ライフサイエンスコーパス: myelin sheath

1 ocyte glycoprotein (MOG that is a protein in myelin sheath).

2 in (MOG), the membrane proteins found in the myelin sheath.

3 d is critical for the genesis of the central myelin sheath.

4 t of axons and subsequent elaboration of the myelin sheath.

5 facilitated by the oligodendrocyte-produced myelin sheath.

6 glial cell size to generate a multilamellar myelin sheath.

7 NF155), and apposes the inner mesaxon of the myelin sheath.

8 etabolite diffusion across the layers of the myelin sheath.

9 rrents can be short-circuited underneath the myelin sheath.

10 ents for the formation and maturation of the myelin sheath.

11 RNA and translocates from the nucleus to the myelin sheath.

12 adherin alone, but without any defect to the myelin sheath.

13 monolayers important to the adhesion of the myelin sheath.

14 between the paranodal terminal loops of the myelin sheath.

15 role in the formation and maintenance of the myelin sheath.

16 ar sheets of insulating plasma membrane--the myelin sheath.

17 free-radical-induced oxidative damage to the myelin sheath.

18 sion of the multiple, spiraling wraps of the myelin sheath.

19 odel membrane system that closely mimics the myelin sheath.

20 tween the axon and the terminal loops of the myelin sheath.

21 ts by TPPP is critical for elongation of the myelin sheath.

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

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

24 lowed by local translation at the developing myelin sheath.

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

26 tion and maintenance of the peripheral nerve myelin sheath.

27 ructural and functional role in the neuronal myelin sheath.

28 the peripheral nervous system that form the myelin sheath.

29 etween adjacent cytoplasmic membranes of the myelin sheath.

30 he initiation and properties of Schwann cell myelin sheaths.

31 n of dominant-negative Fbxw7 produced longer myelin sheaths.

32 brane around axons to generate multilamellar myelin sheaths.

33 ng to mature cells capable of generating new myelin sheaths.

34 f surviving oligodendrocytes to generate new myelin sheaths.

35 axons or, having achieved this, fail to form myelin sheaths.

36 ligodendrocytes and specifically phagocytose myelin sheaths.

37 localised to both developing and mature CNS myelin sheaths.

38 roduction of myelin proteins to generate new myelin sheaths.

39 med oligodendrocytes frequently generate new myelin sheaths.

40 e in service or intercalating among existing myelin sheaths.

41 nating oligodendrocytes and their contiguous myelin sheaths.

42 millimeters and were organized with compact myelin sheaths.

43 mmon objective of investing nerve axons with myelin sheaths.

44 osis lesions relevant to the regeneration of myelin sheaths.

45 generation of their axons and alterations in myelin sheaths.

46 at beta1 integrins regulate the outgrowth of myelin sheaths.

47 f proteins that are responsible for building myelin sheaths.

48 characterized by distinctive, focally folded myelin sheaths.

49 communication mechanisms as synapses to form myelin sheaths.

50 alterations in the structure of many of the myelin sheaths.

51 urons or indirectly by abnormal formation of myelin sheaths.

52 urvatures are also found in vivo in diseased myelin sheaths.

53 al impulse propagation is facilitated by the myelin sheath, a compact membrane surrounding the axon.

54 Moreover, we observed progressive myelin sheath abnormalities and massive axon degeneratio

55 lls, and loss of CFTR caused ultrastructural myelin sheath abnormalities similar to those in known ne

56 ating axons and of nerve fibers with altered myelin sheaths all correlate with increasing cognitive i

57 The myelin sheath allows axons to conduct action potentials

58 We performed in vivo two-photon imaging of myelin sheaths along single axons of excitatory callosal

59 However, remyelination-the regeneration of myelin sheaths-also depends upon an immune response, and

60 hat interact with axons but fail to assemble myelin sheaths; an oligodendrocyte phenotype described p

61 the lipid composition found in the cytosolic myelin sheath and bovine MBP (bMBP) leads to an atherona

62 y action potential conduction depends on the myelin sheath and clustered Na(+) channels at nodes of R

63 KO)] mice exhibited loss of integrity of the myelin sheath and defective nerve conduction as indicate

64 lin protein 22 (PMP22) is a key component of myelin sheath and has been found mutated and aggregated

65 ous system leading to the destruction of the myelin sheath and resulting in metachromatic leukodystro

66 s in the CNS resulting in destruction of the myelin sheath and surrounding axons.

67 association between the leading edge of the myelin sheath and the axonal membrane to demarcate the n

68 oles of Prx in membrane stabilization of the myelin sheath and the lens fiber cell.

69 egeneration: the Schwann cells degrade their myelin sheaths and dedifferentiate, reverting to a pheno

70 ce, and electron microscopy revealed thinner myelin sheaths and increased myelin periodicity in BACHD

71 ease of the CNS resulting in degeneration of myelin sheaths and loss of oligodendrocytes, which means

72 gpr126 mutant Schwann cells elaborate mature myelin sheaths and maintain krox20 expression for months

73 xhibit hypomyelination with shorter, thinner myelin sheaths and motor coordination deficits.

74 udinal structures forming cylindrical axons (myelin sheaths and neurofilaments) can be locally invisi

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

76 model structural damage is initiated at the myelin sheaths and only later spreads to the oligodendro

77 can regulate the formation and remodeling of myelin sheaths and perhaps additional functions of oligo

78 cies as seen in remyelination; that is, thin myelin sheaths and short internodes.

79 Fbxw7 mutant SCs make thicker myelin sheaths and sometimes appear to myelinate multipl

80 onfirm the persistence and longevity of thin myelin sheaths and the importance of remyelination to th

81 tly, affecting the integrity of the axon and myelin sheaths and thus preventing proper remyelination.

82 in pieces were gradually released from aging myelin sheaths and were subsequently cleared by microgli

83 mely within the tubes' inner core, membrane, myelin sheath, and within the outer medium.

84 n the frequency of structural alterations in myelin sheaths, and an increase in the frequency of occu

85 rase promoter, exhibited thicker PNS and CNS myelin sheaths, and PNS myelin abnormalities, such as to

86 r coordination and spatial learning, thinner myelin sheaths, and reduced myelin gene expression.

87 oles of dominant constituents in cytoplasmic myelin sheaths, and shed new light on mechanisms disrupt

88 e high lipid content of axonal membranes and myelin sheaths, and that elevated serum levels of lipid

89 by myelinating Schwann cells and associated myelin sheaths appeared to be unaffected.

90 internodal length, and the thickness of the myelin sheath are powerful structural factors that contr

91 myelin sheaths than controls and that their myelin sheaths are 50% shorter than controls.

92 In contrast, myelin sheaths are formed in the spinal cord, although t

93 Similarly to neurons and synapses, excess myelin sheaths are produced and selectively eliminated,

94 For % myelination the myelin sheaths are selected using the Frangi vesselness

95 In particular, myelin sheaths are thinner than normal, and some axonal

96 anisms that drive the spiral wrapping of the myelin sheath around axons are poorly understood.

97 Wrapping of the myelin sheath around axons by oligodendrocytes is critic

98 erosis, are characterized by the loss of the myelin sheath around neurons, owing to inflammation and

99 s (SCs), thereby forming and maintaining the myelin sheath around peripheral axons (Grove et al., 201

100 Schwann cells produce myelin sheath around peripheral nerve axons.

101 cells that can both form and stably maintain myelin sheaths around axons and also rapidly dedifferent

102 from multipotent neural crest cells and form myelin sheaths around axons that allow rapid transmissio

103 Specifically, oligodendrocytes form myelin sheaths around axons that enable rapid electrical

104 nd is sufficient for the generation of thick myelin sheaths around remyelinated axons in the adult mo

105 nd significant reduction in the thickness of myelin sheaths around small-diameter axons was observed

106 showed that the grafted OPCs formed central myelin sheaths around the axons in the injured spinal co

107 GRPs formed morphologically normal-appearing myelin sheaths around the axons in the ventrolateral fun

108 s the process by which oligodendrocytes form myelin sheaths around the axons of neurons.

109 accurately characterized by (i) modeling the myelin sheath as a hollow cylinder composed of material

110 iffusion tensor imaging, and by newly formed myelin sheaths, as determined by electron microscopy.

111 arcot-Marie-Tooth neuropathy, but the mature myelin sheath assembly mechanism is unclear.

112 ed to control the different requirements for myelin sheath at each axo-glia interaction.

113 ward deciphering the 3D assembly of a mature myelin sheath at the molecular level.

114 PLP-null specimens, in contrast, many of the myelin sheaths became almost completely decompacted.

115 that in midlife, the structural integrity of myelin sheaths begins breaking down, with an acceleratin

116 mation of the axon insulating and supporting myelin sheath by differentiating oligodendrocytes (OLGs)

117 the ER and reduces the level of P0wt in the myelin sheath by half-a level previously shown to cause

118 s demonstrate that accurate placement of the myelin sheath by oligodendrocytes requires the coordinat

119 Myelin sheaths can be restored in demyelinated axons and

120 oligodendrocytes rather than the single long myelin sheath characteristic of Schwann cells.

121 on of proteolipid protein, a highly abundant myelin sheath component that was previously linked to an

122 transmission electron microscopy, a healthy myelin sheath comprises compacted membrane layers spiral

123 sulcus as an electrophysiologic indicator of myelin sheath damage.

124 13 years that we propose results in the same myelin sheath deficiencies as seen in remyelination; tha

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

126 Myelin sheath disruption is a common characteristic of s

127 in zebrafish, that oligodendrocytes make new myelin sheaths during a period of just 5 hr, with regula

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

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

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

131 bule growth from Golgi outposts and controls myelin sheath elongation, linking microtubule cytoarchit

132 m of cytoplasmic channels within the growing myelin sheath enables membrane trafficking to the leadin

133 The development of the myelin sheath enables rapid synchronized communication a

134 the optic nerve, smaller-caliber axons lack myelin sheaths entirely, whereas many large- and interme

135 r than normal, and some axonal segments lack myelin sheaths entirely.

136 ssembly of septin filaments scaffolds mature myelin sheaths, facilitating rapid nerve conduction in t

137 mance, aberrant pain responses, and abnormal myelin sheath folding.

138 al for ensuring the timely generation of new myelin sheaths following demyelinating injury in the adu

139 Remyelination is the regeneration of myelin sheaths following demyelination.

140 of the Ahr gene in mouse impairs optic nerve myelin sheath formation and results in oculomotor defici

141 that stimulating neuronal activity increased myelin sheath formation by individual oligodendrocytes.

142 macrophage activation in the retina promotes myelin sheath formation by oligodendrocytes generated fr

143 essential for the axon-glial interaction and myelin sheath formation in the PNS.

144 the individual oligodendrocyte, during which myelin sheath formation occurs and the number of sheaths

145 that activity-dependent secretion stabilized myelin sheath formation on select axons.

146 dramatically decreased MBP and P0 levels and myelin sheath formation without affecting expression of

147 allosal connections, sensory processing, and myelin sheath formation.

148 sion molecules coordinate MBP synthesis with myelin sheath formation.

149 ell differentiation, neuronal signaling, and myelin sheath formation.

150 d loss of MBP that correlates with a lack of myelin sheath formation.

151 The new data show that NMDARs exist on the myelin sheath formed by oligodendrocytes, that an uncomp

152 r B and PKC epsilon, regulates the number of myelin sheaths formed by individual oligodendrocytes in

153 hypothalamus (HY), and counted the number of myelin sheath forming oligodendrocytes (OLs) in CTX, CP,

154 The myelin sheath forms by the spiral wrapping of a glial me

155 The myelin sheath forms by the spiral wrapping of a glial me

156 major target of CD4+ T-cell immunity to the myelin sheath from multiple sclerosis brain.

157 hannel protein complexes located beneath the myelin sheath from Na(+) channels located at nodes of Ra

158 ntral nervous system (CNS) that produces new myelin sheaths from adult stem cells.

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

160 ct targets for myelination and regulation of myelin sheath growth are essential for central nervous s

161 Vesicular release from neurons promotes myelin sheath growth on axons.

162 of oligodendrocyte Neurofascin, also impairs myelin sheath growth, likely reflecting its association

163 ofascin reduces CNS myelination by impairing myelin sheath growth.

164 In addition, loss and/or dysfunction of the myelin sheath has been associated with a variety of neur

165 As iron accumulates, a degeneration of myelin sheaths has been observed in the elderly, but the

166 s that are reactive with major components of myelin sheaths have a central role.

167 d in pathogenic autoimmune cells that attack myelin sheath in experimental autoimmune encephalomyelit

168 However, the trophic role of the myelin sheath in long-term axonal survival is incomplete

169 uction of oligodendrocytes and the damage of myelin sheath in MHV-infected CNS and suggests that olig

170 ological events leading to disruption of the myelin sheath in MS.

171 of myelin proteins correlated with a thicker myelin sheath in optic nerves; comparison of quantified

172 , which are responsible for the formation of myelin sheath in the central nervous system, with the hu

173 changes were associated with thinning of the myelin sheath in the corpus callosum.

174 The myelin sheath in the mutant was much thinner than normal

175 In the first, we have followed thin myelin sheaths in a model of delayed myelination during

176 Destruction of oligodendrocytes and myelin sheaths in cortical gray matter profoundly alters

177 EM also revealed reduced or absent myelin sheaths in SG neurons from postnatal month 8 onwa

178 The presence of thin myelin sheaths in the adult CNS is recognized as a marke

179 The effect of aging on myelin sheaths in the rhesus monkey was studied in the v

180 demonstrated vacuolation and swelling of the myelin sheaths in the spinal cord of Lbr(+/-):Dhcr14(Del

181 rve-impulse conduction is greatly speeded by myelin sheaths in vertebrates, oligochaete annelids, pen

182 lds OPCs of high purity capable of producing myelin sheaths in vivo.

183 to describe the fine spatial organization of myelin sheaths in vivo.

184 icroarrays composed of lipids present in the myelin sheath, including ganglioside, sulfatide, cerebro

185 The myelin sheath increases the speed of action potential pr

186 Thinner myelin sheaths, indicated by increased G-ratio of myelin

187 The restriction of P0 immunoreactivity to myelin sheaths indicates that the protein is subject to

188 profound changes in cell shape that lead to myelin sheath initiation and formation.

189 The myelin sheath insulates axons and allows for rapid salut

190 The myelin sheath insulates axons in the vertebrate nervous

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

192 Degradation of the myelin sheath is a common pathology underlying demyelina

193 elination, and longitudinal extension of the myelin sheath is disrupted.

194 The myelin sheath is highly enriched in galactosylceramide (

195 The clearance of damaged myelin sheaths is critical to ensure functional recovery

196 ed disruption in the integrity of internodal myelin sheaths is well described and includes splitting

197 elin basic protein (MBP), a component of the myelin sheath, is mediated by both bone marrow (BM)-deri

198 emistry 4-6 weeks postfertilization, showing myelin sheaths lagging behind growing axons.

199 ss and malfunction of Schwann cells or their myelin sheaths lead to peripheral neuropathies such as C

200 s system, and malformation or destruction of myelin sheaths leads to motor and sensory disabilities.

201 Myelin sheath length directly impacts axonal conduction

202 servation that axon diameters correlate with myelin sheath length, as well as reports that PNS axonal

203 ly a century ago, many studies have observed myelin sheath-length diversity between CNS regions.

204 ces in myelin sheath lengths is unknown; are myelin sheath lengths determined solely by axons or do i

205 What accounts for regional differences in myelin sheath lengths is unknown; are myelin sheath leng

206 ed CNS myelination by reducing the number of myelin sheaths made by individual oligodendrocytes durin

207 The number of myelin sheaths made by individual oligodendrocytes regul

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

209 local synthesis of the major protein in the myelin sheath, myelin basic protein, through Fyn kinase-

210 fe, individual oligodendrocytes can regulate myelin sheath number in vivo.

211 rocyte glycoprotein, an antigen in the outer myelin sheath of central nervous system neurons, are pre

212 g O-GlcNAcylation is mislocalized within the myelin sheath of these mutant animals.

213 In the rhesus monkey, the myelin sheaths of nerve fibers in area 46 of prefrontal

214 With age, the structure of the myelin sheaths of some nerve fibers is altered.

215 Whether AOE can also induce changes in myelin sheaths of the auditory nerve (AN) is an importan

216 ve disease multiple sclerosis (MS), only the myelin sheaths of the CNS are lost, while Schwann cell m

217 on diameter to the diameter of the axon plus myelin sheath) of myelinated axons in regions subject to

218 ase, multiple sclerosis, the regeneration of myelin sheaths often fails due to a default of the resid

219 E(-/-) OLs also display defects when forming myelin sheath on neuronal axons during neonatal developm

220 e model for characterizing the effect of the myelin sheath on the evolution of the NMR signal is an e

221 The myelin sheath on vertebrate axons is critical for neural

222 tissue, which happens in mild injury to the myelin sheaths or axonal neurofilaments.

223 0 axon segments per cell, then spiral around myelin sheaths, penetrating from outer to inner layers.

224 (MBP) and its interaction with lipids of the myelin sheath plays an important part in the pathology o

225 r fails leaving remyelinated axons with thin myelin sheaths potentially compromising function and lea

226 Myelin sheaths provide critical functional and trophic s

227 is well described and includes splitting of myelin sheaths, redundant myelin, and fluctuations in bi

228 ing most membrane proteins from entering the myelin sheath region.

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

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

231 s, even in the presence of apparently normal myelin sheaths, remain unknown.

232 Throughout adulthood, the myelin sheath remained disproportionately thin relative

233 11C]MeDAS uptake in the brain as long as the myelin sheaths remained intact.

234 ferentiation, oligodendrocyte generation and myelin sheath remodeling in the forelimb motor cortex.

235 ly, with age the internodes of many of these myelin sheaths show structural changes, the most common

236 axin (Prx), a PDZ domain protein involved in myelin sheath stabilization, is also a component of adha

237 rs, together with age-related alterations in myelin sheath structure, may result in the inefficient a

238 The myelin sheath surrounding axons ensures that nerve impul

239 S results from destruction of the protective myelin sheath surrounding axons, which prevents the tran

240 s (MS), are characterized by the loss of the myelin sheath surrounding nerve axons.

241 om damage or dysregulation of the insulating myelin sheath surrounding spinal motor axons, causing pa

242 CNS, but other isoforms predominated in the myelin sheath surrounding the Mauthner axon.

243 P0 was localized to myelin sheaths surrounding axons, but was not detected i

244 imaging of the mouse spinal cord to resolve myelin sheaths surrounding individual fluorescently-labe

245 expressing reticulospinal neurons have fewer myelin sheaths than controls and that their myelin sheat

246 mouse spinal cord inherently produce longer myelin sheaths than those from the cortex(2), and single

247 lin proteins and deposit them in the growing myelin sheath that enwraps axons multiple times.

248 In peripheral nerves, Schwann cells form the myelin sheath that insulates axons and allows rapid prop

249 play a crucial role in holding together the myelin sheath that insulates peripheral nerves.

250 In the nervous system, a myelin sheath that originates from oligodendrocytes or S

251 -specific T cells that attack the protective myelin sheath that surrounds CNS nerve axons.

252 the majority of axons were wrapped by intact myelin sheaths that appeared structurally normal.

253 ol homeostasis, a major lipid constituent of myelin sheaths that are formed by oligodendrocytes.

254 disorder that results in the degradation of myelin sheaths that insulate axons in the central nervou

255 in the central nervous system (CNS) produce myelin sheaths that insulate axons to ensure fast propag

256 In unmyelinated segments bordered by myelin sheaths, these proteins were clustered in heminod

257 hed axonal segments even in the absence of a myelin sheath; these clusters persist after oligodendroc

258 sticity - affecting oligodendrocytes and the myelin sheaths they produce - that plays a crucial role

259 endrocyte numbers, a significant increase in myelin sheath thickness and axon transport.

260 They also demonstrate reduced myelin sheath thickness and partial disorganization of t

261 ocytes that contributes to the regulation of myelin sheath thickness and that uncouples the initiatio

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

263 in-1 by BACE1 is speculated to cause reduced myelin sheath thickness in both the central nervous syst

264 he proportion of myelinated axons as well as myelin sheath thickness in les and control rats.

265 We characterized oligodendrocyte numbers and myelin sheath thickness in mice with conditional inactiv

266 nd quantified oligodendrocyte maturation and myelin sheath thickness in remyelinating lesions.

267 ce1 regulates the process of myelination and myelin sheath thickness in the central and peripheral ne

268 n axon ensheathment and in the regulation of myelin sheath thickness in the PNS.

269 However, it appeared that myelin sheath thickness in the sciatic nerves was not in

270 Myelin sheath thickness in the spinal cords of knockout

271 In the proposed treadmilling model, myelin sheath thickness is a dynamic balance between the

272 Myelin sheath thickness is precisely regulated and essen

273 This leads to reduced myelin sheath thickness of optic nerve axons in Myocilin

274 not a recovery from demyelination to normal myelin sheath thickness remains unknown.

275 l development and then maintain a functional myelin sheath throughout adult life.

276 g frequency of degenerative changes in their myelin sheaths throughout middle and old age.

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

278 CD8(+) Treg cells could directly target the myelin sheath to ameliorate EAE.

279 e paranodal junction (PNJ) that attaches the myelin sheath to the axon, are present in the shk centra

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

281 icity stems from oligodendroglia, which form myelin sheaths to regulate the conduction of nerve impul

282 olled, at least in part, by the adherence of myelin sheaths to the axolemma in the adjacent region of

283 quisitely tailor the thickness of individual myelin sheaths to the diameter of their target axons to

284 hy characterized by focal thickenings of the myelin sheath (tomacula), progressive demyelination, axo

285 tral myelin, characterized by thin or absent myelin sheaths, vacuolation, enlarged periaxonal collars

286 Consistent with this, the myelin sheath was thinner, less compact and not properly

287 the cell that synthesizes and maintains the myelin sheath, we analyzed JHMV pathogenesis in transgen

288 To determine whether microglia also prune myelin sheaths, we used zebrafish to visualize and manip

289 Vacuole formation and thinner myelin sheaths were evident also with adult surviving do

290 oligodendrocytes that were actively forming myelin sheaths were identified in 30 of 42 remyelinated

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

292 ls defective or incapable of forming compact myelin sheathes when they differentiated to myelinating

293 ing, mixed microtubule polarity, and shorter myelin sheaths when cultured on 3-dimensional (3D) micro

294 One candidate, Cadm1b, localizes to myelin sheaths where both PDZ binding and extracellular

295 In peripheral nerves, Schwann cells form the myelin sheath, which allows the efficient propagation of

296 to aberrant targeting and destruction of the myelin sheath, which manifests as the clinical syndrome

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

298 In the central nervous system (CNS), the myelin sheaths, which protect axons and allow the fast p

299 ese oligodendrocytes also generate their new myelin sheaths within the same period, despite having va

300 The myelin sheaths wrapped around axons by oligodendrocytes