ライフサイエンスコーパス: demyelination

1 ies, and reservoirs for viruses that trigger demyelination.

2 ty and microglia depletion leads to worsened demyelination.

3 ral and peripheral nervous system (CNS, PNS) demyelination.

4 ide microglia/macrophages from 6 weeks after demyelination.

5 t the proper myelination of axons or lead to demyelination.

6 ular disruption, leukocyte accumulation, and demyelination.

7 elitis mouse model of central nervous system demyelination.

8 d potential latency, a functional measure of demyelination.

9 veloping peripheral neuropathy with abundant demyelination.

10 se of OSE and increased CNS inflammation and demyelination.

11 the regeneration of myelin sheaths following demyelination.

12 emyelination in aged animals following focal demyelination.

13 verified in an ex vivo organotypic model of demyelination.

14 or feeding them toxic substances that induce demyelination.

15 creasing Th17 cell-mediated inflammation and demyelination.

16 ptic neuritis, with reduced inflammation and demyelination.

17 mediator of pathophysiological damage after demyelination.

18 newborn neurons was also impaired following demyelination.

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

20 tivation, inflammatory cell recruitment, and demyelination.

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

22 ion is associated with increased severity of demyelination.

23 ation is altered in MS hippocampus following demyelination.

24 reactive astrocyte response associated with demyelination.

25 ll as motor recovery after cuprizone-induced demyelination.

26 the cuprizone model of neuroinflammation and demyelination.

27 BCCAO rats exhibited neuronal damage and demyelination.

28 been shown to cause SC dedifferentiation and demyelination.

29 monitored them for symptoms of inflammatory demyelination.

30 linically feasible method to assess cortical demyelination.

31 also shown to induce complement-independent demyelination.

32 the first symptom of central nervous system demyelination.

33 by injuring their mitochondria and inducing demyelination.

34 ligodendrocyte progenitor cells (OPCs) after demyelination.

35 emyelination is the regenerative response to demyelination.

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

37 stive of inflammatory central nervous system demyelination.

38 lammation, control of viral replication, and demyelination.

39 tem lesions after lysolecithin-induced focal demyelination.

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

41 at are commonly associated with a process of demyelination.

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

43 eriod significantly reduced or prevented the demyelination.

44 that occurs following central nervous system demyelination.

45 and optic radiations, indicating predominant demyelination.

46 etes and relapsing-remitting immune-mediated demyelination.

47 with characteristic inflammatory lesions and demyelination.

48 tects neurological function but also reduces demyelination.

49 and cortex of Cav1.2 knock-out mice through demyelination.

50 d optic neuritis followed by axonal loss and demyelination.

51 izone (CZ) is a copper chelator that induces demyelination.

52 responsible for astrocyte loss and secondary demyelination.

53 ostics but is conventionally not specific to demyelination.

54 oliferation in the adult mouse SVZ following demyelination.

55 entral nervous system (CNS) inflammation and demyelination.

56 osine levels, attenuated SNHL, and prevented demyelination.

57 y does not correlate well with the extent of demyelination(1), which suggests that other factors cont

58 GALC cause psychosine accumulation, inducing demyelination, a neuroinflammatory "globoid" reaction an

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

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

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

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

63 de riboside slowed the axon degeneration and demyelination, although it did not alter the level of ma

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

65 rease in age-exacerbated lipid peroxidation, demyelination and axon loss.

66 H deficiency in mice leads to severe central demyelination and axon loss.

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

68 neurologic impairment resulting from primary demyelination and axonal damage.

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

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

71 a complex disease involving dysmyelination, demyelination and axonal degeneration.

72 n vivo neuroimaging correlate of smouldering demyelination and axonal loss in chronic active lesions

73 oup of horses are consistent with left sided demyelination and axonal loss, consistent with Recurrent

74 virus-induced neural-cell damage leading to demyelination and axonal loss, which are pathological fe

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

76 The metabolic basis for the demyelination and brain disorder is unknown.

77 e fate mapped SVZ-eNPCs in cuprizone-induced demyelination and found that SVZ endogenous neural stem/

78 ce are more susceptible to cuprizone-induced demyelination and have a reduced capacity to remyelinate

79 demyelination, including toxin-induced focal demyelination and immune-mediated demyelination through

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

81 l allergic encephalomyelitis murine model of demyelination and in postmortem brain tissue of patients

82 is (spEAE), which was associated with severe demyelination and inflammation in the central nervous sy

83 multiple sclerosis-related pathology (focal demyelination and inflammation) was characterized in the

84 oute (lip abrasion) can cause multifocal CNS demyelination and inflammation.

85 explored trajectories of surface morphology, demyelination and iron concentration within the basal ga

86 e sclerosis (e.g. central vein sign, subpial demyelination and lesional rims), which are not included

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

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

89 nversely correlated with imaging measures of demyelination and microstructural damage.

90 ted adenosine caused substantial nerve fiber demyelination and mild hair cell loss.

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

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

93 f galactosylceramidase (GALC), which induces demyelination and neurodegeneration due to accumulation

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

95 Early stages of demyelination and neurodegeneration in active lesions co

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

97 Subclinical inflammatory demyelination and neurodegeneration often precede sympto

98 lper 1 (T(H)1) and T(H)17 cells, which cause demyelination and neurodegeneration.

99 ral adrenoleukodystrophy is characterized by demyelination and neurodegeneration.

100 acterized by focal lymphocytic infiltration, demyelination and neurodegeneration.

101 kocytes into the CNS where these cells cause demyelination and neurodegeneration.

102 n liberation within active lesions amplifies demyelination and neurodegeneration.

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

104 synapse loss occurred independently of local demyelination and neuronal degeneration but coincided wi

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

106 ocate to the retina, and causes only minimal demyelination and no neuronal death.

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

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

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

110 e disease and recovery, and quantitated both demyelination and remyelination along the length of the

111 , a copper chelator, is widely used to study demyelination and remyelination in the CNS, in the conte

112 Although it is a widely used model to study demyelination and remyelination in the context of multip

113 Using zebrafish and mouse models of demyelination and remyelination, Cunha et al. now descri

114 tencies in optic neuritis in MS may identify demyelination and remyelination, this has not been direc

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

116 tral nervous system (CNS) has been linked to demyelination and remyelination.

117 at least two mechanisms: psychosine-induced demyelination and secondary neuroinflammation from galac

118 xhibit dynamic response to cuprizone-induced demyelination and species-specific transcriptomic differ

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

120 Although the metabolic basis for the demyelination and the structural and functional alterati

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

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

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

124 without any evidence of 'strict criteria of demyelination'; and (3) definite responsiveness to immun

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

126 injury, likely reflecting neurodegeneration, demyelination, and astrocytic gliosis in the injured cer

127 meliorated EAE-induced oligodendrocyte loss, demyelination, and axon degeneration, without affecting

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

129 S and EAE are characterized by inflammation, demyelination, and axonal damage, with minimal remyelina

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

131 er multiple sclerosis or monophasic acquired demyelination, and healthy controls.

132 strates of multiple sclerosis (inflammation, demyelination, and neuro-axonal loss).

133 mmune cells into the central nervous system, demyelination, and neuronal damage.

134 ers of proinflammatory cuffs, less extensive demyelination, and reduced expression levels of proinfla

135 d nonuniform, internodal segments suggesting demyelination, and remyelination in progress.

136 proliferation of reactive astrocytes during demyelination; and that attenuation of astrocytic voltag

137 Experimental models of dys-/demyelination are characterized by various levels of mye

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

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

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

141 tion study (NCS) abnormalities suggestive of demyelination are mandatory to fulfil the diagnostic cri

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

143 nderlying oligodendrocyte (OL) cell loss and demyelination are not known.

144 Lipid-processing mechanisms during demyelination are poorly understood.

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

146 ent and a spectrum of central and peripheral demyelination as part of its core clinical phenotype.

147 In MS, the ON damage was less severe, with demyelination as the main pathologic component, whereas

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

149 potential genes involved in contributing to demyelination as well as remyelination being expressed b

150 ota with the aim of limiting immune-mediated demyelination, as occurs in multiple sclerosis.

151 erity and alleviates CNS immunopathology and demyelination, associated with decreased activation of T

152 RSA59 (P)-carrying MHV significantly reduced demyelination at the chronic stage.

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

154 disease of the CNS that is characterized by demyelination, axonal loss, gliosis, and inflammation.

155 ferences in the severity of encephalitis and demyelination between RSA59 (PP) and RSA59 (P) arise fro

156 ates psychosine-induced glial cell death and demyelination both in vitro and ex vivo models.

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

160 Demyelination characteristic of at least some early mult

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

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

163 tiple sclerosis and children with monophasic demyelination demonstrated volume loss in thalamic regio

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

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

166 d myelin clearance to promote progression of demyelination disorders by regulating macrophage infiltr

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

168 hronic axonal degeneration, and inflammatory demyelination due to loss of protective antiviral host i

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

170 ecognition and engulfment, Schwann cell (SC) demyelination, epithelial-mesenchymal transition (EMT),

171 lammatory responses, T cell infiltration and demyelination following focal spinal cord lesion.

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

173 In the aged CNS, increased demyelination has been associated with astrocyte hypertr

174 herapy to restore function, and protect from demyelination in 2 MS models.

175 1 as the etiologic agent of multifocal brain demyelination in a normal host and suggests that vaccina

176 with facial cold sores, and multifocal brain demyelination in an otherwise normal host, the cotton ra

177 neuropathy associated with degeneration and demyelination in axons.

178 Nimodipine therapy also reduces demyelination in both EAE and a model of the early MS le

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

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

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

182 Loss of function in EAE, and demyelination in EAE, and the model of the early MS lesi

183 ukocyte infiltration, neuroinflammation, and demyelination in experimental autoimmune encephalomyelit

184 d SVZ-derived eNPCs during cuprizone-induced demyelination in female mice, the animals displayed redu

185 Remyelination occurred shortly after demyelination in HSV-1-infected cotton rats but could be

186 lex virus (HSV) infection and multifocal CNS demyelination in humans; however, convincing evidence fr

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

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

191 Following lysolecithin demyelination in middle-aged mice, indapamide treatment

192 t myelin quantification that detects diffuse demyelination in normal-appearing tissue in multiple scl

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

194 tensor imaging reflect axonal disruption and demyelination in specific white matter tracts within the

195 CCN3 was transiently up-regulated following demyelination in the brain of cuprizone-fed mice and spi

196 In multiple sclerosis (MS), demyelination in the central nervous system thus leads t

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

198 hronic inflammatory disease characterized by demyelination in the central nervous system.

199 del to study acute and chronic virus-induced demyelination in the central nervous system.

200 r characterized by neuroinflammation-induced demyelination in the central nervous system.

201 Demyelination in the cerebral cortex was related to infl

202 Focal demyelination in the mPFC was sufficient to decrease soc

203 jury, we observed early glial activation and demyelination in the posterior visual projections, evide

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 nimal models of central nervous system (CNS) demyelination, including toxin-induced focal demyelinati

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

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

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

210 Cerebral demyelination is a rare complication of overly rapid cor

211 t recovers with remyelination; while chronic demyelination is characterized by increased tissue stiff

212 dministered in the cuprizone model, in which demyelination is less dependent upon immune cells, we di

213 multiple sclerosis, the mechanisms mediating demyelination is not fully understood.

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

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

216 positive astrocytes during cuprizone-induced demyelination leads to a significant reduction in the de

217 Chronic demyelination leads to damaged axons and irreversible de

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

219 Here we show that in response to demyelination, mature oligodendrocytes (OLG) bordering t

220 accumulation in the weeks after inflammatory demyelination may contribute to lesion repair rather tha

221 acrophage polarization, origin, or different demyelination mechanisms, and paves the way for developi

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

223 We demonstrate that in the lysolecithin demyelination model in young and middle-aged mice, the l

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

225 vely kill SVZ-derived eNPCs in the cuprizone demyelination model, we observed migration of SVZ-eNPCs

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

227 ion and remyelination in a cuprizone-induced demyelination model.

228 Furthermore, studies in mouse demyelination models and white matter lesions from patie

229 cord in both lysolecithin- and EAE-mediated demyelination models.

230 e significantly enriched in 10 of 12 primary demyelination (MS) brain specimens compared to a group o

231 Immediately following demyelination, neurons exhibit hyperexcitability, learni

232 f ALD, cerebral ALD, resulting in regions of demyelination observed on brain magnetic resonance imagi

233 alistic model in which axonal disruption and demyelination occur together in the cord.

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

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

236 Demyelination of central nervous system axons, associate

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

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

239 present with a single attack of inflammatory demyelination of the central nervous system.

240 d VEPs in a model in which there is complete demyelination of the optic nerve, with subsequent remyel

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

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

243 After demyelination, oligodendrocytes derived from these newly

244 The metabolic changes preceded any demyelination or axonal degeneration.

245 5(lo) microglia, but they show no detectable demyelination or neuronal loss.

246 In adult mice with toxin (cuprizone)-induced demyelination, oral GlcNAc prevents neuro-axonal damage

247 Combining chronic demyelination paradigms and cell sorting with RNA sequen

248 We histologically characterized thalamic demyelination patterns and compared neuronal loss and ne

249 te to lesion repair rather than inflammatory demyelination per se.

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

251 Chronic inflammatory demyelination polyneuropathy is a heterogeneous and trea

252 CE STATEMENT In multiple sclerosis patients, demyelination progresses with aging and disease course,

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

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

255 osis that prevents CZ-induced loss of OL and demyelination, providing clear evidence of a copper-iron

256 s are inversely correlated with the level of demyelination, providing critical insight into hippocamp

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

258 phalitis (EAE) and in the cuprizone model of demyelination/remyelination.

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

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

261 uman demyelinated brains indicate that acute demyelination results in decreased tissue stiffness that

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

263 , that is lysolecithin or cuprizone-mediated demyelination, showed that PAR1 knock-out in male mice i

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

265 ted Ca(2+) influx in astrocytes during brain demyelination significantly attenuates brain inflammatio

266 ressive peripheral neuropathy with hypo- and demyelination, slowing of nerve conduction velocities an

267 l feature of NMOSD, in contrast to MS, where demyelination spreads along the entire visual pathway.

268 ther sex injected with nimodipine during the demyelination stage of the cuprizone treatment displayed

269 ated with inflammation and postdated initial demyelination, suggesting that iron is not directly path

270 MS is a more diffuse disease than its focal demyelination suggests.

271 ur results indicate that, in toxic models of demyelination, SVZ-derived eNPCs contribute to support a

272 standard group (1%; one case each of osmotic demyelination syndrome and intracranial haemorrhage).

273 chronic hyponatremia are at risk of osmotic demyelination syndrome.

274 p model, which recapitulates the hippocampal demyelination that occurs in MS patients.

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

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

277 uced focal demyelination and immune-mediated demyelination through experimental autoimmune encephalom

278 reases myelin pattern preservation following demyelination, thus presenting a new target for therapeu

279 o understand the neural substrates that link demyelination to cognitive deficits in MS, we investigat

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

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

282 asc155 IgG4 perturb conduction in absence of demyelination, validating the existence of paranodopathy

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

284 y shows, for the first time, that CZ induces demyelination via ferroptosis-mediated rapid loss of oli

285 In addition, the severity of demyelination was similar between tamoxifen-treated mice

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

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

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

289 Using a viral model of neuroinflammation and demyelination, we demonstrate that genetic silencing of

290 Using an in vivo murine model of focal demyelination, we find that BZA enhances OPC differentia

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

292 In contrast, the axon degeneration and demyelination were delayed, and macrophage accumulation

293 le sclerosis and 73 children with monophasic demyelination were prospectively followed with yearly br

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

299 fect clinical disease, neuroinflammation, or demyelination, yet there was increased remyelination.

300 After transplantation near a site of demyelination, Zfp488 expressing hNSCs migrated to the l