Wallerian Degeneration

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Michael P Coleman - One of the best experts on this subject based on the ideXlab platform.

  • Wallerian Degeneration an emerging axon death pathway linking injury and disease
    Nature Reviews Neuroscience, 2014
    Co-Authors: Laura Conforti, Jonathan Gilley, Michael P Coleman
    Abstract:

    Recent work has identified novel modifiers of axon Degeneration following injury, known as Wallerian Degeneration, and new examples of convergence between this mechanism and axon Degeneration occurring in some neurodegenerative diseases. Coleman and colleagues outline our current understanding of the Wallerian Degeneration pathway and consider its links to disease mechanisms.

  • MEK inhibitor U0126 reverses protection of axons from Wallerian Degeneration independently of MEK-ERK signaling.
    PLOS ONE, 2013
    Co-Authors: Catherine Evans, Michael P Coleman, Simon J. Cook, Jonathan Gilley
    Abstract:

    Wallerian Degeneration is delayed when sufficient levels of proteins with NMNAT activity are maintained within axons after injury. This has been proposed to form the basis of ’slow Wallerian Degeneration’ (Wld S ), a neuroprotective phenotype conferred by an aberrant fusion protein, Wld S . Proteasome inhibition also delays Wallerian Degeneration, although much less robustly, with stabilization of NMNAT2 likely to play a key role in this mechanism. The pan-MEK inhibitor U0126 has previously been shown to reverse the axon-protective effects of proteasome inhibition, suggesting that MEK-ERK signaling plays a role in delayed Wallerian Degeneration, in addition to its established role in promoting neuronal survival. Here we show that whilst U0126 can also reverse Wld S -mediated axon protection, more specific inhibitors of MEK1/2 and MEK5, PD184352 and BIX02189, have no significant effect on the delay to Wallerian Degeneration in either situation, whether used alone or in combination. This suggests that an off-target effect of U0126 is responsible for reversion of the axon protective effects of Wld S expression or proteasome inhibition, rather than inhibition of MEK1/2-ERK1/2 or MEK5-ERK5 signaling. Importantly, this off-target effect does not appear to result in alterations in the stabilities of either Wld S or NMNAT2.

  • intra axonal calcium changes after axotomy in wild type and slow Wallerian Degeneration axons
    Neuroscience, 2012
    Co-Authors: Robert Adalbert, Laura Conforti, Giacomo Morreale, M Paizs, Simon Walker, H L Roderick, Martin D Bootman, Laszlo Siklos, Michael P Coleman
    Abstract:

    Abstract Calcium accumulation induces the breakdown of cytoskeleton and axonal fragmentation in the late stages of Wallerian Degeneration. In the early stages there is no evidence for any long-lasting, extensive increase in intra-axonal calcium but there does appear to be some redistribution. We hypothesized that changes in calcium distribution could have an early regulatory role in axonal Degeneration in addition to the late executionary role of calcium. Schmidt–Lanterman clefts (SLCs), which allow exchange of metabolites and ions between the periaxonal and extracellular space, are likely to have an increased role when axon segments are separated from the cell body, so we used the oxalate-pyroantimonate method to study calcium at SLCs in distal stumps of transected wild-type and slow Wallerian Degeneration (Wld S ) mutant sciatic nerves, in which Wallerian Degeneration is greatly delayed. In wild-type nerves most SLCs show a step gradient of calcium distribution, which is lost at around 20% of SLCs within 3 mm of the lesion site by 4–24 h after nerve transection. To investigate further the association with Wallerian Degeneration, we studied nerves from Wld S rats. The step gradient of calcium distribution in Wld S is absent in around 20% of the intact nerves beneath SLCs but 4–24 h following injury, calcium distribution in transected axons remained similar to that in uninjured nerves. We then used calcium indicators to study influx and buffering of calcium in injured neurites in primary culture. Calcium penetration and the early calcium increase in this system were indistinguishable between Wld S and wild-type axons. However, a significant difference was observed during the following hours, when calcium increased in wild-type neurites but not in Wld S neurites. We conclude that there is little relationship between calcium distribution and the early stages of Wallerian Degeneration at the time points studied in vivo or in vitro but that Wld S neurites fail to show a later calcium rise that could be a cause or consequence of the later stages of Wallerian Degeneration.

  • Wallerian Degeneration wlds and nmnat
    Annual Review of Neuroscience, 2010
    Co-Authors: Michael P Coleman, Marc R Freeman
    Abstract:

    Traditionally, researchers have believed that axons are highly dependent on their cell bodies for long-term survival. However, recent studies point to the existence of axon-autonomous mechanism(s) that regulate rapid axon Degeneration after axotomy. Here, we review the cellular and molecular events that underlie this process, termed Wallerian Degeneration. We describe the biphasic nature of axon Degeneration after axotomy and our current understanding of how WldS—an extraordinary protein formed by fusing a Ube4b sequence to Nmnat1—acts to protect severed axons. Interestingly, the neuroprotective effects of WldS span all species tested, which suggests that there is an ancient, WldS-sensitive axon destruction program. Recent studies with WldS also reveal that Wallerian Degeneration is genetically related to several dying back axonopathies, thus arguing that Wallerian Degeneration can serve as a useful model to understand, and potentially treat, axon Degeneration in diverse traumatic or disease contexts.

  • the progressive nature of Wallerian Degeneration in wild type and slow Wallerian Degeneration wlds nerves
    BMC Neuroscience, 2005
    Co-Authors: Bogdan Beirowski, Robert Adalbert, Diana Wagner, Daniela Grumme, Klaus Addicks, Richard R Ribchester, Michael P Coleman
    Abstract:

    Background The progressive nature of Wallerian Degeneration has long been controversial. Conflicting reports that distal stumps of injured axons degenerate anterogradely, retrogradely, or simultaneously are based on statistical observations at discontinuous locations within the nerve, without observing any single axon at two distant points. As axon Degeneration is asynchronous, there are clear advantages to longitudinal studies of individual degenerating axons. We recently validated the study of Wallerian Degeneration using yellow fluorescent protein (YFP) in a small, representative population of axons, which greatly improves longitudinal imaging. Here, we apply this method to study the progressive nature of Wallerian Degeneration in both wild-type and slow Wallerian Degeneration (WldS) mutant mice.

Bogdan Beirowski - One of the best experts on this subject based on the ideXlab platform.

  • the progressive nature of Wallerian Degeneration in wild type and slow Wallerian Degeneration wlds nerves
    BMC Neuroscience, 2005
    Co-Authors: Bogdan Beirowski, Robert Adalbert, Diana Wagner, Daniela Grumme, Klaus Addicks, Richard R Ribchester, Michael P Coleman
    Abstract:

    Background The progressive nature of Wallerian Degeneration has long been controversial. Conflicting reports that distal stumps of injured axons degenerate anterogradely, retrogradely, or simultaneously are based on statistical observations at discontinuous locations within the nerve, without observing any single axon at two distant points. As axon Degeneration is asynchronous, there are clear advantages to longitudinal studies of individual degenerating axons. We recently validated the study of Wallerian Degeneration using yellow fluorescent protein (YFP) in a small, representative population of axons, which greatly improves longitudinal imaging. Here, we apply this method to study the progressive nature of Wallerian Degeneration in both wild-type and slow Wallerian Degeneration (WldS) mutant mice.

  • a rat model of slow Wallerian Degeneration wlds with improved preservation of neuromuscular synapses
    European Journal of Neuroscience, 2005
    Co-Authors: Bogdan Beirowski, Robert Adalbert, Diana Wagner, Daniela Grumme, Livia Berek, Thomas H Gillingwater, Jane E Haley, Katherine Bridge, Derek Thomson
    Abstract:

    : The slow Wallerian Degeneration phenotype, Wld(S), which delays Wallerian Degeneration and axon pathology for several weeks, has so far been studied only in mice. A rat model would have several advantages. First, rats model some human disorders better than mice. Second, the larger body size of rats facilitates more complex surgical manipulations. Third, rats provide a greater yield of tissue for primary culture and biochemical investigations. We generated transgenic Wld(S) rats expressing the Ube4b/Nmnat1 chimeric gene in the central and peripheral nervous system. As in Wld(S) mice, their axons survive up to 3 weeks after transection and remain functional for at least 1 week. Protection of axotomized nerve terminals is stronger than in mice, particularly in one line, where 95-100% of neuromuscular junctions remained intact and functional after 5 days. Furthermore, the loss of synaptic phenotype with age was much less in rats than in mice. Thus, the slow Wallerian Degeneration phenotype can be transferred to another mammalian species and synapses may be more effectively preserved after axotomy in species with longer axons.

  • quantitative and qualitative analysis of Wallerian Degeneration using restricted axonal labelling in yfp h mice
    Journal of Neuroscience Methods, 2004
    Co-Authors: Bogdan Beirowski, Robert Adalbert, Diana Wagner, Daniela Grumme, Klaus Addicks, Richard R Ribchester, Livia Berek, Michael P Coleman
    Abstract:

    We investigated the usefulness of YFP-H transgenic mice [Neuron 28 (2000) 41] which express yellow fluorescent protein (YFP) in a restricted subset of neurons to study Wallerian Degeneration in the PNS. Quantification of YFP positive axons and myelin basic protein (MBP) immunocytochemistry revealed that YFP was randomly distributed to approximately 3% of myelinated motor and sensory fibres. Axotomy-induced Wallerian Degeneration appeared as fragmentation of fluorescent signals in individual YFP positive axons with a morphology and timing similar to Wallerian Degeneration observed by more traditional methods. In YFP-H transgenic mice co-expressing a high dosage of Wld S , a chimeric gene that protects from Wallerian Degeneration [Nat Neurosci. 4 (2001) 1199], axonal fragmentation in distal tibial nerves after sciatic nerve axotomy was approximately 10 times delayed. Considerable retardations of Wallerian Degeneration using the same transgenic expression system were also observed in cultures of nerve explants, enabling in vitro real-time imaging of axonal fragmentation. Remarkably, single YFP-labelled axons could be traced in peripheral nerves for unusually long distances of up to 2.9 cm exploiting confocal fluorescence imaging. Altogether transgenic YFP-H mice prove to be a valuable tool to study mechanisms of Wallerian Degeneration in vivo and in vitro. © 2003 Elsevier B.V. All rights reserved.

  • Wallerian Degeneration of injured axons and synapses is delayed by a ube4b nmnat chimeric gene
    Nature Neuroscience, 2001
    Co-Authors: Till G A Mack, Bogdan Beirowski, Diana Wagner, Thomas H Gillingwater, Michael Reiner, Weiqian Mi, M Emanuelli, D Thomson, Felipe A Court, Laura Conforti
    Abstract:

    Wallerian Degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene

  • Wallerian Degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene.
    Nature Neuroscience, 2001
    Co-Authors: Till G A Mack, Bogdan Beirowski, Diana Wagner, Thomas H Gillingwater, Michael Reiner, Weiqian Mi, M Emanuelli, D Thomson, Felipe A Court, Laura Conforti
    Abstract:

    Wallerian Degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene

Diana Wagner - One of the best experts on this subject based on the ideXlab platform.

  • the progressive nature of Wallerian Degeneration in wild type and slow Wallerian Degeneration wlds nerves
    BMC Neuroscience, 2005
    Co-Authors: Bogdan Beirowski, Robert Adalbert, Diana Wagner, Daniela Grumme, Klaus Addicks, Richard R Ribchester, Michael P Coleman
    Abstract:

    Background The progressive nature of Wallerian Degeneration has long been controversial. Conflicting reports that distal stumps of injured axons degenerate anterogradely, retrogradely, or simultaneously are based on statistical observations at discontinuous locations within the nerve, without observing any single axon at two distant points. As axon Degeneration is asynchronous, there are clear advantages to longitudinal studies of individual degenerating axons. We recently validated the study of Wallerian Degeneration using yellow fluorescent protein (YFP) in a small, representative population of axons, which greatly improves longitudinal imaging. Here, we apply this method to study the progressive nature of Wallerian Degeneration in both wild-type and slow Wallerian Degeneration (WldS) mutant mice.

  • a rat model of slow Wallerian Degeneration wlds with improved preservation of neuromuscular synapses
    European Journal of Neuroscience, 2005
    Co-Authors: Bogdan Beirowski, Robert Adalbert, Diana Wagner, Daniela Grumme, Livia Berek, Thomas H Gillingwater, Jane E Haley, Katherine Bridge, Derek Thomson
    Abstract:

    : The slow Wallerian Degeneration phenotype, Wld(S), which delays Wallerian Degeneration and axon pathology for several weeks, has so far been studied only in mice. A rat model would have several advantages. First, rats model some human disorders better than mice. Second, the larger body size of rats facilitates more complex surgical manipulations. Third, rats provide a greater yield of tissue for primary culture and biochemical investigations. We generated transgenic Wld(S) rats expressing the Ube4b/Nmnat1 chimeric gene in the central and peripheral nervous system. As in Wld(S) mice, their axons survive up to 3 weeks after transection and remain functional for at least 1 week. Protection of axotomized nerve terminals is stronger than in mice, particularly in one line, where 95-100% of neuromuscular junctions remained intact and functional after 5 days. Furthermore, the loss of synaptic phenotype with age was much less in rats than in mice. Thus, the slow Wallerian Degeneration phenotype can be transferred to another mammalian species and synapses may be more effectively preserved after axotomy in species with longer axons.

  • quantitative and qualitative analysis of Wallerian Degeneration using restricted axonal labelling in yfp h mice
    Journal of Neuroscience Methods, 2004
    Co-Authors: Bogdan Beirowski, Robert Adalbert, Diana Wagner, Daniela Grumme, Klaus Addicks, Richard R Ribchester, Livia Berek, Michael P Coleman
    Abstract:

    We investigated the usefulness of YFP-H transgenic mice [Neuron 28 (2000) 41] which express yellow fluorescent protein (YFP) in a restricted subset of neurons to study Wallerian Degeneration in the PNS. Quantification of YFP positive axons and myelin basic protein (MBP) immunocytochemistry revealed that YFP was randomly distributed to approximately 3% of myelinated motor and sensory fibres. Axotomy-induced Wallerian Degeneration appeared as fragmentation of fluorescent signals in individual YFP positive axons with a morphology and timing similar to Wallerian Degeneration observed by more traditional methods. In YFP-H transgenic mice co-expressing a high dosage of Wld S , a chimeric gene that protects from Wallerian Degeneration [Nat Neurosci. 4 (2001) 1199], axonal fragmentation in distal tibial nerves after sciatic nerve axotomy was approximately 10 times delayed. Considerable retardations of Wallerian Degeneration using the same transgenic expression system were also observed in cultures of nerve explants, enabling in vitro real-time imaging of axonal fragmentation. Remarkably, single YFP-labelled axons could be traced in peripheral nerves for unusually long distances of up to 2.9 cm exploiting confocal fluorescence imaging. Altogether transgenic YFP-H mice prove to be a valuable tool to study mechanisms of Wallerian Degeneration in vivo and in vitro. © 2003 Elsevier B.V. All rights reserved.

  • Wallerian Degeneration of injured axons and synapses is delayed by a ube4b nmnat chimeric gene
    Nature Neuroscience, 2001
    Co-Authors: Till G A Mack, Bogdan Beirowski, Diana Wagner, Thomas H Gillingwater, Michael Reiner, Weiqian Mi, M Emanuelli, D Thomson, Felipe A Court, Laura Conforti
    Abstract:

    Wallerian Degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene

  • Wallerian Degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene.
    Nature Neuroscience, 2001
    Co-Authors: Till G A Mack, Bogdan Beirowski, Diana Wagner, Thomas H Gillingwater, Michael Reiner, Weiqian Mi, M Emanuelli, D Thomson, Felipe A Court, Laura Conforti
    Abstract:

    Wallerian Degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene

Robert Adalbert - One of the best experts on this subject based on the ideXlab platform.

  • intra axonal calcium changes after axotomy in wild type and slow Wallerian Degeneration axons
    Neuroscience, 2012
    Co-Authors: Robert Adalbert, Laura Conforti, Giacomo Morreale, M Paizs, Simon Walker, H L Roderick, Martin D Bootman, Laszlo Siklos, Michael P Coleman
    Abstract:

    Abstract Calcium accumulation induces the breakdown of cytoskeleton and axonal fragmentation in the late stages of Wallerian Degeneration. In the early stages there is no evidence for any long-lasting, extensive increase in intra-axonal calcium but there does appear to be some redistribution. We hypothesized that changes in calcium distribution could have an early regulatory role in axonal Degeneration in addition to the late executionary role of calcium. Schmidt–Lanterman clefts (SLCs), which allow exchange of metabolites and ions between the periaxonal and extracellular space, are likely to have an increased role when axon segments are separated from the cell body, so we used the oxalate-pyroantimonate method to study calcium at SLCs in distal stumps of transected wild-type and slow Wallerian Degeneration (Wld S ) mutant sciatic nerves, in which Wallerian Degeneration is greatly delayed. In wild-type nerves most SLCs show a step gradient of calcium distribution, which is lost at around 20% of SLCs within 3 mm of the lesion site by 4–24 h after nerve transection. To investigate further the association with Wallerian Degeneration, we studied nerves from Wld S rats. The step gradient of calcium distribution in Wld S is absent in around 20% of the intact nerves beneath SLCs but 4–24 h following injury, calcium distribution in transected axons remained similar to that in uninjured nerves. We then used calcium indicators to study influx and buffering of calcium in injured neurites in primary culture. Calcium penetration and the early calcium increase in this system were indistinguishable between Wld S and wild-type axons. However, a significant difference was observed during the following hours, when calcium increased in wild-type neurites but not in Wld S neurites. We conclude that there is little relationship between calcium distribution and the early stages of Wallerian Degeneration at the time points studied in vivo or in vitro but that Wld S neurites fail to show a later calcium rise that could be a cause or consequence of the later stages of Wallerian Degeneration.

  • the progressive nature of Wallerian Degeneration in wild type and slow Wallerian Degeneration wlds nerves
    BMC Neuroscience, 2005
    Co-Authors: Bogdan Beirowski, Robert Adalbert, Diana Wagner, Daniela Grumme, Klaus Addicks, Richard R Ribchester, Michael P Coleman
    Abstract:

    Background The progressive nature of Wallerian Degeneration has long been controversial. Conflicting reports that distal stumps of injured axons degenerate anterogradely, retrogradely, or simultaneously are based on statistical observations at discontinuous locations within the nerve, without observing any single axon at two distant points. As axon Degeneration is asynchronous, there are clear advantages to longitudinal studies of individual degenerating axons. We recently validated the study of Wallerian Degeneration using yellow fluorescent protein (YFP) in a small, representative population of axons, which greatly improves longitudinal imaging. Here, we apply this method to study the progressive nature of Wallerian Degeneration in both wild-type and slow Wallerian Degeneration (WldS) mutant mice.

  • a rat model of slow Wallerian Degeneration wlds with improved preservation of neuromuscular synapses
    European Journal of Neuroscience, 2005
    Co-Authors: Bogdan Beirowski, Robert Adalbert, Diana Wagner, Daniela Grumme, Livia Berek, Thomas H Gillingwater, Jane E Haley, Katherine Bridge, Derek Thomson
    Abstract:

    : The slow Wallerian Degeneration phenotype, Wld(S), which delays Wallerian Degeneration and axon pathology for several weeks, has so far been studied only in mice. A rat model would have several advantages. First, rats model some human disorders better than mice. Second, the larger body size of rats facilitates more complex surgical manipulations. Third, rats provide a greater yield of tissue for primary culture and biochemical investigations. We generated transgenic Wld(S) rats expressing the Ube4b/Nmnat1 chimeric gene in the central and peripheral nervous system. As in Wld(S) mice, their axons survive up to 3 weeks after transection and remain functional for at least 1 week. Protection of axotomized nerve terminals is stronger than in mice, particularly in one line, where 95-100% of neuromuscular junctions remained intact and functional after 5 days. Furthermore, the loss of synaptic phenotype with age was much less in rats than in mice. Thus, the slow Wallerian Degeneration phenotype can be transferred to another mammalian species and synapses may be more effectively preserved after axotomy in species with longer axons.

  • quantitative and qualitative analysis of Wallerian Degeneration using restricted axonal labelling in yfp h mice
    Journal of Neuroscience Methods, 2004
    Co-Authors: Bogdan Beirowski, Robert Adalbert, Diana Wagner, Daniela Grumme, Klaus Addicks, Richard R Ribchester, Livia Berek, Michael P Coleman
    Abstract:

    We investigated the usefulness of YFP-H transgenic mice [Neuron 28 (2000) 41] which express yellow fluorescent protein (YFP) in a restricted subset of neurons to study Wallerian Degeneration in the PNS. Quantification of YFP positive axons and myelin basic protein (MBP) immunocytochemistry revealed that YFP was randomly distributed to approximately 3% of myelinated motor and sensory fibres. Axotomy-induced Wallerian Degeneration appeared as fragmentation of fluorescent signals in individual YFP positive axons with a morphology and timing similar to Wallerian Degeneration observed by more traditional methods. In YFP-H transgenic mice co-expressing a high dosage of Wld S , a chimeric gene that protects from Wallerian Degeneration [Nat Neurosci. 4 (2001) 1199], axonal fragmentation in distal tibial nerves after sciatic nerve axotomy was approximately 10 times delayed. Considerable retardations of Wallerian Degeneration using the same transgenic expression system were also observed in cultures of nerve explants, enabling in vitro real-time imaging of axonal fragmentation. Remarkably, single YFP-labelled axons could be traced in peripheral nerves for unusually long distances of up to 2.9 cm exploiting confocal fluorescence imaging. Altogether transgenic YFP-H mice prove to be a valuable tool to study mechanisms of Wallerian Degeneration in vivo and in vitro. © 2003 Elsevier B.V. All rights reserved.

Laura Conforti - One of the best experts on this subject based on the ideXlab platform.

  • Wallerian Degeneration an emerging axon death pathway linking injury and disease
    Nature Reviews Neuroscience, 2014
    Co-Authors: Laura Conforti, Jonathan Gilley, Michael P Coleman
    Abstract:

    Recent work has identified novel modifiers of axon Degeneration following injury, known as Wallerian Degeneration, and new examples of convergence between this mechanism and axon Degeneration occurring in some neurodegenerative diseases. Coleman and colleagues outline our current understanding of the Wallerian Degeneration pathway and consider its links to disease mechanisms.

  • intra axonal calcium changes after axotomy in wild type and slow Wallerian Degeneration axons
    Neuroscience, 2012
    Co-Authors: Robert Adalbert, Laura Conforti, Giacomo Morreale, M Paizs, Simon Walker, H L Roderick, Martin D Bootman, Laszlo Siklos, Michael P Coleman
    Abstract:

    Abstract Calcium accumulation induces the breakdown of cytoskeleton and axonal fragmentation in the late stages of Wallerian Degeneration. In the early stages there is no evidence for any long-lasting, extensive increase in intra-axonal calcium but there does appear to be some redistribution. We hypothesized that changes in calcium distribution could have an early regulatory role in axonal Degeneration in addition to the late executionary role of calcium. Schmidt–Lanterman clefts (SLCs), which allow exchange of metabolites and ions between the periaxonal and extracellular space, are likely to have an increased role when axon segments are separated from the cell body, so we used the oxalate-pyroantimonate method to study calcium at SLCs in distal stumps of transected wild-type and slow Wallerian Degeneration (Wld S ) mutant sciatic nerves, in which Wallerian Degeneration is greatly delayed. In wild-type nerves most SLCs show a step gradient of calcium distribution, which is lost at around 20% of SLCs within 3 mm of the lesion site by 4–24 h after nerve transection. To investigate further the association with Wallerian Degeneration, we studied nerves from Wld S rats. The step gradient of calcium distribution in Wld S is absent in around 20% of the intact nerves beneath SLCs but 4–24 h following injury, calcium distribution in transected axons remained similar to that in uninjured nerves. We then used calcium indicators to study influx and buffering of calcium in injured neurites in primary culture. Calcium penetration and the early calcium increase in this system were indistinguishable between Wld S and wild-type axons. However, a significant difference was observed during the following hours, when calcium increased in wild-type neurites but not in Wld S neurites. We conclude that there is little relationship between calcium distribution and the early stages of Wallerian Degeneration at the time points studied in vivo or in vitro but that Wld S neurites fail to show a later calcium rise that could be a cause or consequence of the later stages of Wallerian Degeneration.

  • Wallerian Degeneration of injured axons and synapses is delayed by a ube4b nmnat chimeric gene
    Nature Neuroscience, 2001
    Co-Authors: Till G A Mack, Bogdan Beirowski, Diana Wagner, Thomas H Gillingwater, Michael Reiner, Weiqian Mi, M Emanuelli, D Thomson, Felipe A Court, Laura Conforti
    Abstract:

    Wallerian Degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene

  • Wallerian Degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene.
    Nature Neuroscience, 2001
    Co-Authors: Till G A Mack, Bogdan Beirowski, Diana Wagner, Thomas H Gillingwater, Michael Reiner, Weiqian Mi, M Emanuelli, D Thomson, Felipe A Court, Laura Conforti
    Abstract:

    Wallerian Degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene