Number Of Myelin Research Articles

Advanced Magnetic Resonance Imaging Biomarkers of the Injured Spinal Cord: A Comparative Study of Imaging and Histology in Human Traumatic Spinal Cord Injury.

A significant problem in the diagnosis and management of traumatic spinal cord injury (tSCI) is the heterogeneity of secondary injury and the prediction of neurological outcome. Imaging biomarkers specific to myelin loss and inflammation after tSCI would enable detailed assessment of the pathophysiological processes underpinning secondary damage to the cord. Such biomarkers could be used to biologically stratify injury severity and better inform prognosis for neurological recovery. While much work has been done to establish magnetic resonance imaging (MRI) biomarkers for SCI in animal models, the relationship between imaging findings and the underlying pathology has been difficult to discern in human tSCI because of the paucity of human spinal cord tissue. We utilized post-mortem spinal cords from individuals who had a tSCI to examine this relationship by performing ex vivo MRI scans before histological analysis. We investigated the correlation between the histological distribution of myelin loss and inflammatory cells in the injured spinal cord and a number of myelin and inflammation-sensitive MRI measures: myelin water fraction (MWF), inhomogeneous magnetization transfer ratio (ihMTR), and diffusion tensor and diffusion kurtosis imaging-derived fractional anisotropy (FA) and axial, radial, and mean diffusivity (AD, RD, MD). The histological features were analyzed by staining with Luxol Fast Blue (LFB) for myelin lipids and Class II major histocompatibility complex (Class II MHC) and CD68 for microglia and macrophages. Both MWF and ihMTR were strongly correlated with LFB staining for myelin, supporting the use of both as biomarkers for myelin loss after SCI. A decrease in ihMTR was also correlated with the presence of Class II MHC positive immune cells. FA and RD correlated with both Class II MHC and CD68 and may therefore be useful biomarkers for inflammation after tSCI. Our work demonstrates the utility of advanced MRI techniques sensitive to biological tissue damage after tSCI, which is an important step toward using these MRI techniques in the clinic to aid in decision-making.

810 Aberrant Immune Activation Drives Chronic White Matter Loss After Experimental Traumatic Brain Injury

INTRODUCTION: Epidemiological studies suggest a single traumatic brain injury (TBI) initiates progressive neurodegeneration, including extensive white matter (WM) injury; yet, the majority of demyelination and WM atrophy occurs in the years following TBI in both rodents and humans. Chronic immune activation correlates with neurological dysfunction after TBI, but the underlying mechanisms remain undefined. METHODS: To define the molecular changes associated with focal TBI, unbiased Nanostring arrays were utilized after controlled cortical impact, a pre-clinical model of focal TBI, in adult mice. Immune activation was monitored using flow cytometry and neurodegeneration was assessed at 8 weeks post-TBI, by histology, electron microscopy, and magnetic resonance imaging. RESULTS: Genomic profiling revealed acute upregulation of gene classes associated with leukocyte activation, phagocytosis, antigen presentation, lymphocyte activation, and metabolism whereas genes associated with axon/dendrite structure and neural connectivity were downregulated. Infiltrating macrophages, which phagocytosed myelin debris, represented the predominant antigen presenting cells (APCs) within the CNS after TBI. Similarly, a time dependent increase in the number of myelin containing macrophages was observed within cerebrospinal fluid of severe TBI patients. Functionally, APCs stimulated with myelin ex vivo or isolated after TBI increased T-helper (TH) cell proliferation and enhanced pro-inflammatory TH1/TH17 polarization. Myeloid-selective activation of the key metabolic regulator, 5’-adenosine monophosphate-activated protein kinase (AMPK), suppressed myelin reactive T-cells, and reduced neurodegeneration after TBI. CONCLUSIONS: The infiltrating myeloid cells after TBI undergo metabolic dysfunction following phagocytosis of myelin debris and orchestrate the generation of myelin autoreactive T-cells resulting in progressive neurodegeneration.

Corrigendum: Myelination Increases the Spatial Extent of Analog-Digital Modulation of Synaptic Transmission: A Modeling Study

[This corrects the article DOI: 10.3389/fncel.2020.00040.].

Efektivitas Otak Anak Usia Dini dalam Mengenal Calistung

The introduction of calistung in AUD focuses on brain optimization of children. The child's brain has a trillion brain cells and trillions of brain-nerve cell connections. Brain nerves. influenced by the number of myelin that awakened at the age of 0-2 years which will determine the ability of abstract thinking, scientific thinking at the formal stage of operations. The backbone and cerebral cortex are the central nervous system for humans. the physical body of the child can be trained through mild exercise. Other parts of the brain in the form of cerebral cortex handle the functions of intellectual and language. Parents or nannies can provide stimulation as needed. The results suggest that children from families with high language intake received higher IQ scores at age three. So is the case with children who get more cognitive stimulation, they are more skilled in language activities. Age of AUD precisely began to learn to read if it has reached the mental age, ie 5-5.5 years.

Wrapping Up the Axon

The regulation of myelin sheath thickness is extremely important for neural function because it regulates nerve conduction velocity. Myelin thickness is proportional to axon size--small axons have little myelin, whereas large-caliber axons have a thick myelin sheath. Schwann cells deliver the correct number of myelin wraps, but how do Schwann cells "sense" the diameter of the engulfed axon? Michailov et al. (see the cover and the Perspective by ffrench-Constant et al. ) now suggest that Schwann cells respond to an axonal growth factor, neuregulin-1, and integrate this cell surface signal to create a biochemical measure of axon caliber. Altering the extent of neuregulin-1 signaling alters myelin thickness, and reduced neuregulin-1 gene dosage in mice "misleads" the Schwann cell as to the true caliber of the axonal segment, which results in reduced myelination and slowing of nerve conduction velocity. G. V. Michailov, M. W. Sereda, B. G. Brinkmann, T. M. Fischer, B. Haug, C. Birchmeier, L. Role, C. Lai, M. H. Schwab, K.-A. Nave, Axonal neuregulin-1 regulates myelin sheath thickness. Science 304 , 700-703 (2004). [Abstract] [Full Text] C. ffrench-Constant, H. Colognato, R. J. M. Franklin, The mysteries of myelin unwrapped. Science 304 , 688-689 (2004). [Summary] [Full Text]

Myelination determines the caliber of dorsal root ganglion neurons in culture

In order to understand the relationship of supporting cells to the differentiation of neurons in culture, we have used morphometry to study myelination of dorsal root ganglion (DRG) neurons by central or peripheral supporting cells. Dissociated DRG cultures from 15-day rat embryos, free of Schwann cells and fibroblasts, were prepared, and supporting cells were added from spinal cord or DRG; myelination commenced after 2 weeks. Control cultures received no supporting cells. At 7, 14, and 24 days, a total of 22 cultures were processed for electron microscopy. Three fascicles from defined points were sampled from each culture. In cultures containing glial cells, smaller fibers (p less than 0.001) were myelinated (mean of median diameter, 1.13 +/- 0.13 (SD) micron) than in cultures containing Schwann cells (1.67 +/- 0.17 micron), although there was no difference (p greater than 0.1) in the degree of myelination expressed as number of myelin lamellae/fiber. A new finding concerned the relationship of axonal diameter to the presence or absence of myelinating cells. In control cultures without supporting cells or in areas where supporting cells were absent, the range of neurite diameter (0.05 to 1.25 micron) and the median diameter (mean of median, 0.24 +/- 0.03 micron) were similar at different times (7, 14, and 24 days), demonstrating a stable population of neurite diameters throughout the period. In myelinated fascicles, a different distribution of neurite diameters was present. Myelinated neurites had a greater median diameter (measured to inner border of myelin) and a different range of fiber diameters compared to bare neurites. For Schwann cells, this range was 0.7 to 3.4 micron, and the mean of median diameters was 1.67 +/- 0.17 micron; for glial cells, the range was 0.6 to 2.4 micron, and the mean of median diameters 1.13 +/- 0.13 micron. Differences between myelinated and bare fibers were all highly significant (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

La Responsibilite Medicale (5th Edn)

In order to understand the relationship of supporting cells to the differentiation of neurons in culture, we have used morphometry to study myelination of dorsal root ganglion (DRG) neurons by central or peripheral supporting cells. Dissociated DRG cultures from 15-day rat embryos, free of Schwann cells and fibroblasts, were prepared, and supporting cells were added from spinal cord or DRG; myelination commenced after 2 weeks. Control cultures received no supporting cells. At 7, 14, and 24 days, a total of 22 cultures were processed for electron microscopy. Three fascicles from defined points were sampled from each culture. In cultures containing glial cells, smaller fibers (p less than 0.001) were myelinated (mean of median diameter, 1.13 +/- 0.13 (SD) micron) than in cultures containing Schwann cells (1.67 +/- 0.17 micron), although there was no difference (p greater than 0.1) in the degree of myelination expressed as number of myelin lamellae/fiber. A new finding concerned the relationship of axonal diameter to the presence or absence of myelinating cells. In control cultures without supporting cells or in areas where supporting cells were absent, the range of neurite diameter (0.05 to 1.25 micron) and the median diameter (mean of median, 0.24 +/- 0.03 micron) were similar at different times (7, 14, and 24 days), demonstrating a stable population of neurite diameters throughout the period. In myelinated fascicles, a different distribution of neurite diameters was present. Myelinated neurites had a greater median diameter (measured to inner border of myelin) and a different range of fiber diameters compared to bare neurites. For Schwann cells, this range was 0.7 to 3.4 micron, and the mean of median diameters was 1.67 +/- 0.17 micron; for glial cells, the range was 0.6 to 2.4 micron, and the mean of median diameters 1.13 +/- 0.13 micron. Differences between myelinated and bare fibers were all highly significant (p less than 0.001).