Klaus‐Armin Nave

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

This study uses snATAC-seq and snRNA-seq to identify TE-derived regulatory elements involved in adult hippocampal neurogenesis in response to rhEPO stimulation.

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.

This study shows that mutant SOD1 aggregates in myelinic nanochannels and accelerates ALS progression in mice, highlighting the role of myelin channel integrity in disease.

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.

The paper shows that microglia and astrocytes extract myelinoid bodies via tethers, preserving myelin sheath integrity through tension-driven scission and fusion.

This study identifies CRH-expressing OPCs that prevent premature differentiation following CNS injury and in early development, highlighting CRHR1's role in oligodendrogenesis.

This study shows EPO induces chromatin remodeling in adult mouse hippocampal neurons, revealing a transposon-mediated mechanism for neurogenesis.

The paper shows that deleting EPO in the forebrain of mice leads to increased expression of EPOR and EphB4, which may explain the lack of cognitive deficits in these mutants.

This study investigates how erythropoietin (EPO) and its receptor (EPOR) regulate oligodendrocyte lineage dynamics in the adult mouse hippocampus, showing EPO promotes differentiation and maturation, and suggests potential therapeutic applications for remyelination.

This study shows that erythropoietin treatment improves behavioral and phenotypical symptoms in Zbtb20+/- mice, a model of Primrose syndrome.

This study identifies novel protein-protein interactions of PMP22 using optimized co-immunoprecipitation and mass spectrometry across multiple cell types.

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.

The paper shows oligodendrocytes contribute to amyloid-β plaques in Alzheimer's disease, but neurons are required for plaque formation.

This study shows that erythropoietin (EPO) reduces inhibitory potential in hippocampal interneurons, enhancing pyramidal neuron excitability and potentially improving neuropsychiatric symptoms.

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

The paper challenges the view that axonal degeneration in MS results from immune-mediated damage by proposing that myelin itself increases axonal degeneration risk under inflammatory conditions.

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 uses single-nucleus RNA sequencing to show that erythropoietin treatment restructures transcriptional networks in hippocampal pyramidal neurons, increasing their numbers and altering gene expression related to neurodifferentiation and cognition.

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 demonstrates that oligodendrocytes mediate axo-vascular coupling in the mouse optic nerve by regulating vascular dilation in response to axonal activity.

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 shows that TDP-43 loss affects oligodendrocyte survival and myelination differently at various stages of maturation, leading to morphological defects and neurological impairments.

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

The paper shows that myelin acts as an energy reserve in the brain under glucose deprivation, supporting oligodendrocytes and axons through fatty acid oxidation.

This study identifies PI3K/Akt/mTOR signaling as a therapeutic target for HNPP by showing that mTOR inhibitors reduce hypermyelination in HNPP mouse models.

The paper shows that neuronal cholesterol synthesis is critical for remyelination in chronic demyelination models and MS patients.

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 oligodendrocytes contribute to sustained stimulus perception in complex auditory tasks, beyond their role in increasing axonal conduction velocity.

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.