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Oligodendrocytes in health and disease
Neuropharmacology 110 (2016) 537e538
Contents lists available at ScienceDirect
Neuropharmacology journal homepage: www.elsevier.com/locate/neuropharm
Editorial
Oligodendrocytes in health and disease
Oligodendrocytes generate myelin sheaths, synchronize and speed up neuronal impulses, and provide metabolic support to CNS axons. Remarkably oligodendrocyte lineage cells are highly dynamic in the adult CNS, appearing to respond to environmental influences and neuronal activity, and can regenerate myelin spontaneously after CNS injury. In this Special Issue of Neuropharmacology, we review recent studies on the role of oligodendrocytes in CNS function in health and disease. Myelination is one of the most critical steps in the development of the mammalian CNS, occurring for the most part postnatally, and continuing well into adulthood. However, in the adult CNS, a significant portion of oligodendrocyte lineage cells remain in an immature and proliferative state thus raising the question whether oligodendrocyte progenitor cells may have additional roles in the adult CNS other than as a reservoir of myelinating cells. Tognatta and Miller here review the contribution of oligodendrocyte lineage cells in CNS functionality, and how they contribute to the pathology of neurodegenerative diseases, such as ALS and Alzheimer's disease. Additionally, in the review by Tomlinson et al., we see how exercise and environmental enrichment affects oligodendrocyte lineage progression and myelination during CNS homeostasis and repair. They also describe potential metabolites and stress effectors in influencing oligodendrogenesis and myelin plasticity. By comparison, Purger et al., review the role of neuronal activity in modulating oligodendrocyte lineage progression and myelination, and how this plays a role in learning. They propose possible cellular, molecular and epigenetic mechanisms that contribute to myelin plasticity. Spitzer et al., review the potential for glutamate signaling as being a mechanism for oligodendrocyte lineage cells to sense neuronal activity, and thus mediate myelin plasticity. Several reviews in this special issue highlight recently identified intracellular signals in oligodendrocyte linage progression. In the review by Gonsalvez et al., we see that extracellular related kinases 1 and 2 (Erk1/2) is a critical signal that stimulates myelinspecific transcription factors to promote oligodendrocyte lineage progression and myelination. Moreover, new imaging strategies have recently been developed to allow the visualization of oligodendrogenesis and myelination in vivo. In the review by Rassul et al., we learn the recent progress in live-imaging of oligodendrocyte-axon interaction and myelination in the developing CNS and after injury. The correlation of myelination abnormality with neurological impairment is evident in disorders such as certain leukodystrophies, periventricular leukomalacia (PVL), and autism. In the adult
http://dx.doi.org/10.1016/j.neuropharm.2016.06.034 0028-3908/© 2016 Published by Elsevier Ltd.
CNS, oligodendrocyte and myelin loss, such as in the chronic demyelinating disorder multiple sclerosis (MS), and in various forms of white matter injury profoundly impair CNS function and contribute to neuronal degeneration. Chew and DeBoy in this issue review demyelination and white matter damages that occur in perinatal and adult brain injuries, and how certain pharmacological agents may attenuate tissue damage by preventing excitotoxicity and increasing oligodendrocyte lineage cell survival. In addition, Baltan reviews the effect of ischemic white matter injury on oligodendrocyte and axon dysfunction, focusing on the effect of ageassociated changes on NMDA receptor redistribution in oligodendrocytes. Following demyelination, oligodendrocytes lineage cells readily regenerate and replace myelin. However, remyelination failure is frequently observed in the chronic progressive phase of MS, which is characterized by profound neurodegeneration. Thus therapeutic strategies to encourage remyelination may not only restore axonal conduction but also maintain neuronal function. Chamberlain et al., review the importance of oligodendrocyte regeneration in maintaining axonal conduction and integrity in MS and the signaling mechanisms involved in oligodendrocyte regeneration/remyelination. Additionally, Sedel et al., reviews the recent clinical trial on high dose biotin as a promising treatment for improving MSrelated disability, and its potential effect in reducing axonal hypoxia by enhancing energy production. Finally, white matter pathology and demyelination are also observed in different forms of traumatic brain injury (TBI). Armstrong et al., review myelin pathology and demyelination in TBI, and discuss remyelination as a potential strategy to promote functional recovery. We would like to thank all the contributors in this Special Issue of Neuropharmacology for providing new insights to the role of oligodendrocytes in CNS function and disease. We would also like to thank all the reviewers for their time and thoughtful comments, and the editors and staff at Neuropharmacology for making this Special Issue possible. References Armstrong, R.C., Mierzwa, A.J., Sullivan, G.M., Sanchez, M.A., 2016. Myelin and oligodendrocyte lineage cells in white matter pathology and plasticity after traumatic brain injury. Neuropharmacology 110, 654e659. Baltan, S., 2016. Age-specific localization of NMDA receptors on oligodendrocytes dictates axon function recovery after ischemia. Neuropharmacology 110, 626e632. Chamberlain, K.A., Nanescu, S.E., Psachoulia, K., Huang, J.K., 2016. Oligodendrocyte regeneration: its significance in myelin replacement and neuroprotection in multiple sclerosis. Neuropharmacology 110, 633e643.
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Editorial / Neuropharmacology 110 (2016) 537e538
Chew, L.J., DeBoy, C.A., 2016. Pharmacological approaches to intervention in hypomyelinating and demyelinating white matter pathology. Neuropharmacology 110, 605e625. Gonsalvez, D., Ferner, A.H., Peckham, H., Murray, S.S., Xiao, J., 2016. The roles of extracellular related-kinases 1 and 2 signaling in CNS myelination. Neuropharmacology 110, 586e593. Purger, D., Gibson, E.M., Monje, M., 2016. Myelin plasticity in the central nervous system. Neuropharmacology 110, 563e573. Rassul, S.M., Neely, R.K., Fulton, D., 2016. Live-imaging in the CNS: new insights on oligodendrocytes, myelination, and their responses to inflammation. Neuropharmacology 110, 594e604. Sedel, F., Bernard, D., Mock, D.M., Tourbah, A., 2016. Targeting demyelination and virtual hypoxia with high-dose biotin as a treatment for progressive multiple sclerosis. Neuropharmacology 110, 644e653. rado ttir, R.T., 2016. Glutamate signalling: a Spitzer, S., Volbracht, K., Lundgaard, I., Ka multifaceted modulator of oligodendrocyte lineage cells in health and disease. Neuropharmacology 110, 574e585. Tognatta, R., Miller, R.H., 2016. Contribution of the oligodendrocyte lineage to CNS repair and neurodegenerative pathologies. Neuropharmacology 110, 539e547. Tomlinson, L., Leiton, C.V., Colognato, H., 2016. Behavioral experiences as drivers of oligodendrocyte lineage dynamics and myelin plasticity. Neuropharmacology 110, 548e562.
Jeffrey K. Huang, Guest Editor* Dept. of Biology, Georgetown University, 37th and O St., NW, Washington, DC 20057, USA ttir, Guest Editor** Ragnhildur T. K arado Wellcome Trust e MRC Stem Cell Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK *
Corresponding author.
**
Corresponding author. E-mail address: [email protected] (J.K. Huang). rado ttir). E-mail address: [email protected] (R.T. Ka Available online 20 August 2016
Contents lists available at ScienceDirect
Neuropharmacology journal homepage: www.elsevier.com/locate/neuropharm
Editorial
Oligodendrocytes in health and disease
Oligodendrocytes generate myelin sheaths, synchronize and speed up neuronal impulses, and provide metabolic support to CNS axons. Remarkably oligodendrocyte lineage cells are highly dynamic in the adult CNS, appearing to respond to environmental influences and neuronal activity, and can regenerate myelin spontaneously after CNS injury. In this Special Issue of Neuropharmacology, we review recent studies on the role of oligodendrocytes in CNS function in health and disease. Myelination is one of the most critical steps in the development of the mammalian CNS, occurring for the most part postnatally, and continuing well into adulthood. However, in the adult CNS, a significant portion of oligodendrocyte lineage cells remain in an immature and proliferative state thus raising the question whether oligodendrocyte progenitor cells may have additional roles in the adult CNS other than as a reservoir of myelinating cells. Tognatta and Miller here review the contribution of oligodendrocyte lineage cells in CNS functionality, and how they contribute to the pathology of neurodegenerative diseases, such as ALS and Alzheimer's disease. Additionally, in the review by Tomlinson et al., we see how exercise and environmental enrichment affects oligodendrocyte lineage progression and myelination during CNS homeostasis and repair. They also describe potential metabolites and stress effectors in influencing oligodendrogenesis and myelin plasticity. By comparison, Purger et al., review the role of neuronal activity in modulating oligodendrocyte lineage progression and myelination, and how this plays a role in learning. They propose possible cellular, molecular and epigenetic mechanisms that contribute to myelin plasticity. Spitzer et al., review the potential for glutamate signaling as being a mechanism for oligodendrocyte lineage cells to sense neuronal activity, and thus mediate myelin plasticity. Several reviews in this special issue highlight recently identified intracellular signals in oligodendrocyte linage progression. In the review by Gonsalvez et al., we see that extracellular related kinases 1 and 2 (Erk1/2) is a critical signal that stimulates myelinspecific transcription factors to promote oligodendrocyte lineage progression and myelination. Moreover, new imaging strategies have recently been developed to allow the visualization of oligodendrogenesis and myelination in vivo. In the review by Rassul et al., we learn the recent progress in live-imaging of oligodendrocyte-axon interaction and myelination in the developing CNS and after injury. The correlation of myelination abnormality with neurological impairment is evident in disorders such as certain leukodystrophies, periventricular leukomalacia (PVL), and autism. In the adult
http://dx.doi.org/10.1016/j.neuropharm.2016.06.034 0028-3908/© 2016 Published by Elsevier Ltd.
CNS, oligodendrocyte and myelin loss, such as in the chronic demyelinating disorder multiple sclerosis (MS), and in various forms of white matter injury profoundly impair CNS function and contribute to neuronal degeneration. Chew and DeBoy in this issue review demyelination and white matter damages that occur in perinatal and adult brain injuries, and how certain pharmacological agents may attenuate tissue damage by preventing excitotoxicity and increasing oligodendrocyte lineage cell survival. In addition, Baltan reviews the effect of ischemic white matter injury on oligodendrocyte and axon dysfunction, focusing on the effect of ageassociated changes on NMDA receptor redistribution in oligodendrocytes. Following demyelination, oligodendrocytes lineage cells readily regenerate and replace myelin. However, remyelination failure is frequently observed in the chronic progressive phase of MS, which is characterized by profound neurodegeneration. Thus therapeutic strategies to encourage remyelination may not only restore axonal conduction but also maintain neuronal function. Chamberlain et al., review the importance of oligodendrocyte regeneration in maintaining axonal conduction and integrity in MS and the signaling mechanisms involved in oligodendrocyte regeneration/remyelination. Additionally, Sedel et al., reviews the recent clinical trial on high dose biotin as a promising treatment for improving MSrelated disability, and its potential effect in reducing axonal hypoxia by enhancing energy production. Finally, white matter pathology and demyelination are also observed in different forms of traumatic brain injury (TBI). Armstrong et al., review myelin pathology and demyelination in TBI, and discuss remyelination as a potential strategy to promote functional recovery. We would like to thank all the contributors in this Special Issue of Neuropharmacology for providing new insights to the role of oligodendrocytes in CNS function and disease. We would also like to thank all the reviewers for their time and thoughtful comments, and the editors and staff at Neuropharmacology for making this Special Issue possible. References Armstrong, R.C., Mierzwa, A.J., Sullivan, G.M., Sanchez, M.A., 2016. Myelin and oligodendrocyte lineage cells in white matter pathology and plasticity after traumatic brain injury. Neuropharmacology 110, 654e659. Baltan, S., 2016. Age-specific localization of NMDA receptors on oligodendrocytes dictates axon function recovery after ischemia. Neuropharmacology 110, 626e632. Chamberlain, K.A., Nanescu, S.E., Psachoulia, K., Huang, J.K., 2016. Oligodendrocyte regeneration: its significance in myelin replacement and neuroprotection in multiple sclerosis. Neuropharmacology 110, 633e643.
538
Editorial / Neuropharmacology 110 (2016) 537e538
Chew, L.J., DeBoy, C.A., 2016. Pharmacological approaches to intervention in hypomyelinating and demyelinating white matter pathology. Neuropharmacology 110, 605e625. Gonsalvez, D., Ferner, A.H., Peckham, H., Murray, S.S., Xiao, J., 2016. The roles of extracellular related-kinases 1 and 2 signaling in CNS myelination. Neuropharmacology 110, 586e593. Purger, D., Gibson, E.M., Monje, M., 2016. Myelin plasticity in the central nervous system. Neuropharmacology 110, 563e573. Rassul, S.M., Neely, R.K., Fulton, D., 2016. Live-imaging in the CNS: new insights on oligodendrocytes, myelination, and their responses to inflammation. Neuropharmacology 110, 594e604. Sedel, F., Bernard, D., Mock, D.M., Tourbah, A., 2016. Targeting demyelination and virtual hypoxia with high-dose biotin as a treatment for progressive multiple sclerosis. Neuropharmacology 110, 644e653. rado ttir, R.T., 2016. Glutamate signalling: a Spitzer, S., Volbracht, K., Lundgaard, I., Ka multifaceted modulator of oligodendrocyte lineage cells in health and disease. Neuropharmacology 110, 574e585. Tognatta, R., Miller, R.H., 2016. Contribution of the oligodendrocyte lineage to CNS repair and neurodegenerative pathologies. Neuropharmacology 110, 539e547. Tomlinson, L., Leiton, C.V., Colognato, H., 2016. Behavioral experiences as drivers of oligodendrocyte lineage dynamics and myelin plasticity. Neuropharmacology 110, 548e562.
Jeffrey K. Huang, Guest Editor* Dept. of Biology, Georgetown University, 37th and O St., NW, Washington, DC 20057, USA ttir, Guest Editor** Ragnhildur T. K arado Wellcome Trust e MRC Stem Cell Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK *
Corresponding author.
**
Corresponding author. E-mail address: [email protected] (J.K. Huang). rado ttir). E-mail address: [email protected] (R.T. Ka Available online 20 August 2016