Pushing Forward: Remyelination as the New Frontier in CNS Diseases
The evolutionary acquisition of myelin sheaths around large caliber axons in the central nervous system (CNS) represented a milestone in the development of vertebrate higher brain function. Myelin ensheathment of axons enabled saltatory conduction and thus accelerated information processing. However...
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Veröffentlicht in: | Trends in neurosciences (Regular ed.) 2016-04, Vol.39 (4), p.246-263 |
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description | The evolutionary acquisition of myelin sheaths around large caliber axons in the central nervous system (CNS) represented a milestone in the development of vertebrate higher brain function. Myelin ensheathment of axons enabled saltatory conduction and thus accelerated information processing. However, a number of CNS diseases harm or destroy myelin and oligodendrocytes (myelin-producing cells), ultimately resulting in demyelination. In the adult CNS, new oligodendrocytes can be generated from a quiescent pool of precursor cells, which – upon differentiation – can replace lost myelin sheaths. The efficiency of this spontaneous regeneration is limited, which leads to incomplete remyelination and residual clinical symptoms. Here, we discuss CNS pathologies characterized by white matter degeneration and regeneration and highlight drugs that could potentially serve as remyelination therapies. |
doi_str_mv | 10.1016/j.tins.2016.02.004 |
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Myelin ensheathment of axons enabled saltatory conduction and thus accelerated information processing. However, a number of CNS diseases harm or destroy myelin and oligodendrocytes (myelin-producing cells), ultimately resulting in demyelination. In the adult CNS, new oligodendrocytes can be generated from a quiescent pool of precursor cells, which – upon differentiation – can replace lost myelin sheaths. The efficiency of this spontaneous regeneration is limited, which leads to incomplete remyelination and residual clinical symptoms. 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Myelin ensheathment of axons enabled saltatory conduction and thus accelerated information processing. However, a number of CNS diseases harm or destroy myelin and oligodendrocytes (myelin-producing cells), ultimately resulting in demyelination. In the adult CNS, new oligodendrocytes can be generated from a quiescent pool of precursor cells, which – upon differentiation – can replace lost myelin sheaths. The efficiency of this spontaneous regeneration is limited, which leads to incomplete remyelination and residual clinical symptoms. Here, we discuss CNS pathologies characterized by white matter degeneration and regeneration and highlight drugs that could potentially serve as remyelination therapies.</description><subject>Animals</subject><subject>Cell Differentiation - physiology</subject><subject>Cellular biology</subject><subject>Demyelinating Diseases</subject><subject>Drug therapy</subject><subject>Humans</subject><subject>myelin repair</subject><subject>Myelin Sheath - physiology</subject><subject>Nerve Regeneration - physiology</subject><subject>Nervous system</subject><subject>Neural Stem Cells - cytology</subject><subject>Neurological disorders</subject><subject>Neurology</subject><subject>neuroregeneration</subject><subject>Neurosciences</subject><subject>Oligodendroglia - cytology</subject><subject>oligodendroglial cells</subject><subject>therapies</subject><subject>white matter</subject><issn>0166-2236</issn><issn>1878-108X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkkFv1DAQhS0EokvhD3BAlrhwSRg7tuMgVAkWtkWqCqIg9WY5ziz1knWKnVDtv6-jLVTqAXGyJX_vjWfeEPKcQcmAqdebcvQhlTzfS-AlgHhAFkzXumCgLx6SRX5QBeeVOiBPUtoAMKGZeEwOuGqUkCAW5P2XKV368IOuhnhtY_eGfsXtDnsf7OiHQG2i4yXSM7ymqziE0WOkPtDl2Tn94BPahOkpebS2fcJnt-ch-b76-G15Upx-Pv60fHdaOFnpsbBa5qpd09agreRcAjhmO7tWlUCrrWu7lrEaRVdxjrIRnLfCqaqSUFkp2-qQvNr7XsXh14RpNFufHPa9DThMybBaZ9uaQ_0faF03On8LMvryHroZphhyI7Mhy-VVwzPF95SLQ0oR1-Yq-q2NO8PAzGGYjZnDMHMYBrjJYWTRi1vrqd1i91fyZ_oZeLsHMI_tdx6tSc5jcNj5iG403eD_7X90T-5ybt7Z_ifuMN31YVIWmPN5HeZtYAoAuL6obgDfpKzX</recordid><startdate>20160401</startdate><enddate>20160401</enddate><creator>Kremer, David</creator><creator>Göttle, Peter</creator><creator>Hartung, Hans-Peter</creator><creator>Küry, Patrick</creator><general>Elsevier Ltd</general><general>Elsevier Sequoia S.A</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20160401</creationdate><title>Pushing Forward: Remyelination as the New Frontier in CNS Diseases</title><author>Kremer, David ; 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subjects | Animals Cell Differentiation - physiology Cellular biology Demyelinating Diseases Drug therapy Humans myelin repair Myelin Sheath - physiology Nerve Regeneration - physiology Nervous system Neural Stem Cells - cytology Neurological disorders Neurology neuroregeneration Neurosciences Oligodendroglia - cytology oligodendroglial cells therapies white matter |
title | Pushing Forward: Remyelination as the New Frontier in CNS Diseases |
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