The microenvironment surrounding sensory neurons in dorsal root ganglia responds differently to peripheral and central injuries, revealing that non-neuronal cells can be manipulated to promote axon regeneration after central injury.
Axonal metabolic flux analysis demonstrates that expression of NMNAT1 blocks axonal degeneration in cultured mouse neurons not by altering NAD+ synthesis, but rather by inhibiting injury-induced, SARM1-dependent NAD+ consumption.
Proteins of the reticulon and REEP families, homologous to the products of human Hereditary Spastic Paraplegia disease genes, contribute to shaping and continuity of the axonal endoplasmic reticulum network in Drosophila.
In the injured sciatic nerve, blood-derived monocytes and macrophages eat dying leukocytes, thereby contributing to nerve debridement and inflammation resolution, and this correlates with neuronal regeneration.
Motor axons undergo dynamic branch-specific changes for weeks before complete neuronal degeneration in a model of amyotrophic lateral sclerosis, highlighting the importance of peripheral factors, intrinsic and extrinsic to motoneurons.
Regenerating neural progenitors of the Xenopus tropicalis tail prioritize differentiation to motor neuron types earlier than proliferation, a decision partly regulated by the transcription factors Pbx3 and Meis1.