A comprehensive compendium of myelin proteins in the peripheral nervous system has been created, alongside a method to address molecular diversity of myelin sheaths in health and disease.

The ORMDL proteins function to restrain the de novo sphingolipid biosynthetic pathway during myelination, when there is a high demand for sphingolipids to prevent excessive accumulation of metabolic intermediates.

A trial of mitofusin activation shows neuron regeneration and phenotype reversal in vitro and in vivo in experimental Charcot–Marie–Tooth disease type 2A caused by mitofusin 2 mutations.

In the peripheral nervous system, the large GTPase dynamin 2 is required for Schwann cell survival, developmental radial sorting of axons, myelination, and myelin maintenance.

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

In models of chronic migraine, neuronal complexity is diminished in head-pain processing regions but restored through HDAC6 inhibition, which increases tubulin acetylation and cytoskeletal flexibility, and CGRP receptor blockade.

A mutagenesis screen in budding yeast sheds light on dynein regulation and function, and reveals the molecular basis for disease in patients suffering from neuropathies caused by dynein dysfunction.

Comparing humans and mice, the protein composition of central nervous system myelin and the transcriptional profiles of myelin-producing oligodendrocytes are largely similar with respect to abundant structural myelin constituents but show divergent expression of a range of other distinct genes.