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Wrap it up: Myelination of transplanted neurons for repair.

Front. Cell. Neurosci. 19:1635551 (2025)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Degeneration or damage of neuronal circuits in the central nervous system can lead to an irreversible loss of neurons and function in the affected brain region. Neuronal transplantation is a promising therapeutic approach consisting of introducing healthy cells into the damaged or diseased regions to restore lost circuits. To achieve successful neuronal transplantation, proper integration of the graft in the host circuitry is necessary. This includes the restoration of connectivity as well as the recapitulation of the physiological characteristics of the lost endogenous neurons. An often-overlooked aspect to assess the integration of transplanted neurons is the acquisition of cell-extrinsic features, such as myelination. This review explores the interaction between transplanted cells and endogenous oligodendroglia, the evidence of myelination in different neuronal transplantation models, and the checkpoints that can influence graft myelination in the injured or diseased brain. Additionally, it discusses how appropriate myelin ensheathment could help overcome some challenges faced in the field of neuronal replacement.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Cns Repair ; Myelination ; Neurodegeneration ; Neuronal Graft ; Neuronal Replacement ; Neuronal Transplantation ; Oligodendrocytes ; Stroke; Neural Stem-cells; Promote Locomotor Recovery; Rat Spinal-cord; Functional Recovery; Huntingtons-disease; Cns Remyelination; Neurite Outgrowth; Progenitor Grafts; Pyramidal Neurons; Dopamine Neurons
e-ISSN 1662-5102
Quellenangaben Band: 19, Heft: , Seiten: , Artikelnummer: 1635551 Supplement: ,
Verlag Frontiers
Verlagsort Avenue Du Tribunal Federal 34, Lausanne, Ch-1015, Switzerland
Begutachtungsstatus Peer reviewed
Förderungen SyNergy
German Research Foundation
EU in the Consortium NSC Reconstruct
NSERC
SSHRC
Boehringer Ingelheim Fonds (BIF) PhD fellowship
German Research Foundation TRR274