Publications by authors named "Clara Mutschler"

Glial cells have a remarkable plasticity. Recent studies using zebrafish as a model highlight conserved cellular behavior in health and disease in the central nervous system (CNS) between zebrafish and humans. These findings inform our understanding of their function and how their dysregulation in pathogenesis can be determinant.

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Article Synopsis
  • The peripheral nervous system can regenerate after nerve damage, but achieving full functional recovery is rare and heavily relies on Schwann cells, which help repair nerve damage and support axon regrowth.
  • New research reveals that nerve injury stimulates communication between fat cells and glial cells, with the adipokine leptin playing a crucial role in helping Schwann cells adapt metabolically during recovery.
  • Leptin receptors in Schwann cells help regulate energy processes needed for nerve repair, suggesting that targeting this intercellular communication could improve therapeutic strategies for nerve injuries.
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Myelinating Schwann cell (SC)-dorsal root ganglion (DRG) neuron cocultures are an important technique for understanding cell-cell signalling and interactions during peripheral nervous system (PNS) myelination, injury, and regeneration. Although methods using rat SCs and neurons or mouse DRG explants are commonplace, there are no established protocols for compartmentalised myelinating cocultures with dissociated mouse cells. There consequently is a need for a coculture protocol that allows separate genetic manipulation of mouse SCs or neurons, or use of cells from different transgenic animals to complement in vivo mouse experiments.

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Since SARM1 mutations have been identified in human neurological disease, SARM1 inhibition has become an attractive therapeutic strategy to preserve axons in a variety of disorders of the peripheral (PNS) and central nervous system (CNS). While SARM1 has been extensively studied in neurons, it remains unknown whether SARM1 is present and functional in myelinating glia? This is an important question to address. Firstly, to identify whether SARM1 dysfunction in other cell types in the nervous system may contribute to neuropathology in SARM1 dependent diseases? Secondly, to ascertain whether therapies altering SARM1 function may have unintended deleterious impacts on PNS or CNS myelination? Surprisingly, we find that oligodendrocytes express mRNA in the zebrafish spinal cord and that SARM1 protein is readily detectable in rodent oligodendrocytes and .

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The peripheral nervous system (PNS) has a remarkable regenerative capacity in comparison to the central nervous system (CNS), a phenomenon that is impaired during ageing. The ability of PNS axons to regenerate after injury is due to Schwann cells (SC) being reprogrammed into a repair phenotype called Repair Schwann cells. These repair SCs are crucial for supporting axonal growth after injury, myelin degradation in a process known as myelinophagy, neurotropic factor secretion, and axonal growth guidance through the formation of Büngner bands.

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