ライフサイエンスコーパス: myelination

1 ighted by MR relaxation rates (influenced by myelination).

2 ors and G protein-coupled receptors, control myelination.

3 nds SC precursor pools and blocks peripheral myelination.

4 endent changes in neurovascular coupling and myelination.

5 ORC1 function in Schwann cells (SCs) hampers myelination.

6 ) signaling in regulating distinct stages of myelination.

7 ligodendrocyte process extension and thereby myelination.

8 ajor feature of normal brain development and myelination.

9 n potentials, and that such process promotes myelination.

10 oligodendrocyte morphology and capacity for myelination.

11 e essential for proper nerve development and myelination.

12 differentiation and subsequent initiation of myelination.

13 ial pathogenic mechanism because it inhibits myelination.

14 is potentially important for promoting axon myelination.

15 eneration, tumorigenesis, and suppression of myelination.

16 g to ensure the correct timing and amount of myelination.

17 tion neither impaired myelin nor reactivated myelination.

18 predict lncRNA functions in oligodendrocyte myelination.

19 has an essential role in the early events of myelination.

20 iously unknown role for the Hippo pathway in myelination.

21 e that Kif13b is a negative regulator of CNS myelination.

22 e development of mature oligodendrocytes and myelination.

23 arget of rapamycin (mTOR), a major driver of myelination.

24 le of QKI in oligodendrocyte development and myelination.

25 cells, enhances AKT activation and promotes myelination.

26 ion arrest and apoptosis, and failure of CNS myelination.

27 ion regulators in cooperation with SOX10 for myelination.

28 ritic cue is necessary to prevent non-axonal myelination.

29 y for radial sorting of axons and subsequent myelination.

30 at Akt controls several key steps of the PNS myelination.

31 ntials from the eye to the SC due to lack of myelination.

32 ligodendroglial cells is critical for normal myelination.

33 pression during Schwann cell development and myelination.

34 promoting myelin growth during developmental myelination.

35 uding brain development, synaptogenesis, and myelination.

36 ndifferentiated SCs incompatible with normal myelination.

37 PI3K/Akt/mTOR pathway, a powerful driver of myelination.

38 exquisite examples of membrane remodeling is myelination.

39 otransmitter release into activity-dependent myelination.

40 pathways involved in regenerative process of myelination.

41 equired in neurons and in OLs for normal CNS myelination.

42 d by L-VOCCs in OPCs is necessary for normal myelination.

43 ition, chromatin reorganization and impaired myelination.

44 g postnatal days 0-4 (P0-P4), preceding most myelination.

45 rucial role in radial axonal sorting and PNS myelination.

46 ecruits and cooperates with Sox10 to promote myelination.

47 sion levels and properties may change during myelination.

48 Sip1), is essential for differentiation and myelination.

49 ystem (PNS) and central nervous system (CNS) myelination.

50 ells, but not in neurons, is detrimental for myelination.

51 l as promoted oligodendrocyte maturation and myelination.

52 6/Adgrg6 is essential for SC development and myelination.

53 monstrated that electrical activity promotes myelination.

54 growth, lung maturation and brain growth and myelination.

55 ation in neural features like morphology and myelination.

56 on in the presence of complement, and impair myelination.

57 known to regulate key aspects of peripheral myelination.

58 CL4 is necessary for proper peripheral nerve myelination.

59 e differentiation and central nervous system myelination.

60 on.Axon-glial communication is important for myelination.

61 involved in peripheral nervous system (PNS) myelination.

62 4,5)P3 is sufficient to trigger all steps of myelination.

63 mote oligodendrocyte differentiation and (re)myelination.

64 gy, reduces axon-OL interactions and impairs myelination.

65 phasize the essential role lysosomes play in myelination.

66 f Krox20 (Egr2), the master regulator of PNS myelination.

67 ize that Shp2 is a negative regulator of CNS myelination.

68 godendrocyte lineage specification and nerve myelination.

69 A) activation, which is required to initiate myelination.

70 growth overcoming signals that normally end myelination.

71 odendrocytes, may lastingly disrupt cortical myelination, a fundamental feature of cerebral connectiv

72 In the present study, we investigated how myelination affects ion channel expression and function,

73 Recent analyses have indicated that myelination along axons of distinct neuronal subtypes ca

74 In stark contrast, myelination along tetanus-toxin-expressing CoPA neuron a

75 fluorescent fusion protein reporter to study myelination along the axons of distinct neuronal subtype

76 promoting rapid, efficient nerve conduction, myelination also made possible the development of the la

77 failure, accumulating evidence suggests that myelination also regulates the structural properties and

78 ze sulfated N-glycans and exhibited abnormal myelination and axonal degeneration in the PNS.

79 f the oligodendrocyte (OL) lineage, delaying myelination and causing persistent motor deficits.

80 maging in these individuals reveals delay in myelination and cerebral atrophy.

81 ure work to investigate how these changes in myelination and conduction velocity contribute to signal

82 ied depending on activity levels, and axonal myelination and conduction velocity exhibited no adaptat

83 e observed upregulation of genes involved in myelination and downregulation of genes related to memor

84 ficiently to accelerate axonal regeneration, myelination and function are restored after injury.SIGNI

85 terized by seizures, leads to alterations in myelination and glia reactivity.

86 anscriptional regulation at the inception of myelination and implicate abnormal timing of myelination

87 niques allowing us to quantify the degree of myelination and iron accumulation via markers of tissue

88 The MAPK/ERK pathway promotes developmental myelination and its sustained activation in SCs induced

89 These cells are responsible for myelination and maintenance of axonal energy metabolism

90 omatin-modifying complexes in control of CNS myelination and myelin repair.

91 demonstrates that GlcNAc6ST-1 modulates PNS myelination and myelinated axonal survival through the G

92 adult and is compatible with restoration of myelination and nerve function after injury.

93 ss and IVH-induced inflammation and restores myelination and neurologic recovery in preterm rabbits w

94 ibition by intramuscular perampanel restored myelination and neurologic recovery in rabbits with IVH.

95 ation, promotes OPC maturation, and restores myelination and neurological function in rabbits with IV

96 e show the relationship between cholesterol, myelination and neurological parameters in mouse models

97 m-based strategies that effectively enhanced myelination and neurological recovery in preterm rabbit

98 treatment reduced inflammation and enhanced myelination and neurological recovery in rabbits with IV

99 has a low side-effect profile, also enhances myelination and neurological recovery in rabbits with IV

100 from vertebrate Schwann cells causes loss of myelination and neuropathies, results attributed to loss

101 MII) enhances central but impairs peripheral myelination and NMII has been implicated in cellular res

102 However, whether enhancing myelination and oligodendrocyte differentiation could be

103 This was associated with enhanced myelination and oligodendrocyte differentiation in the p

104 However, whether enhancing myelination and oligodendrocyte differentiation is benef

105 ght into the signaling mechanisms regulating myelination and propose that Shp2 acts as a transient br

106 lities that include hydrocephalus, defective myelination and reduced lifespan.

107 markedly delayed onset of both developmental myelination and remyelination after injury.

108 te that miR-219 alleles are critical for CNS myelination and remyelination after injury.

109 inactivation of lncOL1 causes defects in CNS myelination and remyelination following injury.

110 ice cultures, Treg accelerated developmental myelination and remyelination, even in the absence of ov

111 fferences in the regulation of developmental myelination and remyelination.

112 Brg1 and is required for proper onset of CNS myelination and remyelination.

113 TSC has different functions in developmental myelination and remyelination.SIGNIFICANCE STATEMENT Mye

114 Adolescent cortical myelination and shrinkage were coupled and specifically

115 h, our findings suggest that BACE1's role in myelination and some sensorimotor functions is consisten

116 omatodendritic compartment directly inhibits myelination and suggest a model in which broadly indiscr

117 nal neurobiological modifications, including myelination and synapse formation, but also pruning of a

118 ired in Schwann cells for radial sorting and myelination and that Yap is redundant with Taz.

119 spatial correspondence between the degree of myelination and the strength of the tonotopic signal acr

120 strong concordance in the degree of cortical myelination and the strength of tonotopic activation acr

121 erstanding of how different neurons regulate myelination and thus their own function within specific

122 mical network had greater rates of shrinkage/myelination and were associated with overexpression of t

123 sal agenesis and pontine hypoplasia, delayed myelination and, less frequently, thalamic signal intens

124 ly and negatively impacts programs governing myelination, and acts on myelinating oligodendrocyte (OL

125 godendrocyte count and decreased spinal cord myelination, and display related neurological phenotypes

126 by affecting oligodendrocyte development and myelination, and mouse behavior.

127 es inflammation and restores OPC maturation, myelination, and neurologic recovery in preterm newborns

128 administration would restore OPC maturation, myelination, and neurological function in survivors with

129 It also promoted OPC maturation, myelination, and neurological recovery.

130 -independent and activity-dependent modes of myelination are beginning to crystallize in a model of m

131 e statement: Oligodendrocyte development and myelination are highly dynamic processes influenced by e

132 rting and the role of mechanotransduction in myelination are largely unknown.

133 ligodendrocyte precursor cells, and promotes myelination as well as clinical recovery in preterm rabb

134 n and myelination, both during developmental myelination as well as during myelin regeneration.

135 s associated with cell process outgrowth and myelination, as well as with metabolic activity.

136 ter demyelination, are suitable for in vitro myelination assays, disease modeling, and screening of p

137 we show that, despite a developmental delay, myelination at the onset and during cuprizone-induced de

138 he function and maturation of OLs to promote myelination.Axon-glial communication is important for my

139 ndrocyte progenitor cell differentiation and myelination both in vitro and after transplantation into

140 iator of oligodendrocyte differentiation and myelination, both during developmental myelination as we

141 on of red blood cells, DNA synthesis, neural myelination, brain development, and growth.

142 in oligodendrocyte differentiation and early myelination, but is not necessary for myelin maintenance

143 ndrocyte differentiation, and viability, and myelination, but their mechanisms of action are incomple

144 +) channels (VGCCs) are important for normal myelination by acting at several critical steps during o

145 ], but it is not known whether regulation of myelination by activity is common to all neuronal subtyp

146 To investigate how activity regulates myelination by different neuronal subtypes, we express t

147 AP/TAZ regulate both developmental and adult myelination by driving TEAD1 to activate Krox20.

148 One possibility is that cholesterol promotes myelination by facilitating signal transduction within t

149 Whereas regulation of central nervous system myelination by GPR17 is well established, verification o

150 Regulation of myelination by oligodendrocytes in the CNS has important

151 Understanding the regulation of myelination by oligodendrocytes is therefore critical fo

152 How action potentials regulate myelination by oligodendrocytes is uncertain.

153 in Schwann cells Kif13b positively regulates myelination by promoting p38gamma mitogen-activated prot

154 e that while some neuronal subtypes modulate myelination by synaptic vesicle release to a striking de

155 y aspects of oligodendrocyte development and myelination can be modulated by extrinsic signals includ

156 Activity-dependent modulation of myelination can dynamically alter action potential condu

157 The enhanced myelination capacity of the SMF stimulated oligodendrocy

158 gy utilization affect both cell survival and myelination capacity.

159 xpectedly opened new avenues of insight into myelination-centered mechanisms of neural plasticity.

160 saccharide reduced inflammation and enhanced myelination, conceivably by depleting HC-HA levels.

161 A lack of sufficient oligodendrocyte myelination contributes to remyelination failure in demy

162 function as an 'inhibitor of inhibitors' in myelination control.

163 elopment and Tead1 binding is induced during myelination, correlating with Pmp22 expression.

164 However, these defects and myelination could be rescued by pharmacological mTORC1 i

165 the beneficial effect of Perk deficiency on myelination could derive from neurons.

166 are regulated by NECL4 and affect peripheral myelination currently remain unclear.

167 The CNS myelination defect results from a cell-autonomous requir

168 Accordingly, human GPR56 mutations cause myelination defects and brain malformations.

169 From a forward genetic screen for myelination defects in zebrafish, we identified a mutati

170 restricted solely to Schwann cells reversed myelination defects, significantly improved neuromuscula

171 esponse, which improved both morphologic and myelination defects.

172 del displays not only axonal damage but also myelination deficits and glial activation in different b

173 Kernicterus presents as axonopathy with myelination deficits at different brain regions, includi

174 Schwann cell differentiation and myelination depends on chromatin remodeling, histone ace

175 ur data indicate that Akt is crucial for PNS myelination driving axonal wrapping by unmyelinated and

176 ed thin myelin sheaths in a model of delayed myelination during a period of 13 years that we propose

177 ensure the correct onset and progression of myelination during both development and following periph

178 s in regulating oligodendrocyte survival and myelination during CNS development.

179 Disruption of myelination during development has been implicated in a

180 nsensus that neuronal activity regulates CNS myelination (e.g., [5-9]) through local axon-oligodendro

181 ration arrest followed by apoptosis, and CNS myelination fails.

182 h results in arrested maturation of OPCs and myelination failure.

183 bited unusual structural adaptations in axon myelination for increased conduction velocity.

184 Here we review insights into myelination, from target selection to axon wrapping and

185 serine/threonine kinase Akt in promoting CNS myelination has been demonstrated, its role in the PNS h

186 to increasing the speed of nerve conduction, myelination has emerged as a source of plasticity in neu

187 ificant enrichment for genes associated with myelination, hormone stimulus, and abnormal hormone leve

188 though nodal proteins cluster in response to myelination, how myelin-forming glia influence nodal ass

189 esis, resulted in significantly retarded CNS myelination; however, myelin appeared normal at 3 months

190 n schizophrenia and provide support for the "myelination hypothesis" of the disease.

191 lum was the area most affected, with greater myelination impairment and glia burden, and showing a ma

192 measure cortical thickness and intracortical myelination in 297 population volunteers aged 14-24 y ol

193 e PI3K/AKT signaling pathway, which controls myelination in both PNS and CNS.

194 e beam performance, pain response, and nerve myelination in both species.

195 isingly, the phenotypes ranged from arrested myelination in nerve development to focal hypermyelinati

196 that BACE1 inhibition significantly impairs myelination in our co-culture system.

197 proposed in vitro as a negative regulator of myelination in Schwann cells.

198 elopment, with less coherent fibers and less myelination in SCR and PCR only in male infants, but the

199 2 (JAM2) as an inhibitor of somatodendritic myelination in spinal cord neurons, thereby elucidating

200 Myelination in the CNS is an ongoing process that starts

201 -glial communication are required for proper myelination in the developing brain.

202 myelination and implicate abnormal timing of myelination in the pathogenesis of childhood-onset dysto

203 ce, sustained Sox2 expression in vivo blocks myelination in the peripheral nerves and maintains Schwa

204 Schwann cell (SC) myelination in the peripheral nervous system is essentia

205 NRG1) is a key signalling factor controlling myelination in the peripheral nervous system, via signal

206 its potential to play a role in disorders of myelination in the peripheral nervous system.

207 The signaling pathways that regulate myelination in the PNS remain poorly understood.

208 ry mechanisms underlying axonal wrapping and myelination in the PNS.

209 ial avoidance and change gene expression and myelination in the prefrontal cortex.

210 prolonged social isolation display impaired myelination in the prefrontal cortex.

211 ing regulates oligodendrocyte maturation and myelination in TSC.

212 enhance oligodendrocyte differentiation and myelination in vitro, for 2 weeks in adult mice followin

213 iator of oligodendrocyte differentiation and myelination in vitro.

214 ndrocyte progenitor cell differentiation and myelination in vitro.

215 as a physiological regulator of Schwann cell myelination in vivo and its potential to play a role in

216 wished to test fully whether Sox2 regulates myelination in vivo and show here that, in mice, sustain

217 omplex in anterograde mbp mRNA transport and myelination in vivo.

218 ized by clustering of activated MG, aberrant myelination, increased inflammation, and lysosomal anoma

219 Axon myelination increases the conduction velocity and precis

220 PERK may interfere with myelination, independent of its role in ER stress.

221 During myelination, individual oligodendrocytes initially over-

222 nd that THAP1 is essential for the timing of myelination initiation during CNS maturation.

223 ferentiated state to ensure proper timing of myelination initiation.

224 Myelination is a biosynthetically demanding process in w

225 Our data suggest that promoting adult myelination is a potential strategy for reversing depres

226 d axons following injury and we show that re-myelination is also blocked by Sox2 expression in Schwan

227 Myelination is critical for rapid propagation of action

228 Correct myelination is crucial for the function of the periphera

229 t that this activity-dependent alteration of myelination is important for modifying the conductive pr

230 t preexisting oligodendrocytes, after active myelination is largely terminated.

231 frontotemporal dementia, but its relation to myelination is not understood.

232 Emerging evidence indicates that myelination is sensitive to environmental experience and

233 gest a model in which broadly indiscriminate myelination is tailored by inhibitory signaling to meet

234 ch molecule controls both axonal sorting and myelination is unclear.

235 The molecular trigger of CNS myelination is unknown.

236 ure OLs in the adult mouse CNS to reinitiate myelination, leading to new myelin wraps and functional

237 Thus, enhancing myelination may be a potential means of reversing depres

238 es designed to push mature OLs to reinitiate myelination may be beneficial both for enhancing remyeli

239 on for binaural auditory processing, reduced myelination might augment sensorineural hearing impairme

240 f ASO treatment after disease onset restored myelination, MNCV, and CMAP almost to levels seen in WT

241 e current study suggests that changes in CNS myelination occur as a downstream mechanism following pe

242 Myelination occurs selectively around neuronal axons to

243 cells (NG2 cells) could be key to rendering myelination of axons dependent on neuronal activity, but

244 Myelination of axons facilitates rapid impulse propagati

245 In the vertebrate nervous system, myelination of axons for rapid impulse propagation requi

246 The myelination of axons in peripheral nerves requires preci

247 Re-myelination of CNS nerves after injury is ineffective.

248 s, elimination of exuberant projections, and myelination of established tracts.

249 r the ability of this pathway to promote the myelination of human sensory axons.

250 tivity in the transgenic mice did not induce myelination of nonmyelinating Schwann cells in the sympa

251 oligodendrocyte differentiation and de novo myelination of parallel fibers.

252 role that it plays in these cells and in the myelination of the peripheral nervous system (PNS) is un

253 defeat induces molecular changes that reduce myelination of the prefrontal cortex, which may be an un

254 y chemical cross-linking results in aberrant myelination of the somatodendritic compartment of neuron

255 ants leads to cerebral inflammation, reduced myelination of the white matter, and neurological defici

256 rogenitor cell (OPC) maturation, and reduced myelination of the white matter.

257 ulation of a gene set enriched for decreased myelination, oligodendrocyte differentiation, and expres

258 opmental oligodendrocyte differentiation and myelination, oligodendrocyte-specific deletion of tubero

259 However, if mTORC1 was hyperactivated after myelination onset, radial hypermyelination was observed.

260 upregulation commenced during developmental myelination or was induced later during adulthood in qui

261 ion cortex had faster rates of shrinkage and myelination over the course of adolescence.

262 However, this default myelination process can be modulated by changes in neuro

263 ts as a transient brake to the developmental myelination process.

264 es in type IIb FCD are due to defects of the myelination processes and maturation, impaired by the pr

265 l blockade of the NRG1-ErbB pathway prevents myelination, providing direct evidence for the ability o

266 ought to be more sensitive to differences in myelination (putatively indexed by the [quantitative] lo

267 mpromising axonal fiber number, density, and myelination, rather than processes leading to spatial di

268 unctions, but their roles in oligodendrocyte myelination remain undefined.

269 odifies beta-catenin signalling and controls myelination remains elusive.

270 Plasticity of myelination represents a mechanism to tune the flow of i

271 concept has emerged that activity-regulated myelination represents an important form of nervous syst

272 chwann cell development and peripheral nerve myelination require the serial expression of transcripti

273 ilored by inhibitory signaling to meet local myelination requirements.

274 Myelination requires oligodendrocyte-neuron communicatio

275 s were used to measure WM microstructure and myelination, respectively.

276 ental process of synaptic pruning and limits myelination, resulting in age-specific reductions in cor

277 uberty followed by selective elimination and myelination, resulting in volume loss and thinning.

278 h, compensating for the absence of essential myelination signals.

279 Myelination starts after the AIS as well as the distribu

280 ed for Schwann cell (SC) differentiation and myelination; sustained embryonic MAPK/ERK activation in

281 ted with oligodendrocyte differentiation and myelination that were validated via cross-species compar

282 Contrary to developmental myelination, there were no changes in OPC or oligodendro

283 ER stress, suggesting that Perk may modulate myelination through a pathway independent of the UPR.

284 ffectors TAZ and YAP in SC proliferation and myelination through modulating G-protein expression and

285 cline in mTORC1 activity is crucial to allow myelination to start, while remaining mTORC1 activity dr

286 inic compound that has been shown to enhance myelination under demyelinating conditions, successfully

287 muli on mechanisms governing programs of CNS myelination under normal and pathological conditions.

288 ole of the MAPK/ERK pathway in developmental myelination versus remyelination and the importance of s

289 chwann cells that regulates peripheral nerve myelination via its cognate receptor ADAM22 expressed by

290 The reduced myelination was accompanied by an important decline in t

291 Developmental myelination was imaged noninvasively in live zebrafish.

292 Impaired myelination was rescued by oral clemastine treatment, an

293 s involved in oligodendrocyte maturation and myelination, we used a conditional knock-out mouse for v

294 Age-related increases in cortical myelination were maximized approximately at the internal

295 d in vitro, and the patterning and extent of myelination were perturbed in the CNS of p35(-/-) mice.

296 on of Discs large 1 (Dlg1), a known brake on myelination, which downregulates the phosphatidylinosito

297 e a molecular model for MDL formation during myelination, which is of importance when understanding m

298 ll-derived sensory neurons strongly enhances myelination, while conversely pharmacological blockade o

299 rain structural measurements implied greater myelination within vmPFC in misophonic individuals.

300 k loss of function in Schwann cells restores myelination without diminishing accumulation of P0 or ma