ライフサイエンスコーパス: remyelination

1 ation) within the CNS and failure of repair (remyelination).

2 treatment options are available to establish remyelination.

3 yte precursor cell (OPC) differentiation and remyelination.

4 ing immune activation of OPCs may facilitate remyelination.

5 terol synthesis gene expression and enhanced remyelination.

6 nd metabolites in lesions over the course of remyelination.

7 y in adult OPCs to examine its relevance for remyelination.

8 ferentiation and ultrastructural evidence of remyelination.

9 e to serve as a therapeutic agent to promote remyelination.

10 4) promotes oligodendrocyte regeneration and remyelination.

11 sustain adult OPC-derived OLs and efficient remyelination.

12 ough which SERMs may mediate their effect on remyelination.

13 lination of the optic nerve, with subsequent remyelination.

14 myelination, and axonal damage, with minimal remyelination.

15 the mechanisms of neuroinflammation and CNS remyelination.

16 croglia as a potential approach to promoting remyelination.

17 c inflammation, neuroaxonal degeneration and remyelination.

18 havioral intervention provides no benefit to remyelination.

19 Tsc1 deletion from NG2(+) OPCs accelerated remyelination.

20 f TSC has not been studied in the context of remyelination.

21 ferentiation, explaining its adverse role in remyelination.

22 n and validated CCL19 as a target to improve remyelination.

23 -gated Ca(2+) influx in OPCs is critical for remyelination.

24 pendent oligodendrocyte apoptosis during CNS remyelination.

25 n is a critical determinant of its effect on remyelination.

26 et little is known about T cell functions in remyelination.

27 AE and spinal cord degeneration and promoted remyelination.

28 on and oligodendrocyte maturation throughout remyelination.

29 ameters in mouse models of demyelination and remyelination.

30 supports oligodendrocyte differentiation and remyelination.

31 eneration, coupled to the lower capacity for remyelination.

32 ocyte progenitor cells (OPCs) and suppresses remyelination.

33 entiating oligodendrocytes, is beneficial to remyelination.

34 the effect of FSD-C10 on neuroprotection and remyelination.

35 ch as genetic programs that coordinate adult remyelination.

36 otein (PLP)-positive oligodendrocytes slowed remyelination.

37 hanisms by which we might enhance endogenous remyelination.

38 vironment that impairs axon regeneration and remyelination.

39 tter, they may represent a valid therapy for remyelination.

40 regulation of developmental myelination and remyelination.

41 fen to demyelinated rats in vivo accelerates remyelination.

42 ent and spontaneous oligodendrocyte-mediated remyelination.

43 rough TNFR1, while tmTNF promotes repair and remyelination.

44 ired for proper onset of CNS myelination and remyelination.

45 ated oligodendrocytes can also contribute to remyelination.

46 herapeutic potential for promoting efficient remyelination.

47 ) lesions feature demyelination with limited remyelination.

48 no compensatory increase in oligodendrocyte remyelination.

49 ng diseases in a regenerative process called remyelination.

50 axons is followed by a period of spontaneous remyelination.

51 the index of demyelination; and the index of remyelination.

52 , axonal regrowth, motor neuron survival and remyelination.

53 tosterone, and androgen receptor (AR) in CNS remyelination.

54 eurons were reversed to normal levels during remyelination.

55 nds which induce IL-33 are likely to promote remyelination.

56 A1 (eEF1A1) negatively regulates PNS and CNS remyelination.

57 n dynamics and evaluate treatments aiming at remyelination.

58 nd detrimental roles played by astrocytes in remyelination.

59 future translational studies on PNS and CNS remyelination.

60 epair as reflected by oligodendrogenesis and remyelination.

61 rated to play a pivotal role in OSM-mediated remyelination.

62 m (CNS) has been linked to demyelination and remyelination.

63 CD1 as a novel therapeutic target to promote remyelination.

64 and showed a faster and more efficient brain remyelination.

65 , ONLR-NPCs may enable glial replacement and remyelination.

66 can accumulate and inhibit tissue repair and remyelination.

67 the chronically demyelinated CNS established remyelination.

68 and in the cuprizone model of demyelination/remyelination.

69 is a known inhibitor of axonal regrowth and remyelination.

70 and TAZ are redundantly required for optimal remyelination.

71 the top up-regulated pathways in OLCs during remyelination.

72 nd that BZA enhances OPC differentiation and remyelination.

73 ic acid receptor-beta (RARbeta) signaling in remyelination.

74 pies aimed at promoting CNS regeneration and remyelination.

75 ch was previously implicated as a target for remyelination.

76 n, or demyelination, yet there was increased remyelination.

77 el function for both RARbeta and RARalpha in remyelination.

78 n OLs plays key roles in CNS myelination and remyelination.

79 re correlated with the suppression of timely remyelination.

80 and the role that microRNAs (miRNAs) play in remyelination, 2',3'-cyclic-nucleotide 3'-phosphodiester

81 rofile from patients exhibiting high and low remyelination ability, we identified novel molecules inv

82 duced myelin debris clearance and diminished remyelination after a demyelinating insult.

83 rocytes, which impairs myelin production and remyelination after demyelinating injury.

84 onset of both developmental myelination and remyelination after injury.

85 alleles are critical for CNS myelination and remyelination after injury.

86 ng peripheral nerve development and inhibits remyelination after injury.

87 ole in regulating Wallerian degeneration and remyelination after PNS injury.

88 udy identifies novel therapeutic targets for remyelination after PNS-CNS injury.

89 roborate the function of this pathway during remyelination after WMI.

90 very, and quantitated both demyelination and remyelination along the length of the nerves.

91 n the adult CNS is recognized as a marker of remyelination, although the reason there is not a recove

92 igodendrocytes do not normally contribute to remyelination and are therefore not a promising target f

93 genitor cell (OPC) microRNAs (miRNAs) during remyelination and development in vivo and differentiatio

94 pathways that regulate neuroinflammation and remyelination and facilitate the development of therapie

95 blation influences the degree of spontaneous remyelination and functional recovery following spinal c

96 igodendrocytes and increases MBP, leading to remyelination and functional recovery of mice.

97 that Nrg1 signalling regulates central axon remyelination and functional repair and drives the trans

98 odendrocyte progenitor cell responses during remyelination and further our understanding of how mamma

99 is leads to attenuated axon damage, enhanced remyelination and improved motor learning.

100 igodendroglial cells is necessary for normal remyelination and is an essential Ca(2+) channel for OPC

101 ass of ERbeta ligands that offer significant remyelination and neuroprotection as well as modulation

102 agonists, have previously been implicated in remyelination and neuroprotection, following a heavy foc

103 Although axons grew rapidly, remyelination and nodal ion channel clustering was much

104 icient mice exhibited substantially impaired remyelination and oligodendrocyte differentiation, which

105 autonomous and SC-nonautonomous functions in remyelination and peripheral nerve repair.

106 However, whether these approaches allow remyelination and promote the reestablishment of AIS and

107 ble to increase myelin clearance and improve remyelination and recovery.

108 yte loss and an inhibitory milieu compromise remyelination and recovery.

109 dividually) in SCs resulted in impaired axon remyelination and target reinnervation following nerve i

110 pathway in developmental myelination versus remyelination and the importance of signaling between SC

111 endrocyte precursor cells (OPCs) to complete remyelination and to sustain axonal survival.

112 critical for favorable axonal regeneration, remyelination, and clinical improvement.

113 ound significant reestablishment of RGC AIS, remyelination, and even reassembly of nodes in regions p

114 s known about the astrocytic contribution to remyelination, and highlight future avenues of investiga

115 suppresses the immune response and increases remyelination, and in addition, inhibition of GSK3 limit

116 increased axon and myelin pathology, reduced remyelination, and increased loss of oligodendrocyte pre

117 proinflammatory macrophage density, enhances remyelination, and rescues remyelination impairment in I

118 central nervous system (CNS) myelination and remyelination, and we sought to investigate the expressi

119 However, nerve regeneration and remyelination are both perturbed, demonstrating that Zeb

120 Although drugs that are intended to promote remyelination are entering clinical trials, the mechanis

121 onnections, treatments effectively promoting remyelination are pivotal in halting disease progression

122 d with a significant increase in spinal cord remyelination as reflected by g-ratio analysis within th

123 bly, deletion of Cxcr2 resulted in increased remyelination, as assessed by g-ratio (the ratio of the

124 proteoglycans contributes to the failure in remyelination associated with multiple sclerosis.

125 tibility, particularly due to the failure of remyelination associated with progressive MS.

126 The primary endpoint was remyelination at 24 weeks, measured as recovery of affec

127 Remyelination began near the retina, progressed distally

128 in contributing to demyelination as well as remyelination being expressed by both microglia and macr

129 We found that eNPCs are dispensable for remyelination but protect partially from increased axona

130 driven demyelination occurs with inefficient remyelination, but therapies are limited, especially tho

131 the nervous system is capable of spontaneous remyelination, but this regenerative process often fails

132 accumulate following demyelination, inhibit remyelination by blocking the differentiation of rat oli

133 NOTCH1 signalling contributes to defective remyelination by impairing differentiation of oligodendr

134 Remyelination by oligodendrocyte progenitor cells (OPCs)

135 lipid-laden microglia/macrophages to support remyelination by oligodendrocytes.

136 on factor 88 (MyD88) signaling in supporting remyelination by promoting myeloid cell-mediated inflamm

137 velopment of oligodendrocytes, as well as in remyelination by Schwann cells after nerve trauma.

138 In multiple sclerosis, remyelination can fail despite abundant oligodendrocyte

139 further investigation on patients with high remyelination capacities will provide new pro-regenerati

140 nd turnover - that might influence their pro-remyelination capacity.

141 nd will provide a surrogate marker in future remyelination clinical trials.

142 Remyelination, conversely, involves a striking cell shor

143 rafish and mouse models of demyelination and remyelination, Cunha et al. now describe a novel role fo

144 Our data are the first to show remyelination defects in individuals with a single mutan

145 INTERPRETATION: Remyelination did not differ significantly between the o

146 While endogenous remyelination, driven by resident oligodendrocyte precur

147 , GALC +/- animals had significantly reduced remyelination during recovery.

148 Sox10 target genes and increases PNS and CNS remyelination efficiency.

149 ted correlation between disease severity and remyelination emphasizes the importance of identifying f

150 oligodendrocytes did not impact the ensuing remyelination, eNPC-ablated mice experienced increased a

151 eg accelerated developmental myelination and remyelination, even in the absence of overt inflammation

152 cyte-specific deficiency of Scd1 accelerated remyelination ex vivo and in vivo.

153 , for reasons that remain poorly understood, remyelination fails in the progressive phase of multiple

154 Why remyelination fails or succeeds in multiple sclerosis pa

155 elinating diseases, the myelin formed during remyelination fails to achieve normal thickness, increas

156 oost maturation of resident OPCs to overcome remyelination failure and halt disease progression.

157 ndings provide insight into aging-associated remyelination failure and suggest therapeutic interventi

158 Remyelination failure by oligodendrocytes contributes to

159 s, as an environmental factor, contribute to remyelination failure by perturbing oligodendrocyte prog

160 inflammatory demyelinating disorder in which remyelination failure contributes to persistent disabili

161 t oligodendrocyte myelination contributes to remyelination failure in demyelinating disorders.

162 her cholesterol insufficiency contributes to remyelination failure in MS, is unclear.

163 senescence as a process that contributes to remyelination failure in PMS, which may impact how this

164 uced remyelinating oligodendrocyte death and remyelination failure in the cuprizone model (male mice)

165 NIFICANCE STATEMENT Therapeutics targeted at remyelination failure, which results in axonal degenerat

166 otential of CNS progenitors in diseases with remyelination failure.

167 cytes into a reparative mode contributing to remyelination following disease.

168 lncOL1 causes defects in CNS myelination and remyelination following injury.

169 represent an endogenous mechanism to improve remyelination following injury.

170 insights into the implications for SERMs in remyelination for MS and hormonal research at large.SIGN

171 overy from demyelinating injury via enhanced remyelination from new and surviving oligodendrocytes.

172 ents remains largely unknown, mainly because remyelination has never been studied within a humanized

173 Promotion of remyelination has opened a new therapeutic avenue, but h

174 ffects that such interventions might have on remyelination have not yet been explored.

175 imental flexibility to analyze mechanisms of remyelination, here we discuss the challenges in underst

176 density, enhances remyelination, and rescues remyelination impairment in IL4Ralpha deficient mice.

177 ncreased proinflammatory macrophage density, remyelination impairment, and axonal injury in central n

178 Addition of FSD-C10 directly promoted remyelination in a chemical-induced demyelination model

179 f oligodendrocyte precursor cells (OPCs) and remyelination in a cross talk between neuronal RA recept

180 (CNS) nervous systems during myelination and remyelination in a cuprizone-induced demyelination model

181 creased 2-arachidonoylglycerol tone promotes remyelination in a model of progressive multiple scleros

182 neuroinflammation, but its deletion enhances remyelination in a preclinical model of the human demyel

183 yte (OL) development and is essential during remyelination in adult mice.

184 egenerative capacity of aged OPCs, improving remyelination in aged animals following focal demyelinat

185 ination may be beneficial both for enhancing remyelination in demyelinating diseases and for increasi

186 he cellular mechanisms sustaining endogenous remyelination in demyelinating disorders, we focused our

187 MP-1 have the therapeutic potential to boost remyelination in demyelinating disorders.

188 ow that the inflammatory response during CNS remyelination in mice is modulated by antibiotic or prob

189 perties and safety profile, improves in vivo remyelination in mouse and increases both adult mouse an

190 at the onset of inflammation resolution and remyelination in mouse central nervous system lesions af

191 Regenerative medicines that promote remyelination in multiple sclerosis (MS) are making the

192 cause BMPs may be involved in the failure of remyelination in multiple sclerosis (MS), we characteriz

193 sted that opicinumab treatment might enhance remyelination in patients with CNS demyelinating disease

194 may offer a therapeutic avenue for enhancing remyelination in patients with demyelinating diseases.

195 fferentiation and that anti-LINGO-1 promotes remyelination in preclinical animal models for MS and in

196 nodal segments suggesting demyelination, and remyelination in progress.

197 tically targeted to enhance SC-mediated axon remyelination in the adult CNS.SIGNIFICANCE STATEMENT Nu

198 Successful remyelination in the CNS generally depends on the activa

199 r, is widely used to study demyelination and remyelination in the CNS, in the context of MS.

200 widely used model to study demyelination and remyelination in the context of multiple sclerosis, the

201 ecified PP population suggest that enhancing remyelination in the human CNS with opicinumab might be

202 is not required for efficient myelination or remyelination in the murine CNS in vivo.

203 astrophic failure of axonal regeneration and remyelination in the PNS.

204 rve injury could be used to foster effective remyelination in the treatment of demyelinating disorder

205 ir potent effects on OPC differentiation and remyelination in vivo and highlight EBP, an enzyme in th

206 SN promoted OPC differentiation in vitro and remyelination in vivo Furthermore, coexpression of cGSN

207 rinogen decreases BMP signaling and enhances remyelination in vivo.

208 plex role for TSC in oligodendrocytes during remyelination in which the timing of Tsc1 deletion is a

209 vel toxin-based spinal cord model of de- and remyelination in zebrafish and showed that pro-inflammat

210 te progenitor cells (OPCs), thereby impeding remyelination, in the demyelinating disease multiple scl

211 Concomitant with hippocampal remyelination induced by withdrawal of Cup/Rap, prolifer

212 The failure to undergo remyelination is a critical impediment to recovery in mu

213 evelopment of pharmacotherapies that promote remyelination is a high priority for multiple sclerosis

214 ing clinical trials, the mechanisms by which remyelination is controlled and how microglia are involv

215 Subsequent remyelination is dependent on recruitment and differenti

216 aques, but its beneficial or adverse role in remyelination is elusive.

217 Spontaneous remyelination is largely mediated by Schwann cells, wher

218 ory diseases such as multiple sclerosis (MS) remyelination is often incomplete.

219 al Nrg1 mutants (where Schwann cell-mediated remyelination is prevented), but not immunoglobulin-spec

220 Here, we show that remyelination is severely delayed after nerve-crush inju

221 Remyelination is the default pathway after myelin loss i

222 Remyelination is the regeneration of myelin sheaths foll

223 Remyelination is the regenerative response to demyelinat

224 d molecules serve as extrinsic inhibitors of remyelination is unknown.

225 ENTARY ON THIS ARTICLE: Myelin regeneration (remyelination) is a spontaneous process that occurs foll

226 eceptor (GPCR) Gpr126/Adgrg6 is required for remyelination, macrophage recruitment, and axon regenera

227 er rates of axon degeneration and more rapid remyelination make relapsing MS more resilient than the

228 stosterone dependency of CNS oligodendrocyte remyelination may have roots in the evolutionary history

229 es interact over the disease course and when remyelination might occur.

230 Remyelination occurred shortly after demyelination in HS

231 Spontaneous remyelination occurs after spinal cord injury (SCI), but

232 ed demyelination, although apparently normal remyelination occurs at a delayed time point.

233 he challenges in understanding where and how remyelination occurs in MS.

234 x system to study the function of TSC in the remyelination of a focal, lysolecithin-demyelinated lesi

235 n compared to controls, suggesting increased remyelination of axons.

236 s were dispensable for Schwann cell-mediated remyelination of central axons after spinal cord injury.

237 r Nrg1 is required for Schwann cell-mediated remyelination of central dorsal column axons and whether

238 Remyelination of CNS axons by Schwann cells (SCs) is not

239 wing learning to enhance oligodendrogenesis, remyelination of denuded axons and the ability of surviv

240 e augmentation of epidermal nerve fibers and remyelination of sciatic nerves.

241 which results in neo-oligodendrogenesis and remyelination of spinal cords.

242 1.2 deletion in OPCs leads to less efficient remyelination of the adult brain.

243 Ca(2+) channel for OPC maturation during the remyelination of the adult brain.SIGNIFICANCE STATEMENT

244 dult OPCs is also essential for an effective remyelination of the mouse brain.SIGNIFICANCE STATEMENT

245 ncies decreased in association with complete remyelination of the optic nerve but remained prolonged

246 Remyelination of the peripheral and central nervous syst

247 ne cells, we did not observe improvements in remyelination, oligodendrocyte numbers, and effects on m

248 omising therapeutic candidates which enhance remyelination: oncostatin M (OSM), a member of the inter

249 fferentiation observed in patients with high remyelination pattern.

250 from different patients, we observed diverse remyelination patterns reproducing for the first time th

251 terventions to improve brain and spinal cord remyelination, paving the way for the translation of thi

252 f OLCs in vivo in corpus callosum during the remyelination phase of a chronic cuprizone model with ax

253 Furthermore, during the remyelination phase of the CPZ model, the corpus callosu

254 aturation and myelin regeneration across the remyelination phase of the cuprizone model.

255 tem/precursor cells are recruited during the remyelination phase to the corpus callosum (CC) and are

256 deficiency completely abolished spontaneous remyelination, phenocopying OSMRbeta KO mice.

257 on of patients depending on their individual remyelination potential, which significantly correlates

258 h lesion size and positively correlated with remyelination potential.

259 -negative cultures explained the accelerated remyelination previously observed in St8sia4(-/-) mice.

260 n NG2-positive OPCs significantly delays the remyelination process in the adult brain.

261 endrocyte progenitor cells (OPCs) during the remyelination process is essential to developing new the

262 reduced maturational rate through the entire remyelination process.

263 rocytes and myelin production throughout the remyelination process.

264 ke multiple sclerosis (MS), where failure of remyelination promotes permanent neuro-axonal damage.

265 pecific mutants (where Schwann cell-mediated remyelination remains intact), providing robust evidence

266 Lack of robust remyelination represents one of the major barriers to re

267 Here we reveal that efficient remyelination requires death of proinflammatory microgli

268 Remyelination requires innate immune system function, bu

269 However, remyelination, restoration of oligodendrocyte densities,

270 However, partial remyelination restores neuronal and behavioral function,

271 newly-formed progenitors provide functional remyelination, restoring normal conduction.

272 imental signaling environment that precludes remyelination.SIGNIFICANCE STATEMENT As an environmental

273 odendrocyte progenitor cells with subsequent remyelination.SIGNIFICANCE STATEMENT In multiple scleros

274 t functions in developmental myelination and remyelination.SIGNIFICANCE STATEMENT Myelin loss in demy

275 omoting oligodendrocyte viability during CNS remyelination.SIGNIFICANCE STATEMENT We report that crea

276 ately, there are still no neuroprotection or remyelination strategies available.

277 These findings can help to open a pathway to remyelination strategies.

278 e same myelin sheath deficiencies as seen in remyelination; that is, thin myelin sheaths and short in

279 However, remyelination-the regeneration of myelin sheaths-also de

280 need additional work before efficacious pro-remyelination therapies will be ready for people with mu

281 euritis in MS may identify demyelination and remyelination, this has not been directly confirmed.

282 of thin myelin sheaths and the importance of remyelination to the long-term health and function of th

283 ption factor for PNS and CNS myelination and remyelination, to drag Sox10 out of the nucleus.

284 Failure of remyelination underlies the progressive nature of demyel

285 ial precursor cell (OPC) differentiation and remyelination via its envelope protein pathogenic HERV-W

286 This reduced remyelination was accompanied by an important decline in

287 While remyelination was completely abrogated in OSMRbeta knock

288 In EAE, remyelination was induced with estrogen receptor-beta (E

289 Dynamic remyelination was inversely correlated with clinical dis

290 The selective effect of IL-4 on remyelination was verified in an ex vivo organotypic mod

291 CCs) are required for OPC development during remyelination, we generated an inducible conditional kno

292 reexisting OLs do not normally contribute to remyelination, we show that sustained activation of ERK1

293 olved in oligodendrocyte differentiation and remyelination, we used a conditional knockout mouse for

294 mage, we found that loss of alphaBC impaired remyelination, which correlated with a reduced presence

295 n cells is important for axonal regrowth and remyelination, which is one reason why the PNS is signif

296 dCl) shows particular promise promoting both remyelination while reducing inflammatory cytokines in t

297 ecreased tissue stiffness that recovers with remyelination; while chronic demyelination is characteri

298 e show that lymphocytes play a major role in remyelination whose efficacy is significantly decreased

299 Since incomplete remyelination will irreversibly damage axonal connection

300 establish a mechanism for 2-AG promotion of remyelination with implications in axonal repair in CNS