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

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

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

5 facilitated by the oligodendrocyte-produced myelin sheath.

6 lowed by local translation at the developing myelin sheath.

7 glial cell size to generate a multilamellar myelin sheath.

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

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

10 etabolite diffusion across the layers of the myelin sheath.

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

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

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

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

15 monolayers important to the adhesion of the myelin sheath.

16 between the paranodal terminal loops of the myelin sheath.

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

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

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

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

21 odel membrane system that closely mimics the myelin sheath.

22 ructural and functional role in the neuronal myelin sheath.

23 ation of the newly synthesized MBPs into the myelin sheath.

24 n proteins results in destabilization of the myelin sheath.

25 to maintain the structural integrity of the myelin sheath.

26 the peripheral nervous system that form the myelin sheath.

27 etween adjacent cytoplasmic membranes of the myelin sheath.

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

29 med oligodendrocytes frequently generate new myelin sheaths.

30 e in service or intercalating among existing myelin sheaths.

31 nating oligodendrocytes and their contiguous myelin sheaths.

32 millimeters and were organized with compact myelin sheaths.

33 mmon objective of investing nerve axons with myelin sheaths.

34 osis lesions relevant to the regeneration of myelin sheaths.

35 generation of their axons and alterations in myelin sheaths.

36 at beta1 integrins regulate the outgrowth of myelin sheaths.

37 f proteins that are responsible for building myelin sheaths.

38 characterized by distinctive, focally folded myelin sheaths.

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

40 urons or indirectly by abnormal formation of myelin sheaths.

41 ligodendrocytes, which fail to form complete myelin sheaths.

42 rotein and morphologically normal internodal myelin sheaths.

43 yelin and forms tight junctions (TJs) within myelin sheaths.

44 spite apparently normal initial formation of myelin sheaths.

45 ropathy characterized by abnormal folding of myelin sheaths.

46 segments of neurites associated with nascent myelin sheaths.

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

48 he initiation and properties of Schwann cell myelin sheaths.

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

50 brane around axons to generate multilamellar myelin sheaths.

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

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

53 localised to both developing and mature CNS myelin sheaths.

54 roduction of myelin proteins to generate new myelin sheaths.

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

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

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

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

59 The myelin sheath allows axons to conduct action potentials

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

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

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

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

66 ume such as the periaxonal space between the myelin sheath and the axon in the myelinated axon and th

67 the restricted periaxonal space between the myelin sheath and the axon.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

91 Although myelin sheaths are rare, most large axons are at least p

92 n is well advanced by 3 months (although the myelin sheaths are still thinner than normal), indicatin

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

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

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

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

97 Schwann cells produce myelin sheath around peripheral nerve axons.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 Myelin sheaths can be restored in demyelinated axons and

114 T cell-mediated destruction of the myelin sheath causes inflammatory damage of the CNS in m

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

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

117 sulcus as an electrophysiologic indicator of myelin sheath damage.

118 13 years that we propose results in the same myelin sheath deficiencies as seen in remyelination; tha

119 The molecular mechanisms underlying myelin sheath destruction in multiple sclerosis lesions

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

121 markably, transgenic shiverer mice with thin myelin sheaths display an intermediate phenotype indicat

122 ker K channel normally localized beneath the myelin sheath, display three types of cooling-induced ab

123 Myelin sheath disruption is a common characteristic of s

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

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

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

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

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

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

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

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

132 nodal axon that is normally concealed by the myelin sheath expresses a rich repertoire of K channel s

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

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

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

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

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

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

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

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

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

142 sion molecules coordinate MBP synthesis with myelin sheath formation.

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

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

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

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

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

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

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

150 stering potassium channels located under the myelin sheath from nodal sodium channels.

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

152 s found that the frequency of alterations in myelin sheaths from both locations correlates significan

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

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

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

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

157 as been implicated in destabilization of the myelin sheath in autoimmune demyelinating diseases such

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

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

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

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

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

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

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

165 d no observable effect on the maintenance of myelin sheaths in mature myelinated cocultures.

166 In both media formulations, the number of myelin sheaths in SC/DRGN cultures was far higher than i

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

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

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

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

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

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

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

174 M-20 is incorporated into functional compact myelin sheaths in young animals, our data show that the

175 erations have been examined by comparing the myelin sheaths in young monkeys, 5-10 years old, with th

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

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

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

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

180 The myelin sheath insulates axons and allows for rapid salut

181 The myelin sheath insulates axons in the vertebrate nervous

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

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

184 The Schwann cell myelin sheath is a multilamellar structure with distinct

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

186 The myelin sheath is highly enriched in galactosylceramide (

187 indicate that formation of a normal compact myelin sheath is required for normal maturation of the n

188 While this increase in the thickness of myelin sheaths is occurring in old monkeys, there are al

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

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

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

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

193 Myelin sheath length directly impacts axonal conduction

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

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

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

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

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

199 The number of myelin sheaths made by individual oligodendrocytes regul

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

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

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

203 that membrane proteins are delivered to the myelin sheath of an oligodendrocyte on rafts with a dist

204 constituents of oligodendrocytes and/or the myelin sheath of oligodendrocytes results in the formati

205 e glycoprotein (MOG) is an Ag present in the myelin sheath of the CNS thought to be targeted by the a

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

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

208 our examination of the effects of age on the myelin sheaths of nerve fibers in primary visual cortex.

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

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

211 In monkeys, myelin sheaths of the axons in the vertical bundles of n

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

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

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

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

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

217 The myelin sheath on vertebrate axons is critical for neural

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

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

220 Myelin sheaths provide critical functional and trophic s

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

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

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

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

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

226 Throughout adulthood, the myelin sheath remained disproportionately thin relative

227 11C]MeDAS uptake in the brain as long as the myelin sheaths remained intact.

228 ion and repair of the central nervous system myelin sheath requires an unambiguous identification and

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

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

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

232 The myelin sheath surrounding axons ensures that nerve impul

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

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

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

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

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

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

239 glial contact where sequential layers of the myelin sheath terminate.

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

241 ctional gap junctions are present within the myelin sheath that allow small molecules to diffuse betw

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

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

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

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

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

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

248 the major membrane-linked constituent of the myelin sheaths that coat peripheral nerves.

249 apable of synthesizing these lipids yet form myelin sheaths that exhibit major and minor dense lines

250 nase did not block myelin formation, but the myelin sheaths that formed were shorter, and the rate of

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

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

253 ccompanied by a progressive increase in MBP+ myelin sheaths that were restricted to the periventricul

254 ly localized to the innermost aspects of the myelin sheath, the paranode, the juxtaparanode, and the

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

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

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

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

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

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

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

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

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

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

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

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

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

268 Myelin sheath thickness in the spinal cords of knockout

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

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

271 The effect of age on myelin sheath thickness was determined by an electron mi

272 indicating that CNS neurons are sensitive to myelin sheath thickness.

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

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

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

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

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

278 ost common is splitting of the dense line of myelin sheaths to accommodate electron dense cytoplasm d

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

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

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

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

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

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

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

286 on was common, whereas in the lesion proper, myelin sheaths were consistently transformed into vesicu

287 f axons and the numbers of lamellae in their myelin sheaths were determined.

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

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

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

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

292 ternodal and juxtaparanodal regions of small myelin sheaths, whereas Cx32 staining was restricted to

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

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

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

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

297 to the fact that, in the old monkeys, thick myelin sheaths with more than ten lamellae are more comm

298 and cerebellum showed diffuse unraveling of myelin sheaths with occasional disintegration of neurona

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