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Julia M. Edgar

Researcher at University of Glasgow

Publications -  78
Citations -  4956

Julia M. Edgar is an academic researcher from University of Glasgow. The author has contributed to research in topics: Myelin & Oligodendrocyte. The author has an hindex of 31, co-authored 74 publications receiving 4176 citations. Previous affiliations of Julia M. Edgar include Life Sciences Institute & Max Planck Society.

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Glycolytic oligodendrocytes maintain myelin and long-term axonal integrity

TL;DR: By in vivo magnetic resonance spectroscopy, brain lactate concentrations in mutants were increased compared with controls, but were detectable only in mice exposed to volatile anaesthetics, which indicates that aerobic glycolysis products derived from oligodendrocytes are rapidly metabolized within white matter tracts.
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Axonal Transport Defects in Neurodegenerative Diseases

TL;DR: It is suggested that many AONDs can be categorized as dysferopathies, diseases in which alterations in AT represent a critical component in pathogenesis, and Illumination of such mechanisms provides a framework for the development of novel therapeutic strategies aimed to prevent axonal and synaptic dysfunction in several major Aonds.
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Myelin Membrane Wrapping of CNS Axons by PI(3,4,5)P3-Dependent Polarized Growth at the Inner Tongue

TL;DR: The integrative approach of live imaging, electron microscopy, and genetics are used to show that new myelin membranes are incorporated adjacent to the axon at the innermost tongue, ultimately leading to the formation of a set of closely apposed paranodal loops.
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Oligodendroglial modulation of fast axonal transport in a mouse model of hereditary spastic paraplegia

TL;DR: A novel role for oligodendrocytes in the local regulation of axonal function is demonstrated and implications for the axonal loss associated with secondary progressive multiple sclerosis are implications.
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Neuroprotection and repair in multiple sclerosis

TL;DR: Advances in advances in both areas are reviewed, focusing on the molecular mechanisms underlying axonal loss in acute inflammation and in chronic demyelination, and discussing how the restoration of myelin sheaths via the regenerative process of remyelinated might prevent axon degeneration.