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Myelin Sheath

The myelin sheath is a crucial component of the nervous system, formed by specialized cells called oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system.
This insulating layer surrounds and protects nerve fibers, enabling rapid and efficient signal transmission.
Disruption or damage to the myelin sheath can lead to various neurological disorders, such as multiple sclerosis, Guillain-Barre syndrome, and leukodystrophies.
Understainding the biology and function of the myelin sheath is crucial for developing effective treatments and therapies for these conditions.
Researchers can leverage PubCompare.ai's AI-powered protocol comparison tool to identify the most effective protocols and products for their myelin sheath studies, optimizing their research efforts.

Most cited protocols related to «Myelin Sheath»

Once the parcellation has been created, parcellated representations of data from each modality can be generated using either the group parcellation or the individual subject parcellations. For the statistical cross-validation, we created parcellated myelin, cortical thickness, task fMRI, and resting state functional connectivity datasets using the semi-automated multimodal group parcellation (see Supplementary Methods 7.1). For myelin and cortical thickness, we simply averaged the values of the dense individual subject maps within each area. For task fMRI, we averaged the time series within each area prior to computing task statistics (to benefit from the CNR improvements of parcellation demonstrated in Fig. 4e). For the same reason, we averaged resting state time series within each parcel prior to computing functional connectivity to form a parcellated functional connectome.
For each pair of areas that shared a border in the parcellation, we computed a paired samples two-tailed t-test across subjects on these parcellated data for each feature (ignoring tests that involved the diagonal in the resting state parcellated functional connectome). We thresholded these tests at the Bonferroni-corrected significance level of P < 9 × 10−8 (number of area pairs across both hemispheres (1,050) × number of features (266) × number of tails (2) × 0.05) and an effect size threshold of Cohen’s d > 1. We grouped the features into 4 independent categories (cortical thickness, myelin, task fMRI, and resting state fMRI) to determine for each area pair whether it showed robust and statistically significant differences across multiple modalities. For more details, see Supplementary Methods 7.2.
Publication 2016
Connectome Cortex, Cerebral fMRI Microtubule-Associated Proteins Multimodal Imaging Myelin Sheath Tail
Once the parcellation has been created, parcellated representations of data from each modality can be generated using either the group parcellation or the individual subject parcellations. For the statistical cross-validation, we created parcellated myelin, cortical thickness, task fMRI, and resting state functional connectivity datasets using the semi-automated multimodal group parcellation (see Supplementary Methods 7.1). For myelin and cortical thickness, we simply averaged the values of the dense individual subject maps within each area. For task fMRI, we averaged the time series within each area prior to computing task statistics (to benefit from the CNR improvements of parcellation demonstrated in Fig. 4e). For the same reason, we averaged resting state time series within each parcel prior to computing functional connectivity to form a parcellated functional connectome.
For each pair of areas that shared a border in the parcellation, we computed a paired samples two-tailed t-test across subjects on these parcellated data for each feature (ignoring tests that involved the diagonal in the resting state parcellated functional connectome). We thresholded these tests at the Bonferroni-corrected significance level of P < 9 × 10−8 (number of area pairs across both hemispheres (1,050) × number of features (266) × number of tails (2) × 0.05) and an effect size threshold of Cohen’s d > 1. We grouped the features into 4 independent categories (cortical thickness, myelin, task fMRI, and resting state fMRI) to determine for each area pair whether it showed robust and statistically significant differences across multiple modalities. For more details, see Supplementary Methods 7.2.
Publication 2016
Connectome Cortex, Cerebral fMRI Microtubule-Associated Proteins Multimodal Imaging Myelin Sheath Tail
The evaluation of cytoskeleton density was performed on 10 images of correctly-myelinated axons for each experimental point among three different experiments. Furthermore, we chose those axons that showed at least one region of myelin concentric layers stacking in the myelin sheaths to check the orthogonal sectioning. After an automatic adjustment of brightness and contrast, axons were isolated from the surrounding myelin sheath and the axonal area evaluated. Cytoplasmic organelles were deleted from the micrograph and, following an automatic thresholding of the images the generation of bit-maps, the number of identified particle was counted and normalized for axonal area.
Publication 2016
Axon Cytoplasm Cytoskeleton Microtubule-Associated Proteins Myelin Sheath Organelles
Spatial image preprocessing (distortion correction and image alignment) was carried out using the HCP’s spatial minimal preprocessing pipelines5 (link). This included steps to maximize alignment across image modalities, to minimize distortions relative to the subject’s anatomical space, and to minimize spatial smoothing (blurring) of the data. The data were projected into the 2 mm standard CIFTI grayordinates space, which includes cortical grey matter surface vertices and subcortical grey matter voxels5 (link). This offers substantial improvements in spatial localization over traditional volume-based analyses, enabling more accurate cross-subject and cross-study registrations and avoiding smoothing that mixes signals across differing tissue types or between nearby cortical folds. Additionally, we did minimal smoothing within the CIFTI grayordinates space to avoid mixing across areal borders prior to parcellation.
For cross-subject registration of the cerebral cortex, we used a two-stage process based on the multimodal surface matching (MSM) algorithm14 (link) (see Supplementary Methods 2.1–2.5). An initial ‘gentle’ stage, constrained only by cortical folding patterns (FreeSurfer’s ‘sulc’ measure), was used to obtain approximate geographic alignment without overfitting the registration to folding patterns, which are not strongly correlated with cortical areas in many regions. Previously, we found that more aggressive folding-based registration (either MSM-based or FreeSurfer-based) slightly decreased cross-subject task-fMRI statistics, suggesting that aligning cortical folds too tightly actually reduces alignment of cortical areas14 (link). A second, more aggressive stage used cortical areal features to bring areas into better alignment across subjects while avoiding neurobiologically implausible distortions or overfitting to noise in the data. The areal features used were myelin maps, resting state network maps computed with weighed regression (an improvement over dual regression34 (link) described in the Supplementary Methods 2.3) and resting state visuotopic maps (see Supplementary Methods 4.4). Areal distortion was measured by taking the log base-2 of the ratio of the registered spherical surface tile areas to the original spherical surface tile areas. The mean (across space) of the absolute value of the areal distortion averaged across subjects from both registration stages was 30% less than the standard FreeSurfer folding-based registration and the maximum (across space) of this measure was 54% less. Despite less overall distortion, the areal-feature-based registration delivers substantially more accurate registration of cortical areas than does FreeSurfer folding-based registration as judged by cross-subject task fMRI statistics, an areal feature that was not used to drive the registration14 (link). Because MSM registration preserves topology and is relatively gentle (it does not tear or distort the cortical surface in neurobiologically implausible ways), it is unable to align some cortical areas in some subjects where the areal arrangement differs from the group average (see Supplementary Results and Discussion 1.3–1.4 for more details on atypical areas). Group average registration drift away from the gentle folding-based geographic alignment was removed from the surface registration35 (link) (see Supplementary Methods 2.5) to enable comparisons of this dataset with datasets registered using different areal features (for example, post-mortem cytoarchitecture). Group average registration drift is any consistent effect of the registration during template generation on the mean size, shape, or position of areas on the sphere (as opposed to the desired reductions in cross-subject variation). An obvious example is the 37% increase in average brain volume produced by registration to MNI space4 (link). Uncorrected drifts during surface template generation can cause apparent changes in cortical areal size, shape, and position when comparing across studies.
Resting state fMRI data were denoised for spatially specific temporal artefacts (for example, subject movement, cardiac pulsation, and scanner artefacts) using the ICA+FIX approach, which includes detrending the data and aggressively regressing out 24 movement parameters36 (link),37 (link). We avoided regressing out the ‘global signal’ (mean grey-matter time course) from our data because preliminary analyses showed that this step shifted putative connectivity-based areal boundaries so that they lined up less well with other modalities, likely because of the strong areal specificity of the residual global signal after ICA+FIX clean up. Task fMRI data were temporally filtered using a high pass filter. More details on resting state and task fMRI temporal preprocessing are described in the Supplementary Methods 1.6–1.8. Substantial spatial smoothing was avoided for both datasets, and all images were intensity normalized to account for the receive coil sensitivity field. Artefact maps of large vein effects, fMRI gradient echo signal loss, and surface curvature were computed as described in Supplementary Methods 1.9.
Publication 2016
Autopsy Brain Cortex, Cerebral ECHO protocol fMRI Gray Matter Heart Histocompatibility Testing Hypersensitivity Microtubule-Associated Proteins Movement Multimodal Imaging Myelin Sheath Tears Veins
The multi-modal cortical parcellation used information related to the four areal properties of architecture, function, connectivity, and topography2 (link). Architecture was measured using T1w/T2w myelin content maps plus cortical thickness maps with surface curvature regressed out5 (link),9 (link),10 (link) (Supplementary Methods 1.5). Function was measured using task-fMRI responses to 7 tasks in 86 task contrasts (47 unique; 39 were sign-reversed contrasts). Effect size maps (beta maps) after correction for the receive field were used instead of Z statistic maps because we are interested in regional differences in the magnitude of the BOLD (blood oxygen level dependent) signal change induced by the tasks, rather than differences in the significance of the BOLD signal change. Functional connectivity was measured using pairwise Pearson correlation of the denoised resting state time series of each pair of grayordinates. Topographic organization was explored using resting state time series in visual cortex, with spatial regressors representing polar angle and eccentricity patterns in area V1 combined with a modified ‘dual-regression-like’ approach that weights each surface vertex according to the cortical surface area that it represents (see Supplementary Methods 4.4). The semi-automated multi-modal parcellation was generated using group average data for all of these modalities from the 210P group of subjects (see Supplementary Methods 3.1–3.3 for details on how the group averages were created for each modality). The reproducibility of these group average maps was assessed by correlating the spatial maps for the 210P and 210V groups (see Supplementary Results and Discussion 1.1).
Publication 2016
Blood Oxygen Levels Contrast Media Cortex, Cerebral fMRI Microtubule-Associated Proteins Myelin Sheath Striate Cortex Visual Cortex

Most recents protocols related to «Myelin Sheath»

The microglia were dissociated with trypsin and collected with completed DMEM. Cells were centrifuged at 1500 rpm and resuspended in FACS buffer before being moved to 5 ml of FACS tubes for staining. Microglia cells were incubated in blocking buffer (CD16/32-APC; 1:100; BioLegend) on ice for 10 min to block Fc receptor. Surface antibody cocktails were prepared with CD45/PerCP-Cy5.5 (1:100; BioLegend) and CD11b/APC-Fire 750 (1:100; BioLegend) including viability dye Zombie Aqua. Intracellular staining was performed with MAP2/Alexa Fluor 594 (1:100) and myelin CNPase/Alexa Fluor 647 (1:100).
Publication 2023
2',3'-Cyclic-Nucleotide Phosphodiesterases Alexa594 Alexa Fluor 647 Buffers Cardiac Arrest Cells Combined Antibody Therapeutics CY5.5 cyanine dye Fc Receptor ITGAM protein, human METAP2 protein, human Microglia Myelin Sheath Protoplasm Trypsin
To quantify the counts of immune cell subpopulations in the brain and spleen using fluorescence-activated cell sorting analysis (FACS), single-cell suspensions of brain or spleen tissues were prepared. After mice were anesthetized, the spleens and brains were quickly removed before and after transcardial perfusion with cold PBS, respectively, and then were immersed in cold PBS. Spleens and brains were mechanically homogenized through 70-µm cell strainers (BD Biosciences), and centrifuged. To isolate brain cells, 5 ml of 30% Percoll (GE Healthcare, Sweden) was added to the cell pellets obtained from brain tissues, which were centrifuged at 700×g for 10 min. After the myelin layer and the supernatant were carefully aspirated, the remaining pellets were washed with PBS, and resuspended into single-cell suspensions for FACS. A total of 7 ml Red Blood Cell Lysis Buffer (Solarbio, China) was added to spleen samples for erythrocyte lysis. Finally, single-cell suspensions of splenocytes were prepared.
Publication 2023
Brain Buffers Cells Cold Temperature Erythrocytes Mus Myelin Sheath Pellets, Drug Percoll Perfusion Population Group Spleen Tissues
Animal studies were performed according to the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health and China. The Experimental Animal Centre of Hubei Medical University provided C57BL/6 mice (male, 3–5 months) that met the criteria. The Institutional Animal Care and Use Committee of Hubei Medical University approved the animal protocols (Cat: 2019–111).
For the transduction of adult muscles, C57BL/6 male mice were anesthetized by using an isoflurane vaporizer maintained at 2% isoflurane and 1 L/m oxygen. Gastrocnemius and soleus (SL) muscles were exposed and injected with Ad-Ezrin (1 × 1010 pfu, two points, 50 μm/each) [15 (link)]. Muscles were removed 7 days after transfection, frozen in isopentane cooled in liquid nitrogen, and stored at − 80 °C.
Mutation and deletion of L-periaxin was associated with Charcot-Marie-Tooth (CMT) characterized by progressive muscle weakness and atrophy of distal extremities with sensory impairment through destroying the myelin sheath formed by Schwann cells. Interestingly, Ezrin inhibits the self-association of L-periaxin and participates in myelin sheath maintenance [4 (link), 5 (link)]. To confirm whether L-periaxin/Ezrin independence and interaction participate in CMT and muscular atrophy, a peroneal nerve injury model was prepared. Briefly, C57BL/6 male mice were anesthetized by using an isoflurane vaporizer maintained at 2% isoflurane and 1 L/m oxygen. Peroneal nerves were exposed and clamped for 15 min; subsequently, the gastrocnemius muscle (GA) was injected with Ad-Ezrin, Ad-Periaxin or Ad-shPeriaxin alone (1 × 1010 pfu, three points, 50 μm/each), and combined treatment with Ad-Ezrin (1 × 1010 pfu, three points, 50 μm/each) injection into the GA with Ad-shPeriaxin injection into the GA or Ad-Periaxin incubation within the injured peroneal nerves was incubated with Ad-Periaxin (1 × 1010 pfu, 50 μm/each) [15 (link)]. The sham and PNI groups within the peroneal nerves and GA were treated with equal amounts of normal saline. Muscles were removed 14 days after transfection, frozen in isopentane cooled in liquid nitrogen, and stored at − 80 °C. The myofiber types were measured through double fluorescence immunostaining of MyHC-I (NOQ, ab234431) and MyHC-II (My32, ab51263). Masson and hematoxylin-eosin staining were performed according to the manufacturer’s instructions. The successful establishment of the peroneal nerve injury model is shown in Additional file 1: Figure S1.
Publication 2023
Adult Animals Animals, Laboratory Atrophy Cardiac Arrest Charcot-Marie-Tooth Disease Combined Modality Therapy Deletion Mutation Eosin Fluorescence Freezing Injuries Institutional Animal Care and Use Committees Isoflurane isopentane Males Mice, Inbred C57BL Muscle, Gastrocnemius Muscle Tissue Muscle Weakness Muscular Atrophy Mutation Myelin Sheath Nitrogen Normal Saline Oxygen periaxin Peroneal Nerve Schwann Cells Soleus Muscle Transfection Vaporizers VIL2 protein, human
Musculocutaneous nerves 50 days after BPA and spinal samples 7 days after BPA were prepared for electron microscopy (EM) studies. Briefly, animals were perfused with 2.5% glutaraldehyde (sigma) plus 2% paraformaldehyde, 2-mm distal musculocutaneous nerves or ventral horns of C5–C7 spinal segments were collected for post-fixation at 4 °C overnight. Under dissection microscope, spinal tissues including ventral horn were trimmed into columns and transverse panels were identified for cutting. After washing in PBS, samples were immersed in 0.5% osmic acid, dehydrated in ethanol, and embedded in resin (EMbed 812, Electron Microscope Sciences). Semi-thin (500 nm) transverse sections were stained with 1% Toluidine Blue and images were captured under a 63 × oil objective. For ultrastructural analysis, 50-nm ultrathin sections were prepared for lead staining and the images were captured using a Philips 400 transmission electron microscope. In musculocutaneous nerves, the number of different-sized axons and G-ratio (the inner/the outer diameter of the myelin sheath) were measured using ImageJ.
In spinal sections, motoneurons with large cell bodies (> 35 μm in diameter) were photographed at × 9700 using a transmission electron microscope, and presynaptic terminals on motoneuron membranes were classified as F-type (flattened vesicles) and S-type (spherical vesicles), representing inhibitory and excitatory synapses respectively [17 (link)]. The boutons in 100-μm motoneuron membrane were counted. Three animals were used in each group, and 2 well-identified neurons were analyzed in each sample.
Publication 2023
Animals Axon Cell Body Dissection Electron Microscopy Ethanol Glutaral Horns Microscopy Motor Neurons Myelin Sheath Nerves, Musculocutaneous Neurons Neurons, Efferent Osmium Tetroxide paraform Presynaptic Terminals Psychological Inhibition Resins, Plant Synapses Tissue, Membrane Tissues Tolonium Chloride Transmission Electron Microscopy
The right (experimental/treatment group) and the left (sham/control group) nerve segments were removed en bloc with the surrounding tissue, fixed in neutral-buffered 10% formalin solution, dehydrated in alcohol series, and embedded in paraffin. Then, 5-μm sections were stained with routine haematoxylin and eosin (H&E) for general morphology and with Masson's trichrome for fibrosis. In addition, one group of sections was stained with the Klüver Barrera method to evaluate myelination, while EphA4 receptor immunohistochemistry was applied to another group of sections. Tissues from a rat without any procedure were used to see the healthy sciatic nerve structure and to compare it with other groups.
Publication 2023
Eosin Ethanol Fibrosis Formalin Immunohistochemistry Myelin Sheath Nervousness Paraffin Embedding Receptor, EphA4 Sciatic Nerve Staining Therapies, Investigational Tissues

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Myelin Removal Beads II are a laboratory product designed for the depletion of myelin from cell suspensions. The beads are made of magnetic particles coated with an antibody that specifically binds to myelin. When the cell suspension is incubated with the beads and exposed to a magnetic field, the myelin-containing cells are retained, allowing the desired cell population to be collected.
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The Neural Tissue Dissociation Kit is a laboratory equipment designed to efficiently dissociate neural tissue samples into single-cell suspensions. The kit includes reagents and tools necessary for the mechanical and enzymatic dissociation process, enabling the preparation of viable cells from complex neural tissues for further analysis or experimentation.
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Myelin removal beads are a laboratory tool used to selectively remove myelin from cell samples. They are designed to facilitate the isolation and purification of cells of interest from tissues containing myelin, such as the central nervous system.
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Collagenase D is an enzyme solution used for the dissociation and isolation of cells from various tissues. It is a mixture of proteolytic enzymes that cleave the collagen present in the extracellular matrix, allowing for the release of individual cells.

More about "Myelin Sheath"

The myelin sheath is a crucial component of the nervous system, formed by specialized cells called oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system.
This insulating layer surrounds and protects nerve fibers, enabling rapid and efficient signal transmission.
Disruption or damage to the myelin sheath can lead to various neurological disorders, such as multiple sclerosis, Guillain-Barré syndrome, and leukodystrophies.
Understanding the biology and function of the myelin sheath is crucial for developing effective treatments and therapies for these conditions.
Researchers can leverage PubCompare.ai's AI-powered protocol comparison tool to identify the most effective protocols and products for their myelin sheath studies, optimizing their research efforts.
Myelin is a lipid-rich substance that wraps around the axons of neurons, forming a protective and insulating layer.
This sheath is essential for the rapid and efficient transmission of electrical signals along the nerve fibers.
The process of myelination is carried out by specialized glial cells, such as oligodendrocytes in the central nervous system (CNS) and Schwann cells in the peripheral nervous system (PNS).
In the CNS, oligodendrocytes produce the myelin sheath, while in the PNS, Schwann cells are responsible for this process.
The myelin sheath is composed of multiple layers of lipid-rich membranes that act as an insulator, increasing the speed of signal propagation through the process of saltatory conduction.
Disruption or damage to the myelin sheath can lead to various neurological disorders, including multiple sclerosis, Guillain-Barré syndrome, and leukodystrophies.
In these conditions, the immune system may attack and damage the myelin sheath, leading to impaired nerve function and a range of neurological symptoms.
Understanding the biology and function of the myelin sheath is crucial for the development of effective treatments and therapies for these neurological disorders.
Researchers can utilize tools like Percoll, Myelin Removal Beads II, Neural Tissue Dissociation Kit, DNase I, HT7700, Ascorbic acid, HBSS, and Myelin removal beads to study the myelin sheath and its associated cells and processes.
By leveraging PubCompare.ai's AI-powered protocol comparison tool, researchers can identify the most effective protocols and products for their myelin sheath studies, optimizing their research efforts and accelerating the development of new therapies.