About this Research Topic
Oligodendrocytes form myelin sheath during CNS development (developmental myelination). New concepts have emerged on the role of oligodendroglia and myelination in shaping animal life experience such as motor, cognition, and emotion adaptivity (adaptive myelination). The myelination capacity of oligodendrocytes is controlled by intrinsic molecular programs and extrinsic signals as well from neurons and other glial cell types.
Traditionally thought to be primary targets in demyelinating disorders, oligodendroglia and myelin damage/injury are also common pathology in neurodegenerative diseases long before neuronal/axonal degeneration and behavioral impairment. It has been increasingly appreciated by the neuroscience community that oligodendroglia and myelin are not simply victims in various CNS pathologies, they are active players in promoting or inhibiting neurodegeneration and neuroinflammation depending on disease/injury contexts, a newly emerging concept of myelination-independent functions of oligodendroglia. Identifying molecular mechanisms (intrinsic and extrinsic) underlying oligodendroglial regulation of CNS pathologies is fundamentally important for oligodendroglial biology and will provide novel insights into future therapeutic designs.
We invite submissions of review or original research articles focusing on the cellular and molecular aspects of oligodendroglia biology in various contexts, including myelination during development, the impact of myelination on adaptive functions, and the involvement of oligodendroglia in neurodegenerative diseases. Authors are encouraged to explore topics such as oligodendroglial regulation of CNS pathologies, potential therapeutic targets related to myelination, and the myelination-independent functions of oligodendroglia. Manuscripts utilizing in vitro models or in vivo animal models to investigate these themes are particularly welcome for consideration in this Research Topic.
Traditionally thought to be primary targets in demyelinating disorders, oligodendroglia and myelin damage/injury are also common pathology in neurodegenerative diseases long before neuronal/axonal degeneration and behavioral impairment. It has been increasingly appreciated by the neuroscience community that oligodendroglia and myelin are not simply victims in various CNS pathologies, they are active players in promoting or inhibiting neurodegeneration and neuroinflammation depending on disease/injury contexts, a newly emerging concept of myelination-independent functions of oligodendroglia. Identifying molecular mechanisms (intrinsic and extrinsic) underlying oligodendroglial regulation of CNS pathologies is fundamentally important for oligodendroglial biology and will provide novel insights into future therapeutic designs.
We invite submissions of review or original research articles focusing on the cellular and molecular aspects of oligodendroglia biology in various contexts, including myelination during development, the impact of myelination on adaptive functions, and the involvement of oligodendroglia in neurodegenerative diseases. Authors are encouraged to explore topics such as oligodendroglial regulation of CNS pathologies, potential therapeutic targets related to myelination, and the myelination-independent functions of oligodendroglia. Manuscripts utilizing in vitro models or in vivo animal models to investigate these themes are particularly welcome for consideration in this Research Topic.
Keywords: oligodendroglia, myelination, developmental myelination, adaptive myelination, CNS, neurodegeneration, neuroinflammation, glial cells, demyelinating disorders
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