncover the genetic findings, clinical spectrum, and natural history of HMSN with focally folded myelin sheaths, and to highlight the significant intrafamily uniformity of clinical presentation.. Focally folded myelin sheaths are the pathologic hallmark of certain hereditary neuropathies of wide clinical spectrum. 11-14,21-26 Of the 23 cases reported, 10 patients came from five families, whereas 13 cases were sporadic. In two cases, an autosomal-dominant mode of inheritance was postulated. 24 The reports of Dayan et al., 27 Nordborg et a1., 28 and Lutschg et al. 29 were not included because published pathologic data were not detailed enough for a comparison with ours.. In our family, the genealogic study showing the high consanguinity rate represents strong evidence in favor of an autosomal-recessive pattern of inheritance, confirming the hypothesis postulated ...
Oligodendrocytes in the central nervous system (CNS) produce myelin sheaths that insulate axons to ensure fast propagation of action potentials. beta1 integrins regulate the myelination of peripheral nerves, but their function during the myelination of axonal tracts in the CNS is unclear. Here we show that genetically modified mice lacking beta1 integrins in the CNS present a deficit in myelination but no defects in the development of the oligodendroglial lineage. Instead, in vitro data show that beta1 integrins regulate the outgrowth of myelin sheaths. Oligodendrocytes derived from mutant mice are unable to efficiently extend myelin sheets and fail to activate AKT (also known as AKT1), a kinase that is crucial for axonal ensheathment. The inhibition of PTEN, a negative regulator of AKT, or the expression of a constitutively active form of AKT restores myelin outgrowth in cultured beta1-deficient oligodendrocytes. Our data suggest that beta1 integrins play an instructive role in CNS myelination ...
Bekijk Stockfoto van Cryofracture Preparation Of A Sciatic Nerve Crosssection Showing The Myelin Sheaths Around Nerve Fibers The Myelin Sheath Is Formed From Successive Wrapping Of The Schwann Cell Plasma Membrane Around The Axon. Ga voor hoogwaardige fotos met een hoge resolutie naar Getty Images.
The main myelin sheath function is:. It acts as an electrical insulator for the neuron - it prevents the penetration of electrical impulses through the shield.. In myelin sheath function, The sheath prevents ion migration to or from the neuron / prevents depolarization.. Accelerates the transmission of the electrical impulse in the neuron - impulses cannot pass through the shield (the shield acts as an electrical insulator), instead, the pulses "jump" from the gap in the myelin sheath to another gap (it jumps from one Ranvier node to another).. ...
Myelin sheath serves as an insulator that surrounds the nerves. This includes the nerves in the brain and spinal cord. This layer is made up of fatty substances, as well as protein. Its purpose is to allow impulses to transfer quickly and efficiently along the nerve cells. If the myelin sheath layer is damages the impulses will slow down and it can cause diseases such as multiple sclerosis. In addition, Myelin Sheath is roughly 200 and 800 μm thick and diseases can also thin out the layer causing the level of protection to obviously decrease. ...
The myelination of central nervous system (CNS) axons by oligodendrocytes enables fast and energy‐efficient propagation of action potentials as well as axonal support [[1], [2]]. The absence of the second most abundant CNS myelin protein MBP results in severe hypomyelination, shivering symptoms and premature death in rodents [[3]]. MBP compacts myelin membranes, binds to cytoskeletal proteins and is involved in oligodendroglial calcium signalling [[4], [5]]. Moreover, it regulates the molecular composition of the glial plasma membrane, facilitating the formation of lipid‐rich myelin domains required for effective axon insulation [[6], [7]]. Therefore, appropriate MBP levels are important to maintain oligodendroglial homeostasis as well as functional myelin membrane formation. During oligodendrocyte maturation, MBP transcription precedes translation by about 1 day [[8], [9]], but the mechanisms underlying this translational repression of MBP remain poorly understood. Axon-glial signalling ...
TY - CHAP. T1 - Myelin and Myelination. AU - Aschner, Michael. AU - Toews, A. D.. PY - 2010/8/12. Y1 - 2010/8/12. N2 - A compound may be neurotoxic by virtue of being targeted to perturb some metabolic, structural, or functional property characteristic of myelin or myelinating cells. Myelin and myelination are described in this section, with emphasis on points relevant to understanding neurotoxic mechanisms. More information is readily available in collections of more specialized reviews of subtopics relevant to myelin.. AB - A compound may be neurotoxic by virtue of being targeted to perturb some metabolic, structural, or functional property characteristic of myelin or myelinating cells. Myelin and myelination are described in this section, with emphasis on points relevant to understanding neurotoxic mechanisms. More information is readily available in collections of more specialized reviews of subtopics relevant to myelin.. UR - ...
The mechanisms that regulate myosin II activity in SC and OL during myelination are not yet known. In SC, phosphorylation of the regulatory chain of myosin II (MLC2) is up-regulated at the onset of myelination and then down-regulated (Melendez-Vasquez et al., 2004), following the same pattern of Rho activation in peripheral nerve extracts (unpublished data). Our previous studies revealed an important role for ROCK during the initial events of PNS myelination, possibly by regulating the phosphorylation status of MLC (Melendez-Vasquez et al., 2004). However, inhibition of ROCK did not interfere with the wrapping of the axon, which suggests that another ROCK-independent mechanism controls the actual motor of SC adaxonal membrane progression around the axon. Our current study extends these initial observations and provides further evidence of the important role of polarized actomyosin contraction for SC myelin formation. Similar to our previous results with a ROCK-specific pharmacological inhibitor, ...
Remyelination is the process of propagating oligodendrocyte precursor cells to form oligodendrocytes to create new myelin sheaths on demyelinated axons in the CNS. This is a process naturally regulated in the body and tends to be very efficient in a healthy CNS. The process creates a thinner myelin sheath than normal, but it helps to protect the axon from further damage, from overall degeneration, and proves to increase conductance once again. Demyelinating diseases, such as Multiple Sclerosis, have been of utmost interest within the last couple of decades. Recent research is uncovering some of the many unknown pathways involved with remyelination in hopes of battling demyelinating diseases like MS which can ultimately cripple a person. While no treatment exists yet in preventing remyelination failure in the chronic stages of these diseases, future research may yet prove to unlock key pathways that can be targeted. Remyelination is activated and regulated by a variety of factors surrounding ...
... is a dielectric (electrically insulating) material that forms a layer, the myelin sheath, usually around only the axon of a neuron. It is essential for the proper functioning of the nervous system. Myelin is an outgrowth of a glial cell. The production of the myelin sheath is called myelination. The production of myelin occurs in the fourteenth week of fetal development, while very little amounts of myelin exist in the brain at the time of birth. During infancy myelination occurs quickly and does not stop until the adolescent stages of life. Because of this rapid myelination, it is essential that children under the age of two receive a diet higher in fats than one of an adult.. Schwann cells supply the myelin for peripheral neurons, whereas oligodendrocytes, specifically of the interfascicular type, myelinate the axons of the central nervous system. Myelin is considered a defining characteristic of the (gnathostome) vertebrates, but it has also arisen by parallel evolution in some ...
The myelin membrane synthesised by oligodendrocytes in the central nervous system (CNS) and Schwann cells in the peripheral nervous system (PNS) provides electric insulation to axons thus enabling the fast saltatory impulse conduction essential for vertebrate nervous system function. Moreover, myelinating glial cells provide trophic support to neurons which is not understood in molecular terms. Myelin is produced and maintained in response to bidirectional communication between neurons and glial cells. Abnormal axon-glia interaction and defects in myelin formation result in demyelinating diseases such as leukodystrophies and hereditary neuropathies, which are characterized by severe neurodegeneration resulting in long term disability and in severe cases premature death. In the common demyelinating disease Multiple Sclerosis similar symptoms arise due to destruction of the myelin sheath by invading immune cells.. We are studying the properties of oligodendrocyte precursor cells (OPC) and the ...
Marie Bechler, a senior researcher in the ffrench-Constant laboratory at the MRC Centre for Regenerative Medicine, said: "The aligned Mimetix scaffold fibres from AMSBIO have been an invaluable tool, allowing us to answer fundamental questions regarding how oligodendrocytes form central nervous system (CNS) myelin sheaths. The suppliers of the Mimetix fibres worked with us to create customised three-dimensional fibres, facilitating the development of an oligodendrocyte culture assay. The culture system we developed permits the examination of myelin sheath formation in the absence of neurons. The aligned microfibres used in our research have enabled us to examine both the physical and molecular signals sufficient to drive CNS myelin sheath formation, which could not be assessed in other culture models. This has opened new opportunities to examine the role of physical cues, heterogeneity due to oligodendrocyte origin, and the sufficiency of molecules to control the number and size of myelin ...
We set up the Cambridge Centre for Myelin Repair in 2005, with the aim of developing treatments that promote myelin repair for people with MS.. Since it opened the Cambridge Centre has created a world-class research environment involving researchers from all around the UK - most notably at our Edinburgh Centre for MS Research.. Scientists at both centres have worked together to show that a molecule called RXR-gamma could encourage the brains own stem cells to repair myelin in animal models of MS. Researchers will now test the benefits of a drug that targets RXR-gamma, called bexarotene, in a phase 2 clinical trial.. We announced four more years of funding for the Cambridge Centre in 2016. Researchers will continue to investigate the fundamental mechanisms behind myelin repair, with the hope of developing new treatments.. They will focus on understanding more about the cells capable of repairing myelin, and the impact ageing and lifestyle factors (such as diet and exercise) can have on these ...
Research Grant Recipient: Mi-Hyeon Jang, PhD. Grant Period: 2017-2019. Award Value: $249,998. Site: University of Minnesota. Summary: Multiple sclerosis and other diseases attack the myelin, a sheath that insulates the nerves. Dr. Jang is investigating the underlying molecular mechanisms of myelin regeneration in an effort to develop a therapy to help patients.. Mi-Hyeon Jang, PhD, is an Assistant Professor of Biochemistry and Molecular Biology and Assistant Professor of Neurosurgery at Mayo Clinic.. ...
Glial cells produce myelin and contribute to axonal morphology in the nervous system. Two myelin membrane proteolipids, PLP and DM20, were shown to be essential for the integrity of myelinated axons. In the absence of PLP-DM20, mice assembled compact myelin sheaths but subsequently developed widespread axonal swellings and degeneration, associated predominantly with small-caliber nerve fibers. Similar swellings were absent in dysmyelinated shiverer mice, which lack myelin basic protein (MBP), but recurred in MBP*PLP double mutants. Thus, fiber degeneration, which was probably secondary to impaired axonal transport, could indicate that myelinated axons require local oligodendroglial support. ...
Multiple sclerosis is a debilitating condition that is characterized by damage to the myelin sheath, the insulating layer that protect nerve fibers in the brain to enable efficient communication between the nerve cells and the brain in the central nervous system. A possible MS treatment that researchers look into aim to identify ways to repair the damaged myelin sheath. A promising method being looked into is trying to make use of stem cells to help in myelin repair in people with MS. The potential use of stem cells for myelin repair has recently found a breakthrough as researchers from the Universities of Cambridge and Edinburgh have identified a biological switch that would enable stem cells to regenerate myelin in lab rats. The findings of the said study was published in the journal Nature Neuroscience. In the said study, the researchers looked at how the stem cells of MS patients repair myelin. During the course of the study, they have been able to identify a specific type of molecule called RXR
Myelinogenesis is generally the proliferation of myelin sheaths throughout the nervous system, and specifically the progressive myelination of nerve axon fibers in the central nervous system. This is a non-simultaneous process that occurs primarily postnatally in mammalian species, beginning in the embryo during the midst of early development and finishing after birth. The myelination process allows neuronal signals to propagate down an axon more swiftly without the loss of signal. This enables better connectivity within specific brain regions and also improves broader neuronal pathways connecting spatially separate regions required for many sensory, cognitive, and motor functions. Some scientists consider myelination to be a key human evolutionary advantage, enabling greater processing speeds that lead to further brain specialization. Myelination continues for at least another 10 to 12 years after birth before an individual is fully developed. While the rate at which individual children develop ...
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 ...
1. The lipids of whole brain and subcellular fractions of the rat were analysed during development. 2. The deposition of cholesterol occurred in two phases, one related to increasing wet weight of the brain and the second to myelination. Cerebroside accumulation was related only to myelination. 3. The composition of myelin isolated from 12-day-old rat brain was different in some respects from that of the adult. In the former there was an increase of phospholipid in relation to cholesterol and a marked deficiency in cerebroside. 4. It is suggested that early myelin is extruded glial plasma membrane, which only later becomes mature myelin.. ...
Research on myelination offers centered on identifying molecules capable of inducing oligodendrocyte (OL) differentiation in an effort to develop strategies that promote functional myelin regeneration in demyelinating disorders. of and gene manifestation, mediated from the connection of SMAD3/4 with Sp1 and FoxO1 transcription factors. Our study is the 1st to demonstrate an autonomous and important part of TGF signaling in OL development and CNS myelination, and may provide new avenues in the treatment of demyelinating diseases. studies have shown that O-2A progenitor cells express TGF1 and that TGF signaling activation exerts an anti-mitogenic effect countering PDGFR signaling, in turn promoting cell cycle arrest (McKinnon et al., 1993). Moreover, Activin-A, a member of the TGF superfamily, has been proposed as one of the cytokines secreted by microglial cells that plays a role in OL regeneration and remyelination (Miron et al., 2013). These scholarly research claim that TGF signaling could be ...
Kelton, D E., "Myelin degeneration in the central nervous system of dilute-lethal mice. Abstr." (1961). Subject Strain Bibliography 1961. 484 ...
Interested in MS myelin sheath repair? Chat to the MS community and watch multiple sclerosis researchers explain their work on repairing damaged myelin.
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Discover what role the myelin sheath plays in our day-to-day lives, how it works, and how it can become damaged by certain conditions (multiple sclerosis).
TY - JOUR. T1 - Dysglobulinemic neuropathy. T2 - Absence of immunoglobulin within myelin sheaths. AU - Rodriguez, M.. AU - Powell, H. C.. PY - 1986. Y1 - 1986. UR - http://www.scopus.com/inward/record.url?scp=0022636706&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0022636706&partnerID=8YFLogxK. M3 - Article. VL - 19. SP - 204. EP - 206. JO - Annals of Neurology. JF - Annals of Neurology. SN - 0364-5134. IS - 2. ER - ...
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In MS, myelin in the brain and spinal cord is destroyed. Though HEALTHY human systems have the natural ability to repair myelin damage, in MS where damage occurs, SCARS of hardened sclerotic tissue INHIBIT and/or PREVENT that process from taking place. There is no cure for MS. Myelin loss has also been linked to a number of other neurological diseases including Parkinsons disease, Alzheimers disease, and depression ...
Myelin Sheaths is not front women Cassandra Ward. However, Cassandra Ward is the front women of Myelin Sheaths, the phenomenal garage four piece straight from Canada. I know (honestly I do), how constantly blogs these are gushing about the latest garage flash-in-the-pan, who release a very awesome single only to be ignored next releases time. Well Myelin Sheaths are the real deal. These are tunes from their brand Get On Your Nerves LP of of South Paw Records (who have brought us other lovely release from Young Governor, and The White Wires), are pure Jay Reatard worship and its wonderful. "Gloves/Mutations" in particular is a great ode to "Blood Visions", and the way the band manages to pull of instrumental intro into the chantey main song is proof of their garage-punk hybrid perfection ...
Our results provide direct evidence that the mechanism of Hes5‐dependent regulation of gene expression is dependent on the developmental stage and cellular context and therefore extend our understanding on the mechanism of action of this important transcription factor. In mammalian cells, Hes family members (Hes1, Hes3 and Hes5) have been implicated as modulators of neural (Ohtsuka et al, 1999; Cau et al, 2000; Hatakeyama et al, 2004) and astrocytic (Wu et al, 2003) differentiation during embryonic development. A previous study in embryonic neuroepithelial cells isolated from the murine spinal cord, suggested that Hes5 expression was transient and confined to precursors or very early progenitors and thereby questioned its possible role as direct regulator of myelin gene expression (Wu et al, 2003). Our results in immortalized murine cortical neonatal progenitors are in agreement with several other studies reporting the expression of Hes5 in the postnatal brain (Stump et al, 2002) and in ...
I thought multiple sclerosis sufferers suffer from damaged myelin sheath, and this leads to inflammation and the immune system begins to attack the myelin. I think you are getting confused with the terms. Multiple sclerosis is the disease by which people are diagnosed with it if their immune system attacks the myelin sheath(when it is damaged), thus a weaker nervous system(because the nerve cells can no longer conduct the impulses). Myelin sheath provides protection of the axon and electrical insulation ...
Myelin loss and axonal damage are both observed in white matter injuries. Each may have significant impact on the long-term disability of patients. Currently, there does not exist a non-invasive biological marker that enables differentiation between myelin and axonal injury.. Diffusion tensor imaging (DTI) has been widely applied in the CNS for detailed analyses of tissue morphology and pathology. The primary parameters accessible from DTI, the directional diffusivities, are often combined into summary parameters sensitive to tissue pathology and morphology. However, such parameters lack specificity to detect and differentiate axon vs. myelin degeneration.. His research lab has taken a different approach to analyze DTI parameters for detecting and differentiating axon vs. myelin degeneration in various mouse models of white matter injury. Dr. Song hopes to translate our animal findings into clinical settings. Current studies include the following:. • Examination of demyelination and ...
Dr Jessica Fletcher, funded by an MS Research Australia Postdoctoral Fellowship, with the support of the Trish MS Research Foundation, has been working with Dr Simon Murray and Dr Junhua Xiao at The University of Melbourne, investigating novel molecular targets for promoting remyelination in the brain. Myelin coats the nerve cells in the brain and spinal cord. In MS there is damage to the myelin, and in the early stages of the disease there is some ability to repair the myelin, a process known as remyelination. Over time the bodys ability to remyelinate becomes impaired, leading to incomplete repair and contributing to the progression of MS symptoms. It is crucial to identify potential new treatment targets that can promote myelin repair, prevent nerve damage and halt MS disease progression.. Dr Fletcher has been working on a nerve growth factor, known as brain-derived neurotrophic factor (BDNF), which has been found to promote myelination by activating different receptors, or docking stations, ...
Multiple sclerosis is a serious neurological condition that has no known cure. Although the causes are far from being known, we do know that the immune system erroneously attacks the protective sheaths around nerve fibres. Scientists at Friedrich-Alexander-Universität Erlangen-Nürnberg have discovered how the formation of myelin sheaths is regulated by protein molecules. This knowledge could be used to help MS patients by stimulating the formation of new myelin sheaths after a relapse.
Deibler, G., Driscoll, B., andKies, M. 1978. Immunochemical and biochemical studies demonstrating the identity of a bovine spinal cord protein (SEP) and a basic protein of bovine peripheral myelin (BF). J. Neurochem. 30:401-412.PubMedGoogle Scholar ...
Early in 2016 Dr David Gonsalvez was awarded a prestigious Betty Cuthbert Postdoctoral Fellowship co-funded by National Health and Medical Research Council / MS Research Australia, with MS Research Australias contribution provided with full funding support from the Trish MS Research Foundation. MS results from the damage and loss of myelin, the conductive layer present around nerve fibres in the brain and spinal cord. This makes the nerve fibres unable to transmit their electrical signals, but also leaves the nerves very vulnerable to permanent damage. Myelin can be repaired, but this process is often incomplete and the failure of remyelination is thought to contribute to the development of the secondary progressive form of MS. At the moment there are no treatment options available that promote the repair of myelin to restore lost function and prevent further disability in people with MS. It is known the myelin repair is inhibited by some of the chemicals and physical features associated with ...
Read about the mechanism that may explain why patients with multiple sclerosis (MS) have higher probabilities to suffer from epilepsy.
We know that neurons are encapsulated by myelin. But what makes the myelin? The brain contains two major classes of cells: neurons and glia. Glia are responsible for creating the myelin sheath, as well as having many other functions. There are different kinds of glia, including Schwann cells, oligodendrocytes, astroctytes, microglia, and more. The Schwann cells…
In MS, cells of the immune system attack the central nervous system (CNS), namely myelin, the element that covers and protects nerve cells, and the nerve fibers themselves. CNS inflammation, demyelination, and axon loss are all hallmarks of the disease, which is mostly associated with motor and sensory symptoms. A large percentage of the MS patient population also experience some level of cognitive problems, such as memory loss and difficulty processing information. Because such cognitive impairment is not prevented through current therapies targeting immune system overactivation and myelin damage, the researchers theorized that additional damage was happening to CNS neurons located outside those brain areas known to be affected by myelin loss ...
Fortunately, Im bright enough to evaluate this extraordinary new method:. http://www.sciencedaily.com/releases/2011/09/110913103211.htm#.TnDL-iVvIQs.mailto. There are vague mentions in the literature of myelination in CRPS, but researchers are so busy trying to figure out how to pill CRPS -- a highly pillable disease -- that such mechanistic issues get surprisingly little play. Myelin is the protective sheath of fat that keeps your neurons safe and warm, so they can do their work. Without myelin, your nerves cant fire properly -- or else they cant stop firing. They need the myelin sheath. Little kids need to take in a certain amount of cholesterol so their growing bodies can build good myelination. Demyelination, that is, the loss of that sheath, is most famously known for its role in Lou Gherigs disease. Ive long suspected that demyelination is both an important sign of disease progress and a powerful contributing factor to further degeneration of the peripheral, if not the central, ...
Myelin, a layer that protects nerve fibers in the brain, speeds up transfer of brain signals and boosts them, thus increasing the possibility of new treatments.
It was discovered early on that the myelin - the fatty sheath of insulation surrounding nerve fibres - in the central nervous system is different from that in the periphery. In particular, it inhibits nerve growth. A number of groups have tried to figure out what components of central myelin are responsible for this activity. Myelin is composed of a large number of proteins, as well as lipid membranes. One of these, subsequently named Nogo, was discovered to block nerve growth. This discovery prompted understandable excitement, especially because an antibody that binds that protein was found to promote regrowth of injured spinal nerves in the rat. (It even prompted a film, Extreme Measures, with Gene Hackman and Hugh Grant - an under-rated thriller with some surprisingly accurate science and some very serious medical malfeasance). ...
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This study strongly supports the utility of hiPSCs as a feasible and effective source of cells to treat myelin disorders," said University of Rochester Medical Center (URMC) neurologist Steven Goldman, M.D., Ph.D., lead author of the study. "In fact, it appears that cells derived from this source are at least as effective as those created using embryonic or tissue-specific stem cells.". The discovery opens the door to potential new treatments using hiPSC-derived cells for a range of neurological diseases characterized by the loss of a specific cell population in the central nervous system called myelin. Like the insulation found on electrical wires, myelin is a fatty tissue that ensheathes the connections between nerve cells and ensures the crisp transmission of signals from one cell to another. When myelin tissue is damaged, communication between cells can be disrupted or even lost.. The most common myelin disorder is multiple sclerosis, a condition in which the bodys own immune system attacks ...