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.

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.

Proteomics uncovers thus far unknown age and sex differences in sciatic nerve and skin of naïve mice, highlighting the importance of adequate age matching and parallel investigation of male and female mice in biomedical studies.

When oligodendrocytes lack expression of the low-abundant myelin protein CMTM5, central nervous system axons are myelinated normally but subsequently degenerate involving a Wallerian-like pathomechanism.

Cd59 and developmental inflammation are key players in myelinating glial cell development, highlighting the collaboration between glia and the innate immune system to ensure normal neural development.

APEX2 proximity labeling of genetically targeted neurons enables subcellular and cell type-specific proteomics in the mouse brain, revealing the axonal and somatodendritic proteomes of midbrain dopaminergic neurons.

A newly identified component in the architecture of the axon/myelin-unit – the septin/anillin scaffold – maintains the structure of myelin in the central nervous system, thereby preventing myelin outfoldings.

The maintenance of skeletal muscle function improves the quality of life, and therefore understanding how changes in the genome drive changes in the skeletal muscle proteome has revealed novel regulators of muscle physiology.

APPPS1 microglia express disease-associated proteomic signatures of Alzheimer's disease earlier, compared to the APP-KI, and these differences correlate with the levels of fibrillar Aβ and impaired microglial phagocytic function.

Boosting the function of translation factor eIF2B by chronic small molecule administration prevents pathology in a neurodegenerative model of Vanishing White Matter disease characterized by a maladaptive stress response.