D Wilton

TL;DR: It is concluded that a single glial transcription factor is essential for restoration of damaged nerves, acting to control the transdifferentiation of myelin and Remak Schwann cells to dedicated repair cells in damaged tissue.

TL;DR: Using transgenic mice and cell cultures, it is found that Notch has complex and extensive regulatory functions in Schwann cells, and this finding identifies a signaling pathway that induces myelin breakdown in vivo.

TL;DR: The data suggest that mutant huntingtin impairs neurodevelopmental pathways that could disrupt synaptic homeostasis and increase vulnerability to the pathologic consequence of expanded polyglutamine repeat-associated phenotypes in neural cells and of cognitive impairment and synaptic pathology in HD model R6/2 mice.

TL;DR: In this article, the authors showed that Schwann cells respond to injury by activating/enhancing trophic support for axons through a mechanism that depends on upregulation of the transcription factor c-Jun, resulting in the sparing of axons that would otherwise die.