Neuronal activity and NIBS in developmental myelination and remyelination - Current state of knowledge.

Autor: Scheinok TJ; AIMS Lab, Center for Neurosciences, UZ Brussel, Vrije Universiteit Brussel, Pleinlaan 2, 1050 Brussel, Belgium; Department of Pharmaceutical and Pharmacological Sciences, Research Group Experimental Pharmacology (EFAR), Center for Neurosciences (C4N), Vrije Universiteit Brussel (VUB), Laarbeeklaan 103, 1090 Brussels, Belgium. Electronic address: thomas.jonathan.scheinok@vub.be., D'Haeseleer M; Nationaal Multiple Sclerose Centrum, Vanheylenstraat 16, 1820 Melsbroek, Belgium., Nagels G; AIMS Lab, Center for Neurosciences, UZ Brussel, Vrije Universiteit Brussel, Pleinlaan 2, 1050 Brussel, Belgium; St Edmund Hall, University of Oxford, Queen's Lane, Oxford, UK., De Bundel D; Department of Pharmaceutical and Pharmacological Sciences, Research Group Experimental Pharmacology (EFAR), Center for Neurosciences (C4N), Vrije Universiteit Brussel (VUB), Laarbeeklaan 103, 1090 Brussels, Belgium., Van Schependom J; AIMS Lab, Center for Neurosciences, UZ Brussel, Vrije Universiteit Brussel, Pleinlaan 2, 1050 Brussel, Belgium; Department of Electronics and Informatics (ETRO), Vrije Universiteit Brussel, Pleinlaan 2, 1050 Brussel, Belgium.
Jazyk: angličtina
Zdroj: Progress in neurobiology [Prog Neurobiol] 2023 Jul; Vol. 226, pp. 102459. Date of Electronic Publication: 2023 Apr 29.
DOI: 10.1016/j.pneurobio.2023.102459
Abstrakt: Oligodendrocytes are responsible for myelinating central nervous system (CNS) axons and rapid electrical transmission through saltatory conduction of action potentials. Myelination and myelin repair rely partially on oligodendrogenesis, which comprises oligodendrocyte precursor cell (OPC) migration, maturation, and differentiation into oligodendrocytes (OL). In multiple sclerosis (MS), demyelination occurs due to an inflammatory cascade with auto-reactive T-cells. When oligodendrogenesis fails, remyelination becomes aberrant and conduction impairments are no longer restored. Although current disease modifying therapies have achieved results in modulating the faulty immune response, disease progression continues because of chronic inflammation, neurodegeneration, and failure of remyelination. Therapies have been tried to promote remyelination. Modulation of neuronal activity seems to be a very promising strategy in preclinical studies. Additionally, studies in people with MS (pwMS) have shown symptom improvement following non-invasive brain stimulation. (NIBS) techniques. The aforementioned mechanisms are yet unknown and probably involve both the activation of neurons and glial cells. Noting neuronal activity contributes to myelin plasticity and that NIBS modulates neuronal activity; we argue that NIBS is a promising research horizon for demyelinating diseases. We review the hypothesized pathways through which NIBS may affect both neuronal activity in the CNS and how the resulting activity can affect oligodendrogenesis and myelination.
Competing Interests: Declaration of Competing Interest The authors report no financial interests or potential conflict of interests.
(Copyright © 2023 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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