Membralin mutant mice manifest a severe and early-onset motor neuron disease with defects in endoplasmic reticulum-associated protein degradation.

White matter microstructure in hemianopia patients indicates that blindsight requires an intact connection between the lateral geniculate nucleus and extrastriate cortex.

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.

Genetic and biochemical analysis reveals that MAPK signaling promotes axon degeneration by modulating the turnover of axon-protective proteins.

ATP imaging of spiking optic nerve axons in real time reveals correlation between ATP levels and electrical activity as well as contribution of lactate metabolism to axonal ATP homeostasis.

The utility of split GFP for tissue-specific visualization of ribosomes in live Caenorhabditis elegans demonstrates the link between ribosomes and microtubules.

An unbiased transcriptional profiling screen reveals the secreted matrix metalloproteinase MMP-1 is a transcriptional target of the ensheathing glial receptor Draper following acute axon injury in adult Drosophila.

Ultrastructural and loss-of-function experiments show that oligodendrocyte-encoded Kir4.1 is located near active axonal structures, including within myelin inner tongue, and has critical functions to promote axonal activity and preserve integrity.

Defects in synapse regeneration limit functional circuit recovery after nerve injury by misdirecting information via ectopic dendritic synapses, and also by functional and molecular deficits in reformed axonal synapses.

A function-based genetic screen using the Caenorhabditis elegans axotomy model identifies new regulators and an inhibitory role for NAD⁺ in axon regeneration, expanding the understanding of axon injury responses and regeneration.