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Axonal Transport

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Rogier Q. Hintzen – One of the best experts on this subject based on the ideXlab platform.

  • Axonal Transport deficits in multiple sclerosis: spiraling into the abyss
    Acta Neuropathologica, 2017
    Co-Authors: Robert Berg, Casper C. Hoogenraad, Rogier Q. Hintzen

    Abstract:

    The Transport of mitochondria and other cellular components along the Axonal microtubule cytoskeleton plays an essential role in neuronal survival. Defects in this system have been linked to a large number of neurological disorders. In multiple sclerosis (MS) and associated models such as experimental autoimmune encephalomyelitis (EAE), alterations in Axonal Transport have been shown to exist before neurodegeneration occurs. Genome-wide association (GWA) studies have linked several motor proteins to MS susceptibility, while neuropathological studies have shown accumulations of proteins and organelles suggestive for Transport deficits. A reduced effectiveness of Axonal Transport can lead to neurodegeneration through inhibition of mitochondrial motility, disruption of axoglial interaction or prevention of remyelination. In MS, demyelination leads to dysregulation of Axonal Transport, aggravated by the effects of TNF-alpha, nitric oxide and glutamate on the cytoskeleton. The combined effect of all these pathways is a vicious cycle in which a defective Axonal Transport system leads to an increase in ATP consumption through loss of membrane organization and a reduction in available ATP through inhibition of mitochondrial Transport, resulting in even further inhibition of Transport. The persistent activity of this positive feedback loop contributes to neurodegeneration in MS.

  • Axonal Transport deficits in multiple sclerosis: spiraling into the abyss
    Acta Neuropathologica, 2017
    Co-Authors: Robert Berg, Casper C. Hoogenraad, Rogier Q. Hintzen

    Abstract:

    The Transport of mitochondria and other cellular components along the Axonal microtubule cytoskeleton plays an essential role in neuronal survival. Defects in this system have been linked to a large number of neurological disorders. In multiple sclerosis (MS) and associated models such as experimental autoimmune encephalomyelitis (EAE), alterations in Axonal Transport have been shown to exist before neurodegeneration occurs. Genome-wide association (GWA) studies have linked several motor proteins to MS susceptibility, while neuropathological studies have shown accumulations of proteins and organelles suggestive for Transport deficits. A reduced effectiveness of Axonal Transport can lead to neurodegeneration through inhibition of mitochondrial motility, disruption of axoglial interaction or prevention of remyelination. In MS, demyelination leads to dysregulation of Axonal Transport, aggravated by the effects of TNF-alpha, nitric oxide and glutamate on the cytoskeleton. The combined effect of all these pathways is a vicious cycle in which a defective Axonal Transport system leads to an increase in ATP consumption through loss of membrane organization and a reduction in available ATP through inhibition of mitochondrial Transport, resulting in even further inhibition of Transport. The persistent activity of this positive feedback loop contributes to neurodegeneration in MS.

Florence Besse – One of the best experts on this subject based on the ideXlab platform.

  • Live imaging of Axonal Transport in Drosophila pupal brain explants
    Nature Protocols, 2015
    Co-Authors: Caroline Medioni, Anne Ephrussi, Florence Besse

    Abstract:

    Axonal Transport is essential for the initial growth, maintenance and synaptic plasticity of axons, and altered Axonal Transport has been observed in different models of neurodegenerative pathologies. Dissecting the mechanisms underlying Axonal Transport in developing or degenerating brains requires dynamic imaging of Axonal cargo movement in living samples. Whereas methods exist to image Axonal Transport in Drosophila larval neurons, they are not suitable to follow this process during metamorphosis, when brains undergo extensive remodeling. Here we present a simple method that enables confocal imaging of both fast and slow Axonal Transport in Drosophila pupal brain explants. We describe how to prepare chambers adapted for live imaging, how to maintain brain explants under physiological conditions and how to monitor and quantitatively analyze the movement of fluorescently labeled cargoes. This protocol requires minimal equipment and is ideally suited for experiments that combine genetics, optogenetics and pharmacological approaches. The brains can be prepared for image acquisition in 1.5 h, and the protocol can be performed easily in any fly laboratory. This protocol describes live imaging of Axonal Transport in Drosophila pupal brains. It complements previous techniques for imaging larval neurons by enabling the study of extensive changes occurring during metamorphosis.

  • Live imaging of Axonal Transport in Drosophila pupal brain explants
    Nature Protocols, 2015
    Co-Authors: Caroline Medioni, Anne Ephrussi, Florence Besse

    Abstract:

    Axonal Transport is essential for the initial growth, maintenance and synaptic plasticity of axons, and altered Axonal Transport has been observed in different models of neurodegenerative pathologies. Dissecting the mechanisms underlying Axonal Transport in developing or degenerating brains requires dynamic imaging of Axonal cargo movement in living samples. Whereas methods exist to image Axonal Transport in Drosophila larval neurons, they are not suitable to follow this process during metamorphosis, when brains undergo extensive remodeling. Here we present a simple method that enables confocal imaging of both fast and slow Axonal Transport in Drosophila pupal brain explants. We describe how to prepare chambers adapted for live imaging, how to maintain brain explants under physiological conditions and how to monitor and quantitatively analyze the movement of fluorescently labeled cargoes. This protocol requires minimal equipment and is ideally suited for experiments that combine genetics, optogenetics and pharmacological approaches. The brains can be prepared for image acquisition in 1.5 h, and the protocol can be performed easily in any fly laboratory.

Robert Berg – One of the best experts on this subject based on the ideXlab platform.

  • Axonal Transport deficits in multiple sclerosis: spiraling into the abyss
    Acta Neuropathologica, 2017
    Co-Authors: Robert Berg, Casper C. Hoogenraad, Rogier Q. Hintzen

    Abstract:

    The Transport of mitochondria and other cellular components along the Axonal microtubule cytoskeleton plays an essential role in neuronal survival. Defects in this system have been linked to a large number of neurological disorders. In multiple sclerosis (MS) and associated models such as experimental autoimmune encephalomyelitis (EAE), alterations in Axonal Transport have been shown to exist before neurodegeneration occurs. Genome-wide association (GWA) studies have linked several motor proteins to MS susceptibility, while neuropathological studies have shown accumulations of proteins and organelles suggestive for Transport deficits. A reduced effectiveness of Axonal Transport can lead to neurodegeneration through inhibition of mitochondrial motility, disruption of axoglial interaction or prevention of remyelination. In MS, demyelination leads to dysregulation of Axonal Transport, aggravated by the effects of TNF-alpha, nitric oxide and glutamate on the cytoskeleton. The combined effect of all these pathways is a vicious cycle in which a defective Axonal Transport system leads to an increase in ATP consumption through loss of membrane organization and a reduction in available ATP through inhibition of mitochondrial Transport, resulting in even further inhibition of Transport. The persistent activity of this positive feedback loop contributes to neurodegeneration in MS.

  • Axonal Transport deficits in multiple sclerosis: spiraling into the abyss
    Acta Neuropathologica, 2017
    Co-Authors: Robert Berg, Casper C. Hoogenraad, Rogier Q. Hintzen

    Abstract:

    The Transport of mitochondria and other cellular components along the Axonal microtubule cytoskeleton plays an essential role in neuronal survival. Defects in this system have been linked to a large number of neurological disorders. In multiple sclerosis (MS) and associated models such as experimental autoimmune encephalomyelitis (EAE), alterations in Axonal Transport have been shown to exist before neurodegeneration occurs. Genome-wide association (GWA) studies have linked several motor proteins to MS susceptibility, while neuropathological studies have shown accumulations of proteins and organelles suggestive for Transport deficits. A reduced effectiveness of Axonal Transport can lead to neurodegeneration through inhibition of mitochondrial motility, disruption of axoglial interaction or prevention of remyelination. In MS, demyelination leads to dysregulation of Axonal Transport, aggravated by the effects of TNF-alpha, nitric oxide and glutamate on the cytoskeleton. The combined effect of all these pathways is a vicious cycle in which a defective Axonal Transport system leads to an increase in ATP consumption through loss of membrane organization and a reduction in available ATP through inhibition of mitochondrial Transport, resulting in even further inhibition of Transport. The persistent activity of this positive feedback loop contributes to neurodegeneration in MS.