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Oligodendrocytes, the myelinating cells of the central nervous system (CNS), play a crucial role in myelin generation, maintenance, and repair after CNS injuries and in demyelinating diseases. Beyond their myelin-related functions, recent studies have revealed additional roles for oligodendrocytes and their progenitors in synaptic plasticity and neuronal circuits. Moreover, growing evidence suggests that oligodendrocytes and myelin dysfunction contribute to the onset and progression of neurodegenerative diseases.
With this Collection, the editors at Nature Communications, Communications Biology and Scientific Reports welcome the submission of primary research articles that focus on oligodendrocytes lineage cells in development, physiology, and disease. We particularly encourage studies exploring their non-canonical roles and contribution to neurodegenerative diseases and other CNS disorders. We are also very interested in studies focusing on treatment strategies targeting oligodendrocytes and remyelination. This call welcomes both basic and preclinical studies in animal models, as well as studies involving human tissue.
Human glial progenitor cells (hGPCs) lose mitotic competence with age. Here, the authors show that with maturation, adult hGPCs acquire a set of transcriptional repressors that actively suppress developmental gene expression.
The cell biological mechanisms that govern myelin sheath extension remain incompletely understood. Here, the authors find that calcium signaling in oligodendrocytes is required for the actin-dependent extension of myelin sheaths.
Heterozygous deletions in the ANKS1B gene cause ANKS1B neurodevelopmental syndrome. Here the authors show this syndrome is associated with impaired white matter integrity, and that Anks1b-deficient mouse models display deficits in oligodendrocyte maturation, myelination, and Rac1 function.
How oligodendrocyte precursor cells (OPCs) integrate calcium signals and neuromodulatory cues to regulate fate is unclear. Here, the authors report that locomotion-induced norepinephrine release modulates OPC calcium dynamics and differentiation.
Niemann-Pick type C disease is characterized by deficiency of the endolysosomal cholesterol transporter NPC1. Here, the authors show in Npc1−/− mice that loss of NPC1 impairs oligodendrocyte lineage cell differentiation and developmental myelination through perturbed epigenetic regulation.
The mechanisms regulating central nervous system remyelination efficiency are poorly understood. Here, the authors show that remyelination is driven by astrocytes supporting oligodendrocyte survival, regulated by the Nrf2 and cholesterol pathways.
Oligodendrocytes have been increasingly shown to be involved in Alzheimer’s disease (AD). Here, the authors perform single-cell RNA-sequencing on APP NL-G-F mice and describe a disease-associated oligodendrocyte (DAO) population. They find inhibition of Erk1/2 signaling in DAOs rescues impaired axonal myelination and cognitive decline in an AD mouse model.