Recent Publications

Comprehensive review of CNS and PNS myelination: sheath assembly, axon glia signalling, and the metabolic role of the oligodendrocyte. The modern structural reference.

Myelin grows from the inner tongue outward; PI(3,4,5)P3 at the leading edge drives membrane extension beneath the previously deposited layers.

Disabling oxidative phosphorylation in oligodendrocytes does not cause demyelination; the cells run on aerobic glycolysis and pass the product to the axon.

MCT1 in oligodendrocytes exports lactate to axons. Deleting it causes axon degeneration with the myelin sheath still intact, separating support from insulation.

Single-cell RNA sequencing resolves the mouse oligodendrocyte lineage into distinct transcriptional states across brain regions.

OPC recruitment, the differentiation block in chronic MS, g-ratio as a repair metric, and the therapeutic strategies that follow from each.

Full account of myelin composition and oligodendrocyte biology; the source for the 70 percent lipid, 30 percent protein figure.

Single-cell lineage tracing shows NG2 cell fate narrows with age, and that white matter NG2 cells keep producing oligodendrocytes into adulthood.

Identifies Olig1 and Olig2 as Shh-regulated bHLH transcription factors marking and specifying the oligodendrocyte lineage.

NT-3 promotes OPC proliferation and survival; blocking it causes OPC death. A landmark in oligodendrocyte developmental biology.

Transected axons are present in active MS plaques in proportion to inflammation, establishing axonal injury as an early event rather than a late one.

OPCs are present in chronic MS lesions but are not dividing or maturing. Remyelination failure is a differentiation block, not an absence of precursors.

Definitive description of the cuprizone model: dose, timing, lesion anatomy, and spontaneous recovery. The benchmark for later cuprizone work.

Human mid-gestational neocortex. Maps chromatin looping, accessibility and methylation in four glial populations including OPCs, and prioritises 112 schizophrenia risk variants sitting in glial regulatory elements.

Mouse. Wild-type brainstem OPCs proliferate more slowly and differentiate later than telencephalic OPCs in culture, and the K27M glioma mutation exploits that regional difference.

Human post-mortem. MSA oligodendrocytes carry more somatic SNCA gains than controls (6.3% vs 2.0%); a gain doubles the chance of an alpha-synuclein inclusion in that cell and tracks earlier onset.

Neonatal cortical injury model. OPCs from the subventricular zone reach a lesion by travelling with migrating neuroblasts, held by adherens junctions that form and dissolve as they go.

Mouse. Small axons left without compact myelin in Teneurin-4 knockouts still survive at a year; four 14-3-3 isoforms rise in them, and blocking 14-3-3 hastens their damage.

Mouse. Halving Glut1 lowers brain glucose, glycogen and lactate, and in the striatum turns down oligodendrocyte and galactolipid genes and depletes myelin-enriched lipids.

Rat CSVD model. Histology and transcriptomics documented myelin disruption alongside altered mature oligodendrocyte and OPC marker profiles, blood-brain barrier breakdown, and microvascular rarefaction at successive time points.

Review linking prenatal alcohol exposure to white matter damage via oligodendrocyte deficiency and impaired myelination, in FASD patients and animal models.

Rat, culture and explant. Spinal cord oligodendrocytes generate longer internodes than cortical oligodendrocytes on identical fibres. Internode length differences between CNS regions are intrinsic to the oligodendrocyte, not instructed by the axon; the same regional identity is seen on microfibers, in co-culture, and in explants. Landmark paper establishing oligodendrocyte regional identity.