ライフサイエンスコーパス: demyelination

1 lar atrophy (SMA) and central nervous system demyelination.

2 stive of inflammatory central nervous system demyelination.

3 lammation, control of viral replication, and demyelination.

4 tem lesions after lysolecithin-induced focal demyelination.

5 drocytes, and an increase in the severity of demyelination.

6 tivation, inflammatory cell recruitment, and demyelination.

7 at are commonly associated with a process of demyelination.

8 ased at the site shortly afterward, prior to demyelination.

9 eriod significantly reduced or prevented the demyelination.

10 that occurs following central nervous system demyelination.

11 and optic radiations, indicating predominant demyelination.

12 etes and relapsing-remitting immune-mediated demyelination.

13 cell cytoplasm, thereby priming the cell for demyelination.

14 sting co-presence of axonal degeneration and demyelination.

15 ovide future therapeutic strategies to treat demyelination.

16 o study mechanisms of damage and recovery in demyelination.

17 red for supporting OL regeneration following demyelination.

18 he CNS protecting from neuroinflammation and demyelination.

19 antly reduced CNS inflammation and prevented demyelination.

20 in animal models of autoimmune inflammatory demyelination.

21 a lysolecithin-induced mouse model of focal demyelination.

22 l spread within the CNS, resulting in severe demyelination.

23 lects axonal degeneration without antecedent demyelination.

24 suggests that deletion of SNPH is harmful in demyelination.

25 ng areas, but that these cells do not impact demyelination.

26 regeneration and CNS remyelination following demyelination.

27 ptic neuritis, with reduced inflammation and demyelination.

28 B1 causes progressive central nervous system demyelination.

29 s) after transplantation in a viral model of demyelination.

30 onse of oligodendrocyte against inflammatory demyelination.

31 be to stimulate remyelination while limiting demyelination.

32 ftment in murine models of adult spinal cord demyelination.

33 crophage recruitment into the CNS leading to demyelination.

34 d remyelination after experimentally-induced demyelination.

35 b1 as targets for intervention in autoimmune demyelination.

36 te inflammatory central nervous system (CNS) demyelination.

37 induces microglia/macrophage activation and demyelination.

38 n the extracellular space, such as following demyelination.

39 owed axonal damage but no classical signs of demyelination.

40 ols Th17 cell differentiation and autoimmune demyelination.

41 T cells without blood-derived macrophages or demyelination.

42 e was demonstrated for all major patterns of demyelination.

43 s of traumatic axonal injury and exacerbated demyelination.

44 n in axonal degeneration following acute CNS demyelination.

45 g induction of MAPK/ERK in adulthood induces demyelination.

46 can also generate new oligodendrocytes after demyelination.

47 ce imaging (MRI) and/or clinical features of demyelination.

48 (CCs) of mice subjected to cuprizone-induced demyelination.

49 unopathological heterogeneity in patterns of demyelination.

50 ocyte invasion, and T-cell infiltration) and demyelination.

51 predominantly macrophages and microglia) and demyelination.

52 ion is associated with increased severity of demyelination.

53 ation is altered in MS hippocampus following demyelination.

54 reactive astrocyte response associated with demyelination.

55 mediator of pathophysiological damage after demyelination.

56 ll as motor recovery after cuprizone-induced demyelination.

57 the cuprizone model of neuroinflammation and demyelination.

58 BCCAO rats exhibited neuronal damage and demyelination.

59 been shown to cause SC dedifferentiation and demyelination.

60 monitored them for symptoms of inflammatory demyelination.

61 linically feasible method to assess cortical demyelination.

62 also shown to induce complement-independent demyelination.

63 the first symptom of central nervous system demyelination.

64 by injuring their mitochondria and inducing demyelination.

65 both white matter (WM) and gray matter (GM) demyelination.

66 emyelination is the regenerative response to demyelination.

67 and microglia activation ((11)C-PK11195) and demyelination ((11)C-MeDAS) during normal disease progre

68 eously with MRI and symptoms compatible with demyelination (5 AQ4 positive, 2 MOG positive).

69 Using the cuprizone model of demyelination, a noninflammatory model that allows the a

70 y, oligodendrocyte reduction, and persistent demyelination after prolonged cuprizone treatment.

71 Observations: Cortical atrophy and demyelination along the subpial surface appear early in

72 Our previous data have shown that demyelination alters neuronal gene expression in the hip

73 godendrocytes following lysolecithin-induced demyelination, although apparently normal remyelination

74 Although white matter pathology, including demyelination and axon injury, can lead to secondary gra

75 Demyelination and axon loss are pathological hallmarks o

76 We find that demyelination and axonal damage are not directly initiat

77 autoreactive pathogenic TH cells that elicit demyelination and axonal damage.

78 However, a late onset of demyelination and axonal degeneration occurred at hypere

79 ctin-1 activation causes macrophage-mediated demyelination and axonal injury.

80 recessive neuropathy characterized by severe demyelination and axonal loss in human, with both motor

81 CMT1A is characterized by demyelination and axonal loss, which underlie slowed mot

82 eased EAE severity, accompanied by increased demyelination and axonal loss.

83 7 cells are particularly potent mediators of demyelination and axonopathy.

84 mouse models, resulting in the reduction of demyelination and CNS-infiltrating T helper 1 and T help

85 inactivation of Fig4 in Schwann cells causes demyelination and defects in autophagy-mediated degradat

86 How TREM2 deficiency mediates demyelination and disease is unknown.

87 astrointestinal (GI) distress, to persistent demyelination and even encephalitic death.

88 ng via LPA receptor type 1 activation causes demyelination and functional deficits after spinal cord

89 ectly enhance their repopulation of areas of demyelination and hence their ability to contribute to r

90 e picture of how they become activated after demyelination and how this enables them to contribute to

91 tral striatum iron accumulation is linked to demyelination and impairments in declarative memory.

92 FA supplementation reduced cuprizone-induced demyelination and improved motor and cognitive function.

93 after spinal cord injury results in reduced demyelination and improvement in locomotor recovery.

94 ng sensitive and specific cut-off values for demyelination and incorporating new knowledge on electro

95 Axon injury/loss, demyelination and inflammation are the primary pathologi

96 lis, protects against central nervous system demyelination and inflammation during experimental autoi

97 ckout (alpha1KO) mice with EAE showed severe demyelination and inflammation in the brain and spinal c

98 and individually quantify axon injury/loss, demyelination and inflammation, would not only facilitat

99 Axonal damage precedes extensive demyelination and is characterized by swelling along the

100 Using the cuprizone (CPZ) model of demyelination and mice of either sex, we establish that

101 -) mice demonstrated significantly decreased demyelination and microglial/macrophage accumulation com

102 quent large-fiber involvement and associated demyelination and more severe axonal loss.

103 tional ablation results in severe peripheral demyelination and mouse death.

104 lapse of EAE occurred as a result of reduced demyelination and myeloid cell infiltration into the CNS

105 upregulate netrin-1 expression early during demyelination and netrin-1 receptors are expressed by OP

106 In our study we analysed demyelination and neurodegeneration in a large series of

107 Early stages of demyelination and neurodegeneration in active lesions co

108 a chronic inflammatory disease with primary demyelination and neurodegeneration in the central nervo

109 acrophages accumulate at the sites of active demyelination and neurodegeneration in the multiple scle

110 Subclinical inflammatory demyelination and neurodegeneration often precede sympto

111 acterized by focal lymphocytic infiltration, demyelination and neurodegeneration.

112 ral adrenoleukodystrophy is characterized by demyelination and neurodegeneration.

113 the central nervous system (CNS) leading to demyelination and neurological deficits.

114 tem characterized by oligodendrocyte damage, demyelination and neuronal death.

115 terized by auto-reactive T cells that induce demyelination and neuronal degradation.

116 ological studies have identified substantial demyelination and neuronal loss in the spinal cord grey

117 tor in the molecular mechanism of peripheral demyelination and opens a potential opportunity for the

118 tion in the absence of Myd88 leads to severe demyelination and pathology despite overall reduced infl

119 Arrest of progressive cerebral demyelination and prevention of severe loss of neurocogn

120 rease of axonal mitochondria following acute demyelination and protects against axonal degeneration i

121 n the present study, we used mouse models of demyelination and proteomics analysis to identify molecu

122 disease associated with progressive cerebral demyelination and rapid, devastating neurologic decline.

123 ms and early death, as well as age-dependent demyelination and reduced expression of myelin genes tha

124 d neurological parameters in mouse models of demyelination and remyelination.

125 nerve, visual evoked potentials can indicate demyelination and should be correlated with an imaging o

126 chanisms, including its link to inflammatory demyelination and temporal occurrence in the disease cou

127 es oligodendrocyte differentiation following demyelination and therefore has important therapeutic im

128 d) control rats and of models of spinal cord demyelination and traumatic contusion injury.

129 years, and had a first CIS suggestive of CNS demyelination and typical of relapsing-remitting multipl

130 omplement, but NMO histopathology also shows demyelination, and - importantly - axon injury, which ma

131 ate reduced structural integrity of neurons, demyelination, and abnormalities in the glutamatergic pa

132 , independent of the white matter pathology, demyelination, and axon injury that have been the focus

133 lated with reduced immune cell infiltration, demyelination, and axonal damage in the CNS.

134 SCI leads to oligodendrocyte death and demyelination, and clinical trials have tested glial tra

135 on and in activated adult OPCs responding to demyelination, and is also detected in multiple sclerosi

136 both during development and following focal demyelination, and longitudinal extension of the myelin

137 sclerosis, there is increasing evidence that demyelination, and neuronal damage occurs preferentially

138 d clinical disease coincident with increased demyelination, and succumbed to infection within 3 weeks

139 ritical for EGFR activation in OLs following demyelination, and therefore, for sustaining OL regenera

140 index of myelin content change; the index of demyelination; and the index of remyelination.

141 Memory impairments and hippocampal demyelination are common features in MS patients.

142 The principal risk factors for cerebral demyelination are correction of the serum sodium more th

143 Although the negative effects of demyelination are generally attributed to conduction fai

144 Depletion of oligodendrocyte progenitors and demyelination are major pathological features that are p

145 system where persistent virus infection and demyelination are not factors in long-term neuropatholog

146 i)Rag(-/-) mice during development and after demyelination, are suitable for in vitro myelination ass

147 n restoration following lysolecithin-induced demyelination as well as experimental autoimmune encepha

148 efficiently repairing lysolecithin model of demyelination (astrocyte-free), netrin-1 expression is a

149 s axonal damage, oligodendrocyte cell death, demyelination, autoimmunity, and blood-brain barrier dys

150 th fibrin deposition, microglial activation, demyelination, axonal damage, and clinical severity.

151 Multiple sclerosis (MS) is characterized by demyelination, axonal degeneration, and inflammation.

152 e elements of acute inflammatory CNS injury: demyelination, axonal injury and neuronal degeneration.I

153 of the myelin sheath (tomacula), progressive demyelination, axonal loss, and motor and sensory nerve

154 disseminated encephalomyelitis, tumefactive demyelination, Balo's concentric sclerosis, Schilder's d

155 Neuroprotection was not limited to models of demyelination, but was also observed in another mouse mo

156 ine a detrimental role of IL-27 in promoting demyelination by delaying viral control.

157 CD4(+) T-cell infiltration into the CNS, and demyelination by increasing expression of vascular cell

158 attern in the human disease, where targeting demyelination by therapeutic interventions remains a maj

159 Demyelination can be reduced or eliminated by increasing

160 Neuropathological evidence suggests that demyelination can occur in the relative absence of lymph

161 AQP4-Ab negative first episode CNS acquired demyelination cases (n = 29; females = 55%; all AQP4-Ab

162 Demyelination characteristic of at least some early mult

163 rae PGL-1 induces macrophages to cause nerve demyelination characteristic of human leprosy.

164 g body of evidence suggests that gray matter demyelination, cortical atrophy, and leptomeningeal infl

165 Stimulating prompt OPC recruitment following demyelination could improve myelin repair by providing s

166 el of multiple sclerosis (MS), a devastating demyelination disease.

167 viding new drug targets for the treatment of demyelination diseases.

168 on of the nodes, axon-glia interactions, and demyelination diseases.

169 n oligodendrocyte progenitor cells following demyelination disturbs OL lineage cell expansion and sur

170 ter recovering from oligodendrocyte loss and demyelination, DTA mice develop a fatal secondary diseas

171 ain meninges that were associated with local demyelination during experimental autoimmune encephaliti

172 lecule associated with neurodegeneration and demyelination, elicits NLRP3 and NLRC4 inflammasome acti

173 ole of Sox2 expression in OPCs responding to demyelination, enabling them to effectively contribute t

174 plex pathologic substrate involving cortical demyelination, gray matter atrophy, and meningeal inflam

175 Only 1 of 23 NMDAR patients with signs of demyelination had ovarian teratoma compared with 18 of 5

176 is of SVZ tissue from mice with experimental demyelination identified several proteins that are known

177 of the earliest tissue changes accompanying demyelination in a primate model of multiple sclerosis (

178 cts on lysophosphatidylcholine (LPC) induced demyelination in a three-dimensional brain cell culture

179 neuropathy associated with degeneration and demyelination in axons.

180 bust and accurate quantitative assessment of demyelination in both WM and GM.

181 we demonstrate that progressive inflammatory demyelination in cerebral adrenoleukodystrophy coincides

182 Significant (p < 0.05) demyelination in cuprizone-treated animals was found acc

183 appearing white matter, different degrees of demyelination in different patients and lesions, early n

184 Severe brain-specific inflammation and demyelination in DRB1*0301.DQ8.IFN-gamma(-/-) mice with

185 mod on clinical score, CNS inflammation, and demyelination in EAE was abolished in AhR(-/-) mice.

186 a-host immune symbiosis to reveal autoimmune demyelination in genetically susceptible mice.

187 sive loss of white matter integrity and axon demyelination in MAP.

188 Moreover, lysolecithin-mediated demyelination in mice deficient in the creatine-synthesi

189 nt DeltaDomA, caused neuron degeneration and demyelination in mice infected intracranially, suggestin

190 Cuprizone-induced demyelination in mice is a frequently used model in prec

191 Focal demyelination in mice lacking IL4I1 or interleukin 4 rec

192 ination following experimental toxin-induced demyelination in mice with inducible loss of Sox2 reveal

193 XCL1-transgenic mice reduced the severity of demyelination in mice, arguing for a role for these cell

194 Following cuprizone-elicited demyelination in mice, astrocytes contain BDNF and incre

195 ment of acute optic neuritis (AON) and acute demyelination in multiple sclerosis.Despite facilitating

196 in female-biased spontaneous autoimmune CNS demyelination in myelin oligodendrocyte glycoprotein-spe

197 n mapping enables quantitative assessment of demyelination in normal-appearing brain tissues and show

198 pported a significant contribution of age to demyelination in patients with MS, suggesting that age-a

199 Detecting cortical demyelination in patients with multiple sclerosis (MS) i

200 TMEV) infection in mice induces inflammatory demyelination in the central nervous system.

201 Demyelination in the cerebral cortex was related to infl

202 vical spinal cord; radiculitis; neuritis and demyelination in the spinal roots; and inflammation with

203 During the onset of demyelination in the subcortical white matter (SCWM), ac

204 a rapidly progressive cerebral inflammatory demyelination in up to 60% of affected males.

205 ause major neurological dysfunction, without demyelination, in both multiple sclerosis (MS) and a mou

206 We show that during cuprizone-induced demyelination, in vivo CXCR7 antagonism augmented OPC pr

207 icant clinical correlation was found for the demyelination index.

208 gen) was assessed and related to measures of demyelination, inflammation, and neuronal density.

209 myelin proteins, which accumulate following demyelination, inhibit remyelination by blocking the dif

210 postnatal CNS development or in response to demyelination injury has not been examined.

211 Demyelination is a cardinal feature of multiple sclerosi

212 on is important from other diseases in which demyelination is a feature (eg, neuromyelitis optica spe

213 Cerebral demyelination is a rare complication of overly rapid cor

214 tation into animals in which immune-mediated demyelination is initiated by the viral infection of the

215 nd few bare axons at 10 wpi, indicating that demyelination is relatively rare.

216 hology in which central nervous system (CNS) demyelination is secondary.

217 ing or pharmacological inhibition, prevented demyelination, leading to nerve conduction and neuromusc

218 e and subsequent oligodendrocyte cell death, demyelination, macrophage recruitment, and astroglial ac

219 trate that astrocytes play a pivotal role in demyelination, making them a potential target for therap

220 e larger Ca(2+) influx that occurs following demyelination may contribute to the axonal degeneration

221 iple sclerosis (MS), is characterized by CNS demyelination mediated by autoreactive T cells.

222 alian brain and further suggest that osmotic demyelination might be a consequence of proteostasis fai

223 promoted remyelination in a chemical-induced demyelination model on organotypic slice culture, in a B

224 in loss in brain tissues using the cuprizone demyelination model.

225 lerosis pathologic damage typically includes demyelination, neuro-axonal loss, and astrogliosis.

226 iminish neuroinflammation or the severity of demyelination, nor increase remyelination.

227 t by infected macrophages that patrol axons; demyelination occurs in areas of intimate contact.

228 eurodegenerative disease where immune-driven demyelination occurs with inefficient remyelination, but

229 Demyelination of central nervous system axons, associate

230 were associated with striking JCV-associated demyelination of cortical and subcortical U fibers, sign

231 nn cells within the spinal cord and profound demyelination of dorsal column axons.

232 lammatory disease of the CNS that causes the demyelination of nerve cells and destroys oligodendrocyt

233 s to trigger mitochondrial damage and induce demyelination of nerve cells.

234 and remyelination after lysolecithin-induced demyelination of organotypic cerebellar slice cultures.

235 ollowing traumatic spinal cord injury, acute demyelination of spinal axons is followed by a period of

236 on remyelination after lysolecithin-induced demyelination of spinal cord white matter.

237 for inactivating mutations in TREM2 exhibit demyelination of subcortical white matter and a lethal e

238 de-induced EAE, and reduced inflammation and demyelination of the central nervous system (CNS).

239 dent mechanisms contributing to inflammatory demyelination of the CNS have been explored using experi

240 After lysolecithin-induced demyelination of the male mouse ventral spinal cord whit

241 d model system, in which there is widespread demyelination of the spinal cord and optic nerves, we al

242 mice were subjected to lysolecithin-induced demyelination of the spinal cord, systemic injections of

243 gical deficit, immune cell infiltration, and demyelination of the spinal cords in wild-type mice, but

244 nd the CON, which probably resulted from the demyelination of the white matter.

245 of JCV resulted in infection and subsequent demyelination of these chimeric mice.

246 itochondrial volume increase following acute demyelination of WT CNS axons does not occur in demyelin

247 After demyelination, oligodendrocytes derived from these newly

248 ts included atypical clinical presentations, demyelination on nerve conduction studies (p = 0.0005),

249 core of less than -2.0 criterion, indicating demyelination) on QS maps correlated significantly with

250 Chronic demyelination, on-going inflammation, axonal loss and gr

251 n groups of 2-month-old Cx32 KO mice, before demyelination onset, significantly reduced the ratio of

252 The metabolic changes preceded any demyelination or axonal degeneration.

253 5(lo) microglia, but they show no detectable demyelination or neuronal loss.

254 hanisms responsible for chronic inflammatory demyelination polyneuropathy are broad and may include d

255 Chronic inflammatory demyelination polyneuropathy is a heterogeneous and trea

256 investigate the underlying mechanisms of the demyelination process.

257 the early molecular events that trigger the demyelination program in these diseases remain unknown.

258 ons of lipid layers at an early stage of the demyelination progression, whereas the membrane architec

259 of corpus callosum from mice subjected to a demyelination protocol, this novel inhibitor improved ne

260 t the disease could be primarily caused by a demyelination rather than a primitive axonal damage.

261 In another model mimicking a mild, demyelination-related Charcot-Marie-Tooth type 1 neuropa

262 2(+) axonal swellings and spheroids and less demyelination relative to ACSF-treated mice.

263 tle structural variations at early stages of demyelination remains poorly characterized.

264 icacy of these and other therapies for acute demyelination require re-evaluation using modern, high-p

265 is believed to be the major risk factor for demyelination resulting from astrocyte death, which lead

266 debilitating morbidity is attributed to axon demyelination resulting from direct interaction of the M

267 licating phagocytosing macrophages amplifies demyelination, Schwann cell dedifferentiation and pertur

268 nvolving phagocytosing macrophages amplifies demyelination, Schwann cell dedifferentiation, and pertu

269 Further, areas with demyelination showed increased presence of CD68(+) infla

270 y modifier of the onset of neuroinflammatory demyelination.SIGNIFICANCE STATEMENT Multiple sclerosis

271 1 inhibitors in preclinical murine models of demyelination significantly attenuated disease progressi

272 d in an acute encephalomyelitis, followed by demyelination similar in pathology to the human demyelin

273 ined as a neurological event consistent with demyelination, starting within 90 days of randomisation,

274 After demyelination, such as occurs in multiple sclerosis, rem

275 chronic hyponatremia are at risk of osmotic demyelination syndrome.

276 ens have been reported in a range of central demyelination syndromes and autoimmune encephalopathies

277 ing persistence, coincident with less severe demyelination, the hallmark tissue damage associated wit

278 otein, we found that after focal spinal cord demyelination, the surrounding surviving labeled oligode

279 In the setting of demyelination, these changes may be reversed or persist

280 vivo time-lapse imaging in a mouse model of demyelination to investigate the underlying mechanisms o

281 How Mycobacterium leprae infection causes demyelination to mediate leprosy pathogenesis has been a

282 ough the reason there is not a recovery from demyelination to normal myelin sheath thickness remains

283 ne model of oligodendrocyte degeneration and demyelination, Trem2(-/-) microglia failed to amplify tr

284 r sciatic nerve injury triggers Schwann cell demyelination via ERK1/2, p38, JNK, and c-JUN activation

285 ibodies to CAMs may be pathogenic and induce demyelination via functional blocking activity.

286 Demyelination was not detected by (11)C-MeDAS PET, proba

287 on at the onset and during cuprizone-induced demyelination was unaffected in male Ncam1(-/-) or St8si

288 In subjects with ongoing inflammatory demyelination we observed a sequence of increased capill

289 umulation of microtubules led to progressive demyelination, we analyzed the spinal cord and optic ner

290 Here, using a rat model of osmotic demyelination, we showed that rapid correction of chroni

291 markers of axonal damage, astrogliosis, and demyelination were evaluated as predictors in a prelimin

292 Oligodendrocyte loss results in demyelination, which leads to impaired neurological func

293 g LPA1 linked receptor-mediated signaling to demyelination, which was in part mediated by microglia.

294 as observed in samples from spinal cord with demyelination, while the intensity of the [M + K](+) add

295 to oligodendrocytes (OLs) even in regions of demyelination with intact axons and instead divert into

296 Multiple sclerosis (MS) lesions feature demyelination with limited remyelination.

297 These results suggest early demyelination with loss of cells and/or cell volumes in

298 tical microvacuolization, and patchy foci of demyelination with no evident white matter axonal degene

299 ve animal model combining cuprizone-mediated demyelination with transfer of myelin-reactive CD4(+) T

300 sclerosis (MS) reflect disruption of myelin (demyelination) within the CNS and failure of repair (rem