ライフサイエンスコーパス: myelin

1 with a multilamellar lipid structure called myelin.

2 epresenting perturbed signal conduction from myelin.

3 pezoid body fibers also showed a decrease in myelin.

4 erized by immune-mediated destruction of CNS myelin.

5 f diseases including the primary diseases of myelin.

6 the affected individuals revealed a lack of myelin.

7 characterized by focally thick and redundant myelin.

8 ecting peripheral and central nervous system myelin.

9 al role in production and maintenance of CNS myelin.

10 y but none of the other parameters including myelin.

11 d is essential for inflammatory responses to myelin.

12 by impairing the turnover of gangliosides in myelin.

13 ntifies a cellular mechanism by which subtle myelin abnormalities cause low-grade neuroinflammation a

14 p-deficient and other mutant mice with minor myelin abnormalities.

15 red in psychiatric disorders associated with myelin abnormalities.

16 is indicates that deterioration of axons and myelin after axotomy are mechanistically distinct proces

17 outgrowth inhibition and neuron loss versus myelin alone, and ELISA experiments revealed that myelin

18 ivity in both development and maintenance of myelin and have important implications in the study of m

19 l and nonneuronal cells in the regulation of myelin and identifies an additional therapeutic avenue f

20 otein, the most abundant glycoprotein in PNS myelin and mutations in which at the glycosylation site

21 pposing processes: persistent destruction of myelin and myelin repair by differentiating oligodendroc

22 g to characterize microstructural changes in myelin and neuroaxonal integrity in the cortex and white

23 a result of the estrous cycle are related to myelin and oligodendrocytes and 12 of the 63 DEGs in the

24 racterised by immune-mediated destruction of myelin and progressive neuroaxonal loss.

25 Repair cells are 2- to 3-fold longer than myelin and Remak cells and 7- to 10-fold longer than imm

26 Furthermore, the origin of these cells from myelin and Remak cells and their ability to give rise to

27 ic assumptions in Schwann cell biology: that myelin and Remak cells generate the elongated cells that

28 relationships between: (1) repair cells and myelin and Remak cells of uninjured nerves and (2) remye

29 sus that, distal to peripheral nerve injury, myelin and Remak cells reorganize to form cellular colum

30 EMENT After injury to peripheral nerves, the myelin and Remak Schwann cells distal to the injury site

31 capacity of oligodendrocytes to (re)generate myelin and that failed interactions with neighboring cel

32 f structural proteins (NF200, Ankyrin G, and Myelin) and ion channels (Pan-Nav , Nav 1.6, and Kv 3.1b

33 Many glycoproteins have been identified in myelin, and a lack of one myelin glycoprotein results in

34 t myelin comprises most of the dry weight of myelin, and its insulative nature is the basis for salta

35 owever, the axonal signals, the receptors on myelin, and the integration of intracellular signaling p

36 ion, such engineered DCs, when pulsed with a myelin antigen, led to myelin-specific suppression of on

37 tamin D 1alpha-hydroxylase and pulsed with a myelin antigen, provide myelin-specific suppression of o

38 response elicited by endogenously presented myelin antigens in vivo, we developed a novel approach u

39 ificantly retarded CNS myelination; however, myelin appeared normal at 3 months of age.

40 ease-related changes to oligodendrocytes and myelin are also suspected of playing a role in developme

41 corporated into central nervous system (CNS) myelin are contributed by astrocytes.

42 Myelin around axons is currently widely studied by struc

43 n, which is of importance when understanding myelin assembly and demyelinating conditions.

44 measured their maturation via expression of myelin-associated genes (hMBP, mMog) in presence and abs

45 led a dominant pattern of down-regulation of myelin-associated genes.

46 We now demonstrate that myelin-associated glycoprotein (MAG), a well known inhib

47 We show that myelin-associated glycoprotein or CNS myelin, in general

48 Anti-MAG (myelin-associated glycoprotein) neuropathy is a disablin

49 injured neurons, promote axon growth, remove myelin-associated growth inhibitors, and guide regenerat

50 xpression of Rtn4b is very low in tissue and myelin at 3-5 days after lesion when axons regenerate.

51 nd quantify the molecular order of lipids in myelin at subdiffraction scales, using label-free polari

52 ined whether MDD is characterized by reduced myelin at the whole-brain level and in NAcc, LPFC, insul

53 orporates both T and B cell recognition of a myelin autoantigen.

54 ensity imaging for assessing microstructural myelin, axonal and dendrite integrity in lesional and no

55 ensor for the simultaneous quantification of Myelin Basic Protein (MBP) and Tau proteins in cerebrosp

56 acked myelin membranes, mostly occupied by a myelin basic protein (MBP) phase.

57 A critical component of myelin is myelin basic protein (MBP), expression of which requires

58 ed cisplatin-induced changes in coherency of myelin basic protein fibers in the cingular cortex and l

59 ereby increasing oligodendrocyte density and myelin basic protein staining in CNS lesions.

60 e in regulatory T cells, with an increase in myelin basic protein-specific T cell proliferation and s

61 rmin (Ermn), and by immunohistochemistry for myelin basic protein.

62 Ac-6-O-sulfation) is highly conserved in PNS myelin between these species.

63 Cholesterol is rate-limiting for myelin biogenesis in the developing CNS; however, whethe

64 on (MPF) mapping demonstrated a promise as a myelin biomarker in human and animal studies with a part

65 present in most astrocytes at sites of acute myelin breakdown, indicating that astroglial myelin phag

66 ders defined by lack of development of brain myelin, but the cellular mechanisms of hypomyelination a

67 We assessed the cellular origin of new myelin by fate mapping platelet-derived growth factor re

68 Because modulation of myelin can, in turn, affect several aspects of conductio

69 emak cells and their ability to give rise to myelin cells after regeneration has not been demonstrate

70 nerves and that such cells can transform to myelin cells after regeneration.SIGNIFICANCE STATEMENT A

71 tor of toxicity was axonopathy and secondary myelin changes accompanied by a reduction in intraepider

72 In situ analyses indicated a spectrum of myelin changes in the presence of morphologically intact

73 knowledge, little is known about AD-related myelin changes, and even when present, they are often re

74 Neutrophil depletion substantially inhibits myelin clearance after nerve injury in both male WT and

75 This promoted myelin clearance but led to abnormalities in nonmyelinat

76 our laboratory has previously reported that myelin clearance in the injured sciatic nerve proceeds u

77 e find that neutrophils play a major role in myelin clearance not only in Ccr2(-/-) mice but also in

78 In the early phase of injury, the rate of myelin clearance was faster.

79 axons, activate FGFR2 in the oligodendrocyte/myelin compartment to increase ERK1/2 activation, which

80 ve blood-nerve barrier, are impacted by this myelin composition change is unknown.

81 nerve despite this change in glial cell and myelin composition, remains unknown.

82 Compact myelin comprises most of the dry weight of myelin, and i

83 Myelin content was detected with carbon 11 ((11)C) Pitts

84 arkers while being sensitive to white matter myelin content.

85 Using anatomical MRI optimized for myelin contrast within gray matter, we also observe a st

86 le explanation for these deficits is loss of myelin, creating conduction block at the site of injury.

87 carriers may have increased vulnerability to myelin damage following injury or disease due to ineffic

88 We expect that clarifying the nature of myelin damage in preclinical AD may be informative on th

89 ion, blood-brain barrier opening, and later, myelin damage.

90 sciences is that the clearance of axonal and myelin debris after a nerve injury is directed primarily

91 t heterozygote GALC mutant mice have reduced myelin debris clearance and diminished remyelination aft

92 llowing injury or disease due to inefficient myelin debris clearance.

93 In all conditions, we found that myelin debris was present in most astrocytes at sites of

94 Functionally, myelin debris was taken up by astrocytes through recepto

95 esions have been shown previously to contain myelin debris, although its significance has not been ex

96 After neonatal implantation into myelin-deficient shiverer mice, SCZ GPCs showed prematur

97 to discriminate and evaluate the severity of myelin deficit in mouse and rhesus monkey brains.

98 lving tool for identification and evaluation myelin deficit in preclinical animals and potentially in

99 shed PCA-tdTHz, we evaluated the severity of myelin deficit lesions in rhesus monkey brain induced by

100 While myelin deficit of the central nervous system leads to se

101 ve index relation of THz spectrum identified myelin deficit without exogenous labeling or any pretrea

102 ere identified in both porcine and mouse PNS myelin, demonstrating that the 6-O-sulfation of N-acetyl

103 ed along nerves containing centrally derived myelin, demonstrating that, although perineurial glial c

104 in healthy subjects but responded instead to myelin-derived self-antigens in patients with MS.

105 but not mouse, iNKT cells directly recognize myelin-derived sulfatide presented by CD1d.

106 While an innate program of myelin development proceeds independently of nervous sys

107 ramified microglia of normal white matter in myelin disease models.

108 om iPSC may facilitate the studying of human myelin diseases and the development of high-throughput s

109 key technology to understand the biology of myelin diseases and to develop treatments for such disor

110 permanent neurological disability in primary myelin diseases.

111 eta KO-mediated neurite growth promotion and myelin disinhibition were abrogated by CRMP2 inhibition

112 correlation and drug screening in any human myelin disorder.

113 Based on cytoarchitecture and myelin distribution, we identified seven Ov subregions,

114 he potential to protect and possibly restore myelin elaborated by existent oligodendrocytes in early

115 Myelin elaborated by oligodendrocytes (OLs) in the centr

116 the master transcription factors controlling myelin formation and development in oligodendrocytes whi

117 sm underlying the important roles of MyRF in myelin formation and development.

118 e for activity-dependent, plastic changes in myelin-forming cells that influence myelin structure and

119 eins cluster in response to myelination, how myelin-forming glia influence nodal assembly is poorly u

120 Macrophages with ingested myelin fragments were identified only once the fragmenta

121 NIFICANCE STATEMENT Nodes of Ranvier are the myelin-free gaps along myelinated axons that allow fast

122 and not required for OL differentiation and myelin gene expression in vivo.

123 ted with altered oligodendrocyte morphology, myelin gene expression, and microtubule dysfunction.

124 , with normal oligodendrocyte morphology and myelin gene expression.

125 sease, hundreds of mutations in the X-linked myelin gene proteolipid protein 1 (PLP1) have been ident

126 Myelin-gene Regulatory Factor (MyRF) is one of the maste

127 tion in some systems, potentially suppresses myelin genes, and has been implicated in demyelinating n

128 uation of myelin growth, expression of major myelin genes, key transcription factor Myrf and extracel

129 rticipate in transcription regulation of the myelin genes.

130 been identified in myelin, and a lack of one myelin glycoprotein results in abnormal myelin structure

131 PNS myelin glycoproteins contain highly abundant sulfated N-

132 However, the roles of glycans on myelin glycoproteins remain poorly understood.

133 mbryonic MAPK/ERK activation in SCs enhances myelin growth overcoming signals that normally end myeli

134 stained activation in SCs induced continuous myelin growth, compensating for the absence of essential

135 ole, excessive SC mTORC1 activity stimulates myelin growth, even overgrowth, in adulthood.

136 r type 1 (FGFR1), resulted in attenuation of myelin growth, expression of major myelin genes, key tra

137 tart, while remaining mTORC1 activity drives myelin growth.

138 r insights into the regulatory mechanisms of myelin growth.

139 etase activity before exposing to MAG or CNS myelin improves SC migration and survival in vitro Furth

140 research is needed to elucidate the role of myelin in affecting emotional, cognitive, behavioral, an

141 timulate this pool of progenitors to replace myelin in demyelinating diseases.

142 NS precursors could be manipulated to repair myelin in lieu of glial transplantation.

143 o have reduced levels of GM1 ganglioside and myelin in neuronal axons.

144 These results suggest a novel role for MAG/myelin in poor SC-myelin interaction and identify p75 cl

145 eripheral activity modifies the thickness of myelin in sensory neurons, not only in development but a

146 is a common autoimmune disease that targets myelin in the central nervous system (CNS).

147 Myelin in the CNS is a specialised extension of the olig

148 Myelin in the CNS is generated by oligodendrocytes and r

149 We show that lipid molecular order of myelin in the mouse spinal cord is significantly reduced

150 w that myelin-associated glycoprotein or CNS myelin, in general, inhibit rodent Schwann cell migratio

151 This first line response of astrocytes to myelin injury may exert beneficial or detrimental effect

152 nse of astrocytes in diseases with prominent myelin injury that results in recruitment of immune cell

153 al nervous system pathologies with prominent myelin injury, namely, progressive multifocal leukoencep

154 To test for stress-induced changes in myelin integrity, aurophosphate (Black Gold) myelin stai

155 ggest a novel role for MAG/myelin in poor SC-myelin interaction and identify p75 cleavage as a mechan

156 Regeneration of CNS myelin involves differentiation of oligodendrocytes from

157 NIFICANCE STATEMENT It is well accepted that myelin is a biologically active membrane in active commu

158 A critical component of myelin is myelin basic protein (MBP), expression of whic

159 Myelin is required for proper nervous system function.

160 wild-type mice and, in corpus callosum, the myelin is thinner than in controls.

161 a fundamental property of brain composition, myelin, is altered in this disorder.

162 s critical for axon function, independent of myelin itself.

163 ed (T2w) images may be sensitive to cortical myelin levels.

164 Although there is strong evidence that in myelin, lipid composition, and lipid membrane morphology

165 ann cells, both at paranodal junctions (with myelin loops) and at nodal gaps (with microvilli).

166 ltiple sclerosis (MS).SIGNIFICANCE STATEMENT Myelin loss and subsequent axon degeneration contributes

167 Remyelination is the default pathway after myelin loss in all mammalian species, in both naturally

168 ion and remyelination.SIGNIFICANCE STATEMENT Myelin loss in demyelinating disorders such as multiple

169 However, the degree and duration of myelin loss, and the extent and mechanisms of endogenous

170 ssue destruction, astrogliosis and secondary myelin loss.

171 gulators of peripheral nerve development and myelin maintenance.

172 early myelination, but is not necessary for myelin maintenance.

173 umerous studies have used Schwann cells, the myelin-making cells of the peripheral nervous system to

174 In vitro, addition of C3 tripled both myelin-mediated neurite outgrowth inhibition and neuron

175 onsistently, the effect of GD1a in restoring myelin membrane formation in the presence of fibronectin

176 aggregated fibronectin-induced inhibition of myelin membrane formation, in vitro, and OPC differentia

177 d glial cells wrap axons with a multilayered myelin membrane in vertebrates.

178 Myelin membranes are thought to be cell-autonomously ass

179 between two cytoplasmic leaflets of stacked myelin membranes, mostly occupied by a myelin basic prot

180 nd elevated chemokine expression compared to myelin-negative, reactive astrocytes.

181 istry for two strongly down-regulated genes, myelin oligodendrocyte glycoprotein (Mog) and ermin (Erm

182 Autoantibodies against myelin oligodendrocyte glycoprotein (MOG) are associated

183 otect a proteolysis-sensitive immunodominant myelin oligodendrocyte glycoprotein (MOG) epitope (resid

184 t are deficient in miR-146a and specific for myelin oligodendrocyte glycoprotein (MOG), an autoantige

185 esistant to EAE induced by immunization with myelin oligodendrocyte glycoprotein (MOG)35-55 The mecha

186 M knockout (KO) mice developed a more severe myelin oligodendrocyte glycoprotein (MOG)35-55-induced e

187 e of antibodies recognizing the autoantigen, myelin oligodendrocyte glycoprotein and tumour target, H

188 self-epitopes such as has been suggested for myelin oligodendrocyte glycoprotein epitope 35-55 (MOG35

189 E mice were given subcutaneous injections of myelin oligodendrocyte glycoprotein fragment1-125 emulsi

190 We evaluated the seroprevalence of myelin oligodendrocyte glycoprotein immunoglobulin G1 (M

191 D4-Cre and crossed these with mice bearing a myelin oligodendrocyte glycoprotein-specific TCR transge

192 is severity by limiting central tolerance to myelin oligodendrocyte glycoprotein.

193 Endogenous myelin peptide presentation to CD4(+) T cells following

194 urial glial cells display plasticity despite myelin perturbations, the blood-nerve barrier is comprom

195 lasticity of perineurial glia in response to myelin perturbations, we identified transforming growth

196 We hypothesized that myelin phagocytosis by astrocytes is an early event duri

197 myelin breakdown, indicating that astroglial myelin phagocytosis is an early and prominent feature.

198 49Asn) that exhibits a combined neuronal and myelin phenotype had overlapping cellular defects involv

199 Phosphatidylcholines are major myelin phospholipids, and several phosphorylated phospha

200 have important implications in the study of myelin plasticity and how this could relate to sensorine

201 ic cues can influence the intrinsic power of myelin plasticity to promote functional recovery.

202 n are beginning to crystallize in a model of myelin plasticity, with broad implications for neurologi

203 n rats were validated in human disease where myelin-positive hypertrophic astrocytes showed increased

204 athic pain and tissue damage mitigation, and myelin preservation.

205 ndent manner, pointing to the involvement of myelin-producing oligodendrocytes.

206 cytokines and neurotrophic factors, support myelin production, and remove synapses and cellular debr

207 Reduced levels of the myelin protein 2'-3'-cyclic nucleotide 3'-phosphodiester

208 MT1A) is caused by duplication of peripheral myelin protein 22 (PMP22) and is the most common heredit

209 is linked with duplication of the peripheral myelin protein 22 (PMP22) gene.

210 d mice, reduced expression of the structural myelin protein CNP is associated with catatonic signs in

211 reated rats also showed a reduction in major myelin protein immunoreactive clusters 7 and 14 days pos

212 MBP is an abundant myelin protein involved in demyelinating diseases, such

213 , its mechanism and association with loss of myelin protein was not elaborated.

214 g as dominant factors in the organization of myelin proteome.

215 In the mammalian nervous system, myelin provides electrical insulation for the neural cir

216 cally stained with Luxol Fast Blue (LFB) for myelin quantification.

217 Using murine myelin-reactive CD4 T cells, we demonstrate that proxima

218 anti-inflammatory cytokines that can counter myelin-reactive T cells and modulate experimental allerg

219 MS risk genes and 40% of signature genes of myelin-reactive T cells in MS changed their expression i

220 6(+) ILCs profoundly impaired the ability of myelin-reactive TH17 cells to invade central nervous sys

221 d maturation may induce positive signals for myelin recovery.

222 developmental myelination as well as during myelin regeneration.

223 tis, a model for multiple sclerosis, even in myelin regions that appear morphologically unaffected.

224 tosis (HFE), fatty acid desaturase 2 (FADS2)/myelin regulatory factor (MYRF), transmembrane protease,

225 most significantly down-regulated genes were myelin-related.

226 Furthermore, central nervous system (CNS) myelin remains an adaptive entity in adulthood, sensitiv

227 d axons in DR6(-/-) animals display profound myelin remodeling.

228 s exhibit intrinsic capacities to coordinate myelin repair and further investigation on patients with

229 spinal cord injury (SCI), but the extent of myelin repair and identity of the cells responsible rema

230 promote oligodendrocyte differentiation and myelin repair as well as motor recovery after cuprizone-

231 cesses: persistent destruction of myelin and myelin repair by differentiating oligodendrocyte progeni

232 fate mapping to demonstrate that spontaneous myelin repair by endogenous oligodendrocyte precursors i

233 Our findings suggest that myelin repair can be achieved even following prolonged d

234 adverse role of polysialic acid (polySia) in myelin repair is a long-standing question.

235 als have tested glial transplants to promote myelin repair.

236 lySia are promising strategies for improving myelin repair.

237 complexes in control of CNS myelination and myelin repair.

238 is and a therapeutic role for miR-219 in CNS myelin repair.

239 Furthermore, miR-219 mimics enhance myelin restoration following lysolecithin-induced demyel

240 l lesion segmentation and 3 T T1/T2-weighted myelin-sensitive imaging and neurite orientation dispers

241 adient strength diffusion and T1/T2-weighted myelin-sensitive magnetic resonance imaging to character

242 n alone, and ELISA experiments revealed that myelin serine proteases cleave C3 to generate active fra

243 Myelin serves essential roles in the functioning of the

244 Thus, [Ca(2+)]i controls myelin sheath development.

245 developing oligodendrocytes in vivo and that myelin sheath elongation is promoted by a high frequency

246 ction level, but not on the axonal tracts or myelin sheath integrity.

247 these receptors that drive the growth of the myelin sheath remain poorly understood in the CNS.

248 regarding axon numbers, axonal calibers, and myelin sheath thickness by electron microscopy.

249 working together to drive the growth of the myelin sheath, thus increasing myelin thickness.SIGNIFIC

250 hinery required for the proper growth of the myelin sheath.

251 lowed by local translation at the developing myelin sheath.

252 that could result in radial fractures of the myelin sheath.

253 (MS) is caused by immune-mediated damage of myelin sheath.

254 n the pinniped optic nerve, those with thick myelin sheaths (elephant seal: 9%, sea lion: 7%) and thi

255 s (elephant seal: 9%, sea lion: 7%) and thin myelin sheaths (elephant seal: 91%, sea lion: 93%).

256 revented BCCAO-induced damage to hippocampal myelin sheaths and oligodendrocytes, enhanced expression

257 Following stabilization, myelin sheaths grow along axons, and we find that higher

258 provide two lines of evidence here that thin myelin sheaths may persist indefinitely in long-lived an

259 We show that the myelin sheaths remain thin and stable on many axons thro

260 y-driven adaptations to both axons and their myelin sheaths to fully understand how myelinated axon p

261 sies and 'onion bulb' formations and/or thin myelin sheaths were observed in 14 (67%) of them.

262 ligodendrocytes initially over-produce short myelin sheaths, which are either retracted or stabilized

263 nostainings and dot blots of optic nerve and myelin showed that expression of Rtn4b is very low in ti

264 uces the clinical severity of EAE induced by myelin-specific CD4(+) T cells.

265 However, the role of myelin-specific CD8 T-cells in disease remains unclear,

266 y, we found the loss-of-function allele of a myelin-specific gene (CNP rs2070106-AA) associated with

267 dendrocyte differentiation and regulation of myelin-specific gene expression, as the cause underlying

268 in the hypothalamus are oligodendrocyte- and myelin-specific genes.

269 y, this has been seen as a by-product of the myelin-specific immune response.

270 se and pulsed with a myelin antigen, provide myelin-specific suppression of ongoing experimental alle

271 s, when pulsed with a myelin antigen, led to myelin-specific suppression of ongoing experimental alle

272 E development following adoptive transfer of myelin-specific T cells and show substantially reduced i

273 halomyelitis (EAE), expansion of pathogenic, myelin-specific Th1 cell populations drives active disea

274 t that immunogenic DCs can be engineered for myelin-specific therapy for MS.

275 this study, we identified a potential novel myelin-specific therapy that works with immunogenic DCs,

276 y tied to central nervous system maturation, myelin stability, and the pathobiology of various de- an

277 Close agreement between histological myelin staining and MPF suggests that fast MPF mapping e

278 myelin integrity, aurophosphate (Black Gold) myelin staining was performed on mPFC sections.

279 s, in conjunction with immunohistochemistry, myelin staining, and a novel three-choice, reversal-lear

280 anges in myelin-forming cells that influence myelin structure and neurological function.

281 d axonopathy, with a secondary disruption in myelin structure within 2 weeks of drug administration.

282 one myelin glycoprotein results in abnormal myelin structures in many cases.

283 zoid body fibers developed thinner axons and myelin than age-matched controls.

284 v1.2(KO) OPCs mature slower and produce less myelin than control oligodendrocytes during the recovery

285 ol of spinal cord oligodendrocytes generates myelin that is of normal thickness.

286 d as a significant "late-stage" regulator of myelin thickness in the CNS, independent of oligodendroc

287 cin (mTOR) pathway is also known to regulate myelin thickness, we examined FGFR2-deficient mice for t

288 ormal with the exception of modestly reduced myelin thickness.

289 growth of the myelin sheath, thus increasing myelin thickness.SIGNIFICANCE STATEMENT It is well accep

290 This includes a unique measurement of myelin tracks within intact tissue using an endogenous f

291 The fundamental role of the brain-specific myelin transcription factor 1-like (MYT1L) gene in cases

292 Thus, our data suggest that myelin uptake is an early response of astrocytes in dise

293 in their plasticity to myelinate and remodel myelin via mTORC1 throughout life.

294 biomarker interactions were observed between myelin water fraction and phosphorylated tau 181/beta-am

295 d transverse relaxation rates as well as the myelin water fraction from each of these individuals.

296 id 42 levels modulate age-related changes in myelin water fraction.

297 inal and transverse relaxation rates and the myelin water fraction.

298 Widespread age-related changes to myelin were observed across the brain, particularly in l

299 f Trem2, both necessary for clearing damaged myelin, were markedly reduced in GALC +/- animals.

300 udy aimed to characterize the development of myelin within the trapezoid body, a central auditory fib