Hauke B. Werner

The paper develops transgenic mouse lines with red fluorescent labeling of myelin, enabling structural and functional imaging compatible with green spectral sensors.

The paper identifies the myelinic channel system as a pathway for microtubule-dependent organelle transport in oligodendrocytes, showing its role in maintaining axonal integrity through neuronal activity and motor proteins.

The paper identifies myelin basic protein (MBP) as an RNA chaperone that facilitates microglial nuclear import of myelin RNA, with implications for multiple sclerosis pathology.

This paper identifies FABP8/PMP2 as a defining feature of human and old-world monkey CNS myelin, revealing molecular heterogeneity in myelin sheaths and its role in cholesterol enrichment.

This study shows that AP2 complex is essential for myelin sheath biogenesis and homeostasis, with loss of AP2 causing hypomyelination and hypermyelination in different developmental stages.

This study shows that CNS axon diameter growth does not require oligodendrocyte ensheathment or myelination, contrasting with PNS findings.

This paper develops nanobodies against CNPase, showing distinct epitopes and functional applications in imaging and as intrabodies.

This study investigates the effects of spastizin mutations in zebrafish, showing axon demyelination and degeneration in M-cells, leading to impaired locomotion.

This study shows that oligodendrocytes use potassium signaling to regulate axonal metabolism and maintain axonal health through metabolic coupling.

This study shows that ageing-related myelin dysfunction drives amyloid-beta deposition in Alzheimer's disease mouse models, suggesting myelin integrity as an upstream risk factor.

This study shows that forebrain-specific myelin loss in mice causes catatonia-like symptoms and isolated executive dysfunction without affecting motor-sensory functions.

The paper compares myelin proteome and oligodendrocyte transcriptome profiles between humans and mice, finding both conservation and divergence in specific proteins and genes.

This study identifies Pinch2 as a critical regulator of central nervous system myelination, showing that its loss leads to hypermyelination and pathological myelin outfoldings.

This study shows that CMTM5 deficiency in oligodendrocytes leads to progressive axonopathy, suggesting its role in maintaining axonal integrity rather than myelin formation.

This study shows that oligodendrocyte exosome secretion supports axonal transport and neuronal viability, and its impairment leads to axonal degeneration in mouse mutants.

This study shows that continuous myelin synthesis is necessary for maintaining white matter integrity, as preventing new myelin formation in adult mice leads to myelin degradation and neurological disease.