Axonal damage sensing kinase DLK is a direct target and mediator of the cAMP effector kinase PKA in a unified mechanism for stimulating axonal regeneration.

4-sulfation at the non-reducing end of chondroitin sulfate glycosaminoglycan chains is essential for inhibition of axonal growth.

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

Inhibiting RNA N6-methyladenosine demethylase ALKBH5 promoted axonal regeneration of dorsal root ganglion neurons by regulating stability of Lpin2 mRNA and enhanced the survival and axonal regeneration of retinal ganglion cells.

Posttranslational modifications of tubulins regulate axonal growth and regeneration by controlling the stabilities of microtubules or modulating their interactions with microtubule-associated proteins.

Dominant optic atrophy (DOA) and DOA plus mutations' effects on optic nerve degeneration distinguished in a novel Drosophila model.

Mature axons lose the ability to regenerate because key growth molecules are excluded through changes in vesicle transport, and restoring transport can restore regeneration.

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.

Transportomic analysis of the changes underlying neurodegeneration reveals the importance of Kif5a for neuronal survival and highlights the need to restore specific anterograde cargo transport to for regeneration.

A mouse model of retinal degeneration reveals a common mechanism for axonal degeneration and photoreceptor cell death and identifies SARM1 as a therapeutic candidate for retinopathies.