ライフサイエンスコーパス: remyelination

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

2 c inflammation, neuroaxonal degeneration and remyelination.

3 fen to demyelinated rats in vivo accelerates remyelination.

4 ent and spontaneous oligodendrocyte-mediated remyelination.

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

6 rough TNFR1, while tmTNF promotes repair and remyelination.

7 ired for proper onset of CNS myelination and remyelination.

8 ated oligodendrocytes can also contribute to remyelination.

9 herapeutic potential for promoting efficient remyelination.

10 ferentiation, explaining its adverse role in remyelination.

11 ) lesions feature demyelination with limited remyelination.

12 no compensatory increase in oligodendrocyte remyelination.

13 ng diseases in a regenerative process called remyelination.

14 axons is followed by a period of spontaneous remyelination.

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

16 , axonal regrowth, motor neuron survival and remyelination.

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

18 ent in the central nervous system tissue for remyelination.

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

20 , enabling them to effectively contribute to remyelination.

21 h there is ongoing balancing between de- and remyelination.

22 sion of OPCs during the recruitment phase of remyelination.

23 bout the role of Sox2, especially during CNS remyelination.

24 myelination provides innovative avenues for remyelination.

25 plex protein Scribble in CNS myelination and remyelination.

26 elopment but also OL regeneration during CNS remyelination.

27 of CNS pathological conditions that require remyelination.

28 on and survival, blunting the process of CNS remyelination.

29 nd myelin sheaths and thus preventing proper remyelination.

30 n and how this enables them to contribute to remyelination.

31 ion and hence their ability to contribute to remyelination.

32 fore, for sustaining OL regeneration and CNS remyelination.

33 of intracellular polarity in myelination and remyelination.

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

35 LGs are key to understanding myelination and remyelination.

36 ng to demyelinating activity and presence of remyelination.

37 the severity of demyelination, nor increase remyelination.

38 injury (SCI) by enhancing OL survival and/or remyelination.

39 sis compromised the rate and extent of adult remyelination.

40 pendent oligodendrocyte apoptosis during CNS remyelination.

41 in stem cell biology, in CNS myelination and remyelination.

42 he demyelinating activity or the presence of remyelination.

43 panied by axonal preservation, and increased remyelination.

44 ide novel targets to therapeutically enhance remyelination.

45 s in demyelinated lesions results in reduced remyelination.

46 tion in demyelinated lesions and accelerated remyelination.

47 that Cdk5 is also an important regulator of remyelination.

48 L lineage cell into mature OL and subsequent remyelination.

49 recruitment and central nervous system (CNS) remyelination.

50 d the number of cells recruited and impaired remyelination.

51 enhance oligodendrocyte differentiation and remyelination.

52 te that ET-1 drastically reduces the rate of remyelination.

53 myelin proteolipid protein gene, initiating remyelination.

54 ntation is one promising strategy to promote remyelination.

55 potential target for therapies that promote remyelination.

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

57 nically-relevant models of demyelination and remyelination.

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

59 AE and spinal cord degeneration and promoted remyelination.

60 ameters in mouse models of demyelination and remyelination.

61 supports oligodendrocyte differentiation and remyelination.

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

63 eneration, coupled to the lower capacity for remyelination.

64 ocyte progenitor cells (OPCs) and suppresses remyelination.

65 entiating oligodendrocytes, is beneficial to remyelination.

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

67 ch as genetic programs that coordinate adult remyelination.

68 otein (PLP)-positive oligodendrocytes slowed remyelination.

69 hanisms by which we might enhance endogenous remyelination.

70 vironment that impairs axon regeneration and remyelination.

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

72 regulation of developmental myelination and remyelination.

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

74 pro-inflammatory environment and failure of remyelination; a combination of effects predicted to exa

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

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

77 oval and show that there can be no efficient remyelination after a primary demyelinating insult if my

78 used delayed myelin debris uptake and slowed remyelination after experimentally-induced demyelination

79 ng peripheral nerve development and inhibits remyelination after injury.

80 ring development and for proper regeneration/remyelination after injury.

81 onset of both developmental myelination and remyelination after injury.

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

83 romotes oligodendroglial cell maturation and remyelination after lysolecithin-induced demyelination o

84 effect of abrogating astrocyte activation on remyelination after lysolecithin-induced demyelination o

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

86 t either improve clinical outcome or enhance remyelination after transplantation into animals in whic

87 roles for neuregulin in schizophrenia and in remyelination after white matter damage.

88 5K function, application of which stimulates remyelination after WMI.

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

90 fy a role for CXCR7 in OPC maturation during remyelination and are the first to use a small molecule

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

92 treatment strategies, such as enhancement of remyelination and CNS repair.

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

94 hin sections confirmed stereotypical thin OL remyelination and few bare axons at 10 wpi, indicating t

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

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

100 egative regulator of OPC differentiation and remyelination and is potentially a therapeutic target to

101 ell source for cell-based therapy to promote remyelination and neuroprotection in myelin diseases.

102 rogression by restoring tissue integrity via remyelination and neuroregeneration.

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

108 dentifying a drug that stimulates endogenous remyelination and/or minimizes axonal degeneration would

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

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

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

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

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

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

115 The mechanisms controlling remyelination are currently poorly understood.

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

117 tration correlates with impaired spontaneous remyelination as evidenced by myelin protein expression,

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

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

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

121 Remyelination began near the retina, progressed distally

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

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

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

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

126 Remyelination by oligodendrocyte progenitor cells (OPCs)

127 In multiple sclerosis, remyelination can fail despite abundant oligodendrocyte

128 ial replacement of lost oligodendrocytes and remyelination can occur as a result of activation and re

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

130 However, the overall remyelination capacity remains inefficient because precu

131 ous repair, including oligodendrogenesis and remyelination, continues for several months after SCI, p

132 Remyelination, conversely, involves a striking cell shor

133 The efficiency of central nervous system remyelination declines with age.

134 We show that oligodendrocyte-mediated remyelination decreases and Schwann cell remyelination i

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

136 INTERPRETATION: Remyelination did not differ significantly between the o

137 flammatory demyelinating disease, endogenous remyelination does occur but is frequently insufficient

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

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

140 We identified an endogenous inhibitor of remyelination, Endothelin-1 (ET-1), which is highly expr

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

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

143 Why remyelination fails or succeeds in multiple sclerosis pa

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

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

146 Remyelination failure by oligodendrocytes contributes to

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

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

149 Remyelination failure correlated with a truncated prolif

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

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

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

153 Remyelination failure plays an important role in the pat

154 yelinating episodes contributes to permanent remyelination failure.

155 otential of CNS progenitors in diseases with remyelination failure.

156 oligodendrocyte lineage resulted in delayed remyelination following demyelinating injury to the adul

157 yelination, but also OL regeneration and CNS remyelination following demyelination.

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

159 ive effect of endothelin 2, analysis of both remyelination following experimental demyelination and o

160 In vivo studies on remyelination following experimental toxin-induced demye

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

162 dase but not another hyaluronidase inhibited remyelination following lysolecithin-induced demyelinati

163 l lineage during both normal myelination and remyelination following toxin-induced, genetic, or autoi

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

165 mics that underlie transplanted NPC-mediated remyelination have not been described.

166 the immune response contributing to impaired remyelination highlights a role for peripheral monocytes

167 imiting their recruitment to axons requiring remyelination; however, few inhibitors have been identif

168 ata define a major distinct role for NPCs in remyelination, identifying them as a key target for enha

169 pomyelination during development and impairs remyelination if injured.

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

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

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

173 number of new oligodendrocytes and enhances remyelination in a lysolecithin-induced mouse model of f

174 tiation during developmental myelination and remyelination in a manner independent of the Wnt/beta-ca

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

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

177 ibers and are a promising model for studying remyelination in adult peripheral nerves.

178 The failure of remyelination in Cdk5 cKO animals was associated with a

179 bited oligodendrocyte differentiation during remyelination in cerebellar slice cultures.

180 ist indazole chloride (Ind-Cl) on functional remyelination in chronic experimental autoimmune encepha

181 e progenitor cell differentiation and induce remyelination in demyelinating disease models.

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

183 sting OLs carries the potential for enhanced remyelination in demyelinating diseases and increased ne

184 Failure of remyelination in diseases, such as multiple sclerosis (M

185 to promote oligodendrocyte regeneration and remyelination in experimental models of MS.

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

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

188 Remyelination in multiple sclerosis (MS) is often incomp

189 out toxic effects with the goal of promoting remyelination in multiple sclerosis.

190 tructurally modified derivatives, to enhance remyelination in patients.

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

192 e of Cdk5 disruption in neural cells because remyelination in slice cultures is blocked by Cdk5 inhib

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

194 lso demonstrate that a reduced efficiency of remyelination in the caudal CC was associated with long-

195 Remyelination in the central nervous system (CNS) is cri

196 toimmune response and progressive failure of remyelination in the central nervous system.

197 The reason for this peripheral type of remyelination in the CNS and what governs it is unknown.

198 nce between Schwann cell and oligodendrocyte remyelination in the CNS, and provides further insight i

199 Animal models that enable the study of remyelination in the context of ongoing inflammation are

200 yet to be an approved therapy that promotes remyelination in the damaged central nervous system (CNS

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

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

203 ng putative MS therapies designed to enhance remyelination in the setting of active inflammation, and

204 nsider measures with the potential to detect remyelination in the spinal cord and in the optic nerve.

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

206 cial approach for therapeutic enhancement of remyelination in those demyelinating diseases where GPR1

207 hich we demonstrate inhibits myelination and remyelination in vitro.

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

209 peripheral monocytes in impairing endogenous remyelination in vivo.

210 eir effects on OPC maturation and functional remyelination in vivo.

211 rinogen decreases BMP signaling and enhances remyelination in vivo.

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

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

214 ted remyelination decreases and Schwann cell remyelination increases in lesioned knockout mice in com

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

216 Understanding the mechanisms of CNS remyelination is central to developing effective means b

217 Subsequent remyelination is dependent on recruitment and differenti

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

219 p35, is increased during myelin repair, and remyelination is impaired in p39(-/-) mice.

220 Spontaneous remyelination is largely mediated by Schwann cells, wher

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

222 Screening for remyelination is problematic, as myelination requires th

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

224 Remyelination is the default pathway after myelin loss i

225 Remyelination is the regenerative response to demyelinat

226 elative contribution of NPCs versus pOPCs to remyelination is unknown.

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

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

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

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

231 Remyelination may fail because oligodendrocyte precursor

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

233 Approaches to stimulate remyelination may lead to recovery from demyelinating in

234 nating disease and identify a new target for remyelination medicines.

235 Here we show, using an in-vivo remyelination model, that demyelinated axons are electri

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

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

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

239 Here we characterize the contribution to remyelination of a subset of adult neural stem cells, id

240 ation, such as occurs in multiple sclerosis, remyelination of axons is often incomplete, leading to l

241 at supports neuronal survival and ultimately remyelination of axons.

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

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

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

245 n the CNS, and provides further insight into remyelination of CNS axons by Schwann cells.

246 Remyelination of damaged axons requires the generation o

247 of endothelin receptor type B also inhibited remyelination of experimentally-generated demyelination

248 1.2 deletion in OPCs leads to less efficient remyelination of the adult brain.

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

250 Remyelination of the mouse hippocampus reversed these ch

251 fferentiation observed in patients with high remyelination pattern.

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

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

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

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

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

257 sion and survival, leading to a delay in the remyelination process.

258 reduced maturational rate through the entire remyelination process.

259 Examination of remyelination processes, both in the mouse model for foc

260 ow that LXRs are involved in myelination and remyelination processes.

261 Endogenous remyelination promotes recovery, but the process is not

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

263 ctional screening for compounds that promote remyelination represents a major hurdle in the developme

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

265 CXCR7-mediated effects on remyelination required CXCR4 activation, as assessed via

266 However, remyelination, restoration of oligodendrocyte densities,

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

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

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

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

271 glia and peripherally derived macrophages as remyelination started.

272 ed to understand the regenerative process of remyelination that can follow CNS demyelination.

273 d a key player in the age-related decline in remyelination that may be targeted by available or newly

274 f TACE in supporting OL regeneration and CNS remyelination that may contribute to the design of new s

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

276 though accumulation of myelin debris impairs remyelination, the mechanisms regulating the clearance o

277 by promoting Notch activation in OPCs during remyelination through induction of Jagged1 expression in

278 eneration and subsequent disability requires remyelination through the generation of new oligodendroc

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

280 mpacted oligodendrogenesis, myelination, and remyelination, transgenic mouse lines were generated in

281 ein also plays a role in OL regeneration and remyelination under demyelinating conditions.

282 In the CNS, the chemokine CXCL12 promotes remyelination via CXCR4 activation on OPCs, resulting in

283 This reduced remyelination was accompanied by an important decline in

284 The influence of netrin-1 on CNS remyelination was examined using gain and loss of functi

285 Therapeutic Ind-Cl-induced remyelination was independent of its effects on the immu

286 Dynamic remyelination was inversely correlated with clinical dis

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

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

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

290 n regions subject to significant NPC-derived remyelination were equivalent to those of unchallenged c

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

292 ith inducible loss of Sox2 revealed impaired remyelination, which was largely due to a profound atten

293 l therapeutic strategy would be to stimulate remyelination while limiting demyelination.

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

295 Since incomplete remyelination will irreversibly damage axonal connection

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

297 oligodendrocyte precursor cells and promoted remyelination within lesions; these pro-regenerative eff

298 Remyelination within the central nervous system (CNS) mo

299 ts on the immune system, as Ind-Cl increased remyelination within the cuprizone diet-induced demyelin

300 In multiple sclerosis, successful remyelination within the injured CNS is largely dependen