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277
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ShareScore release 0.9.0
Dataset results
277 results for “myelin”
Assessing Changes in Multi-parametric MRI in Patients With Acute Demyelinating Lesions Taking Clemastine Fumarate as a Myelin Repair Therapy
ClinicalTrials.gov study NCT06065670. IPD Sharing: NO. Countries: 1. Publications: 5.
Frequency of FCGR3A Gene Polymorphisms in Patients With Neuromyelitis Optica Spectrum Disorders, Anti-oligodendrocyte Myelin Protein Antibody Disease, and Multiple Sclerosis.
ClinicalTrials.gov study NCT06865274. IPD Sharing: NO. Countries: 1. Publications: 30.
Initial Clinical Presentation of Inflammatory Optic Neuritis Associated or Not With Autoantibodies Anti-Myelin-oligodendrocyte-glycoprotein
ClinicalTrials.gov study NCT03345537. IPD Sharing: NO. Countries: 1. Publications: 15.
Effect of the Kv7-channel Opener Flupirtine on the Excitability of Human Peripheral Myelinated Axons in Vivo
ClinicalTrials.gov study NCT01450865. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Human myelinated brain organoids with integrated microglia as a model for myelin repair and remyelinating therapies
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Data from: Myelin basic protein induces neuron-specific toxicity by directly damaging the neuronal plasma membrane
The central nervous system (CNS) insults may cause massive demyelination and lead to the release of myelin-associated proteins including its major component myelin basic protein (MBP). MBP is reported to induce glial activation but its effect on neurons is still little known. Here we found that MBP specifically bound to the extracellular surface of the neuronal plasma membrane and induced neurotoxicity in vitro. This effect of MBP on neurons was basicity-dependent because the binding was blocked by acidic lipids and competed by other basic proteins. Further studies revealed that MBP induced damage to neuronal membrane integrity and function by depolarizing the resting membrane potential, increasing the permeability to cations and other molecules, and decreasing the membrane fluidity. At last, artificial liposome vesicle assay showed that MBP directly disturbed acidic lipid bilayer and resulted in increased membrane permeability. These results revealed that MBP induces neurotoxicity through its direct interaction with acidic components on the extracellular surface of neuronal membrane, which may suggest a possible contribution of MBP to the pathogenesis in the CNS disorders with myelin damage.
Data from: Loss of mTORC2 signaling in oligodendrocyte precursor cells delays myelination
Myelin abnormalities are increasingly being recognized as an important component of a number of neurologic developmental disorders. The integration of many signaling pathways and cell types are critical for correct myelinogenesis. The PI3-K and mechanistic target of rapamycin (mTOR) pathways have been found to play key roles. mTOR is found within two distinct complexes, mTORC1 and mTORC2. mTORC1 activity has been shown to play a major role during myelination, while the role of mTORC2 is not yet well understood. To determine the role of mTORC2 signaling in myelinogenesis, we generated a mouse lacking the critical mTORC2 component Rictor in oligodendrocyte precursors (OPCs). Targeted deletion of Rictor in these cells decreases and delays the expression of myelin related proteins and reduces the size of cerebral white matter tracts. This is developmentally manifest as a transient reduction in myelinated axon density and g-ratio. OPC cell number is reduced at birth without detectable change in proliferation with proportional reductions in mature oligodendrocyte number at P15. The total number of oligodendrocytes as well as extent of myelination, does improve over time. Adult conditional knock-out (CKO) animals do not demonstrate a behavioral phenotype likely due in part to preserved axonal conduction velocities. These data support and extend prior studies demonstrating an important but transient contribution of mTORC2 signaling to myelin development.
Data from: HDAC1/2-dependent P0 expression maintains paranodal and nodal integrity independently of myelin stability through interactions with neurofascins
The pathogenesis of peripheral neuropathies in adults is linked to maintenance mechanisms that are not well understood. Here, we elucidate a novel critical maintenance mechanism for Schwann cell (SC)–axon interaction. Using mouse genetics, ablation of the transcriptional regulators histone deacetylases 1 and 2 (HDAC1/2) in adult SCs severely affected paranodal and nodal integrity and led to demyelination/remyelination. Expression levels of the HDAC1/2 target gene myelin protein zero (P0) were reduced by half, accompanied by altered localization and stability of neurofascin (NFasc)155, NFasc186, and loss of Caspr and septate-like junctions. We identify P0 as a novel binding partner of NFasc155 and NFasc186, both in vivo and by in vitro adhesion assay. Furthermore, we demonstrate that HDAC1/2-dependent P0 expression is crucial for the maintenance of paranodal/nodal integrity and axonal function through interaction of P0 with neurofascins. In addition, we show that the latter mechanism is impaired by some P0 mutations that lead to late onset Charcot-Marie-Tooth disease.
Adrenocorticotropic Hormone (ACTH) Effects on Myelination in Subjects With MS
ClinicalTrials.gov study NCT02446886. IPD Sharing: NO. Countries: 1. Publications: 0.
Data from: Myelin basic protein induces neuron-specific toxicity by directly damaging the neuronal plasma membrane
Open the record for dataset details and reuse information.
Data from: HDAC1/2-dependent P0 expression maintains paranodal and nodal integrity independently of myelin stability through interactions with neurofascins
Open the record for dataset details and reuse information.
Data from: Loss of mTORC2 signaling in oligodendrocyte precursor cells delays myelination
Open the record for dataset details and reuse information.
Role of fatty acid synthase in oligodendrocyte myelination
GEO Series GSE112725. Mus musculus. 7 samples. Type: Expression profiling by high throughput sequencing.
DNA methylation status of myelinating Schwann cells during development and in diabetic neuropathy [Bisulfite-Seq2]
GEO Series GSE51031. Mus musculus. 10 samples. Type: Methylation profiling by high throughput sequencing.
DNA methylation status of myelinating Schwann cells during development and in diabetic neuropathy [Gene Expression Array: GNMT mice]
GEO Series GSE45701. Mus musculus. 4 samples. Type: Expression profiling by array.
PAD2-mediated citrullination contributes to efficient oligodendrocyte differentiation and myelination
GEO Series GSE115929. Mus musculus. 8 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Neuronal APOE4 removal strongly protects against Tau-mediated gliosis, neurodegeneration, and myelin deficits
GEO Series GSE221215. Mus musculus. 11 samples. Type: Expression profiling by high throughput sequencing.
Reactive oligodendrocyte progenitor cells (re-)myelinate the regenerating zebrafish spinal cord [transcriptome]
GEO Series GSE161686. Danio rerio. 20 samples. Type: Expression profiling by high throughput sequencing.
RNA expression in mutants of the miRNA pathway during myelination
GEO Series GSE64880. Mus musculus. 15 samples. Type: Expression profiling by high throughput sequencing.
SRF transcriptionally regulates the oligodendrocyte cytoskeleton during CNS myelination (ChIP-Seq)
GEO Series GSE241559. Rattus norvegicus. 16 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.