ライフサイエンスコーパス: demyelinate

1 positive for ZIKV infection, 27 had GBS (18 demyelinating, 8 axonal, and 1 Miller Fisher syndrome),

2 Lesions were classified according to demyelinating activity and presence of remyelination.

3 Plaque types were classified according to demyelinating activity based on stringent criteria.

4 ced in pediatric lesions irrespective of the demyelinating activity or the presence of remyelination.

5 ese cells has not been well addressed in the demyelinated adult CNS, which has decreased cell plastic

6 therapeutically enhance myelin repair in the demyelinated adult CNS.

7 Following exposure to the demyelinating agent cuprizone, however, GALC +/- animals

8 1w/T2w values significantly differed between demyelinated and myelinated cortex (p < 0.001).

9 e, treated mice exhibited reduced numbers of demyelinated and remyelinated fibers and fewer inflammat

10 gnostic evidence of a length-dependent mixed demyelinating and axonal polyneuropathy.

11 hey differ from multiple sclerosis and other demyelinating and non-demyelinating conditions in their

12 om a general loss of oligodendrocytes in the demyelinated area, we observed a decrease of astroglial

13 cells (OPCs) do not completely migrate into demyelinated areas or OPCs in lesions may not mature int

14 B and the extent of reactive astrogliosis in demyelinating areas and in in vitro assays.

15 use bone marrow-derived cells is abundant in demyelinating areas, but that these cells do not impact

16 sclerosis, but also show that even a single demyelinating attack-when associated with white matter l

17 ability to recover from the T-cell-mediated demyelinating autoimmune disease experimental autoimmune

18 Of interest to the etiology of demyelinating autoimmune disease is the potential to abe

19 Multiple sclerosis is a chronic demyelinating autoimmune disease of the CNS with no know

20 ures for the prevention and treatment of CNS-demyelinating autoimmune disorders.

21 the common forms of either acute or chronic demyelinating autoimmune neuropathy.

22 , using an in-vivo remyelination model, that demyelinated axons are electrically active and generate

23 on microscopic analysis further reveals that demyelinated axons are preserved but reduced in caliber.

24 yelination of WT CNS axons does not occur in demyelinated axons deficient in syntaphilin, an axonal m

25 logical studies, degeneration of chronically demyelinated axons is not a key feature that distinguish

26 Immunofluorescence examination of demyelinated axons showed that betaIV-spectrin, Nav1.6,

27 In contrast, while the AIS in demyelinated axons started more closely to the soma, ank

28 ll recordings demonstrated that neurons with demyelinated axons were intrinsically more excitable, ch

29 its, which become prevalent at internodes in demyelinated axons, may underlie their dysfunctional con

30 eservation of cytoskeletal integrity even in demyelinated axons.

31 When demyelinated, axons deficient in syntaphilin degenerate

32 n modulate oligodendrocyte maturation in the demyelinated brain and suggest that voltage-gated Ca(2+)

33 irus from patients with the frequently fatal demyelinating brain disease progressive multifocal leuko

34 is largely mediated by Schwann cells, where demyelinated central axons, particularly in the dorsal c

35 e the metabolic properties of T cells in the demyelinating CNS in vivo.

36 lls that mediate ongoing inflammation in the demyelinating CNS.

37 nctional deficits underlying diseases with a demyelinating component.

38 o the biology of reprogrammed cells in adult demyelinating conditions and support use of these cells

39 orts oligodendrocyte (OL) regeneration under demyelinating conditions has been a primary goal for reg

40 le sclerosis and other demyelinating and non-demyelinating conditions in their prognosis and treatmen

41 has been shown to enhance myelination under demyelinating conditions, successfully reversed social a

42 e in OL regeneration and remyelination under demyelinating conditions.

43 elitis are considered central nervous system demyelinating conditions.

44 ic relevance in multiple sclerosis and other demyelinating conditions.

45 MOG antibody disease both considered primary demyelinating conditions.

46 tance when understanding myelin assembly and demyelinating conditions.

47 s in the meninges and pronounced in actively demyelinating cortical lesions, retrograde degeneration

48 ler's murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD), a well-established ani

49 r vitamin D in the regenerative component of demyelinating disease and identify a new target for remy

50 ation abnormalities seen in association with demyelinating disease and optic neuritis, although evide

51 irmed that NFM was not a critical Ag driving demyelinating disease because NFM18-30-specific T cells

52 unogenic in C57BL/6 mice but fails to induce demyelinating disease by polyclonal T cells despite havi

53 dy definitively demonstrates that autoimmune demyelinating disease can be driven by distinct Th-polar

54 al leukoencephalopathy (PML) is a lethal CNS demyelinating disease caused by the human neurotropic po

55 sive multifocal leukoencephalopathy (PML), a demyelinating disease in humans.

56 that has been linked to JME, an inflammatory demyelinating disease in Japanese macaques that mimics m

57 yelitis virus (TMEV) induces immune-mediated demyelinating disease in susceptible SJL/J mice but not

58 patient who died from a rapidly progressing demyelinating disease known as progressive multifocal le

59 differentiation and induce remyelination in demyelinating disease models.

60 The demyelinating disease multiple sclerosis (MS) has an ear

61 utes to the pathogenesis of the inflammatory demyelinating disease multiple sclerosis (MS).

62 PCs), thereby impeding remyelination, in the demyelinating disease multiple sclerosis (MS).

63 functional impairment that characterizes the demyelinating disease multiple sclerosis (MS).

64 gical disability in individuals with the CNS demyelinating disease multiple sclerosis.

65 NMOSD is a recently defined demyelinating disease of the central nervous system (CNS

66 ple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS

67 Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS

68 Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system trad

69 h multiple sclerosis, a chronic inflammatory demyelinating disease of the central nervous system with

70 Multiple sclerosis (MS) is a demyelinating disease of the central nervous system, lea

71 sclerosis (MS) (n=43,879), an inflammatory, demyelinating disease of the central nervous system.

72 leukoencephalopathy (PML) is an often-fatal demyelinating disease of the central nervous system.

73 Centres managing patients with demyelinating disease of the CNS across Australia and Ne

74 Multiple sclerosis (MS) is a demyelinating disease of the CNS characterized by inflam

75 sclerosis (MS) is an autoimmune inflammatory demyelinating disease of the CNS that causes disability

76 ultiple sclerosis (MS) is an immune-mediated demyelinating disease of the CNS that has been linked wi

77 of multiple sclerosis (MS), an inflammatory demyelinating disease of the CNS.

78 e sclerosis (MS), a chronic inflammatory and demyelinating disease of the CNS.

79 T Multiple sclerosis (MS) is an inflammatory demyelinating disease of the CNS.

80 tiple sclerosis (MS) is a neuroinflammatory, demyelinating disease of the CNS.

81 ultiple Sclerosis (MS) is an immune-mediated demyelinating disease of the human central nervous syste

82 therapeutic modulation of ERK1/2 activity in demyelinating disease or peripheral neuropathies must be

83 We propose that the inflammatory demyelinating disease process in early multiple sclerosi

84 tion and is the causative agent of the fatal demyelinating disease progressive multifocal leukoenceph

85 ty of the population and can cause the fatal demyelinating disease progressive multifocal leukoenceph

86 compromised individuals results in the fatal demyelinating disease progressive multifocal leukoenceph

87 ssive multifocal leukoencephalopathy, a rare demyelinating disease that occurs in the setting of prol

88 ve multifocal leukoencephalopathy (PML) is a demyelinating disease triggered by infection with the hu

89 hemorrhage, intracranial hemorrhage, spine, demyelinating disease, and epileptic patients.

90 In multiple sclerosis, an inflammatory demyelinating disease, endogenous remyelination does occ

91 In the 2.3% with demyelinating disease, gabapentin was the most likely se

92 yelination similar in pathology to the human demyelinating disease, multiple sclerosis.

93 ression, JCV can infect the brain, causing a demyelinating disease, progressive multifocal leukoencep

94 tral nervous system and chronic inflammatory demyelinating disease, providing an experimental animal

95 composition and low MBP concentration, as in demyelinating disease, show structural instabilities and

96 ler's murine encephalomyelitis virus-induced demyelinating disease.

97 nent role in the development of TMEV-induced demyelinating disease.

98 t leukodystrophy (ADLD), a fatal adult onset demyelinating disease.

99 accelerating myelin clearance and improving demyelinating disease.

100 susceptibility of mice to the development of demyelinating disease.

101 lammatory and proliferative genes to promote demyelinating disease.

102 ENT Multiple sclerosis is a severe, chronic, demyelinating disease.

103 ation in OPCs, contributing to Th17-mediated demyelinating disease.

104 ler's murine encephalomyelitis virus-induced demyelinating disease.

105 te ratio, 0.90 [95% CI, 0.70-1.15]) or other demyelinating diseases (crude incidence rates, 7.54 even

106 spectrum disorders (NMOSD) are inflammatory demyelinating diseases (IDD) with a specific biomarker,

107 neficial both for enhancing remyelination in demyelinating diseases and for increasing neural plastic

108 the potential for enhanced remyelination in demyelinating diseases and increased neural plasticity i

109 Because functional restoration in demyelinating diseases critically depends on the success

110 yelin can be replaced after injury or during demyelinating diseases in a regenerative process called

111 is result in the impairment of recovery from demyelinating diseases in the adult.

112 Progression of demyelinating diseases is caused by an imbalance of two

113 w diagnostic markers in these two autoimmune demyelinating diseases of the central nervous system.

114 reported in patients that recover from acute demyelinating diseases such as Guillain-Barre syndrome.

115 tions including central nervous system (CNS) demyelinating diseases such as multiple sclerosis (MS) a

116 elin regeneration can occur spontaneously in demyelinating diseases such as multiple sclerosis (MS).

117 therapeutic approaches for the treatment of demyelinating diseases such as multiple sclerosis (MS).S

118 nstitute clinically debilitating sequelae in demyelinating diseases such as multiple sclerosis, but t

119 axons, associated with traumatic injury and demyelinating diseases such as multiple sclerosis, cause

120 In demyelinating diseases such as multiple sclerosis, disru

121 o ameliorate the devastating consequences of demyelinating diseases such as multiple sclerosis.

122 ng rates underlies degenerative processes in demyelinating diseases such as multiple sclerosis.

123 approach for potential treatment of chronic demyelinating diseases such as multiple sclerosis.

124 s can be therapeutically enhanced in chronic demyelinating diseases such as multiple sclerosis.

125 loping new therapeutic tools to intervene in demyelinating diseases such as multiple sclerosis.

126 hat Shp2 is a relevant therapeutic target in demyelinating diseases such as multiple sclerosis.SIGNIF

127 iple sclerosis cases and 3300 cases of other demyelinating diseases were identified, of which 73 and

128 peutic enhancement of remyelination in those demyelinating diseases where GPR17 is highly expressed,

129 hich the olfactory system is affected in CNS demyelinating diseases, and raises intriguing questions

130 finding may have important implications for demyelinating diseases, psychiatric disorders, and cogni

131 BP is an abundant myelin protein involved in demyelinating diseases, such as multiple sclerosis.

132 Because, in demyelinating diseases, the myelin formed during remyeli

133 mportant role in the pathogenesis underlying demyelinating diseases.

134 xonal degeneration that occurs in peripheral demyelinating diseases.

135 ying pathogenesis in autoimmune inflammatory demyelinating diseases.

136 e development of multiple sclerosis or other demyelinating diseases.

137 sclerosis and a composite end point of other demyelinating diseases.

138 ral nervous system inflammatory and acquired demyelinating diseases.

139 nt diagnoses of multiple sclerosis and other demyelinating diseases.

140 al relationship between qHPV vaccination and demyelinating diseases.

141 ferentiation in multiple sclerosis and other demyelinating diseases.

142 development of multiple sclerosis and other demyelinating diseases.

143 aluate their roles and clinical relevance in demyelinating diseases.

144 a key target for enhancing myelin repair in demyelinating diseases.

145 his pool of progenitors to replace myelin in demyelinating diseases.

146 ising strategies to advance the treatment of demyelinating diseases.SIGNIFICANCE STATEMENT The benefi

147 dence ratio, 1.05 [95% CI, 0.79-1.38]; other demyelinating diseases: incidence ratio, 1.14 [95% CI, 0

148 mmune cell infiltration in neuroinflammatory demyelinating diseases; yet, the causal link between inf

149 Multiple Sclerosis (MS) is an inflammatory demyelinating disorder in which remyelination failure co

150 ic oligodendrocyte loss, which occurs in the demyelinating disorder multiple sclerosis (MS), contribu

151 s (EAE), an animal model of the inflammatory demyelinating disorder multiple sclerosis (MS).

152 Multiple sclerosis (MS) is a chronic demyelinating disorder of the CNS characterized by immun

153 , optic neuritis presents as an inflammatory demyelinating disorder of the optic nerve, which can be

154 effective remyelination in the treatment of demyelinating disorders and in identifying pathways invo

155 w strategies for therapeutic intervention in demyelinating disorders by promoting oligodendrocyte reg

156 unty population-based cohort of inflammatory demyelinating disorders of the central nervous system we

157 disseminated encephalomyelitis) and from non-demyelinating disorders such as chronic small vessel dis

158 nation.SIGNIFICANCE STATEMENT Myelin loss in demyelinating disorders such as multiple sclerosis resul

159 enues for treatment of neurodegenerative and demyelinating disorders.

160 s may be beneficial in neuroinflammatory and demyelinating disorders.

161 ew strategies for promoting myelin repair in demyelinating disorders.

162 promising new approach for the treatment of demyelinating disorders.

163 new therapeutic avenue for the treatment of demyelinating disorders.

164 a primary goal for regenerative medicine in demyelinating disorders.

165 ons, but also provide potential insight into demyelinating disorders.

166 tion contributes to remyelination failure in demyelinating disorders.

167 al damage was most extensive in early active demyelinating (EA) lesions of pediatric patients and cor

168 nflammatory neuropathy with mixed axonal and demyelinating electrophysiology.

169 recently isolated from JM with inflammatory demyelinating encephalomyelitis (JME).

170 At follow up, 55% had a clinical demyelinating episode involving the brain; 30% of cases

171 In addition, further relapsing demyelinating episodes associated with MOG antibodies we

172 ole of cholesterol in promoting repair after demyelinating episodes.

173 reduces the risk of conversion from a first demyelinating event (also known as a clinically isolated

174 Early treatment following a first clinical demyelinating event (FCDE) delays further disease activi

175 Study with 127 cases having a classic first demyelinating event followed for 5 years from onset.

176 und to attenuate the conversion from a first demyelinating event to clinically definite MS in a phase

177 with isolated optic neuritis (ON) as a first demyelinating event who had a median follow-up of 4.0 ye

178 Eligible patients had a first clinical demyelinating event within 75 days before screening, at

179 efinite MS in patients with a first clinical demyelinating event, when given at the same doses shown

180 rsion in individuals experiencing an initial demyelinating event.

181 y, we evaluated the role of CRYAB in primary demyelinating events.

182 gical tests were consistent with the primary demyelinating form of the disease.

183 opathy with liability to pressure palsies or demyelinating forms of Charcot-Marie-Tooth disease.

184 neuropathological changes in myelinated and demyelinated hippocampi from postmortem MS brains.

185 ocytes within regions previously shown to be demyelinated in later stages of this syndrome.

186 d a 'paranodopathy' rather than a subtype of demyelinating inflammatory neuropathy.

187 late remyelination may lead to recovery from demyelinating injuries and protect axons.

188 yelinating drug for the treatment of chronic demyelinating injury in multiple sclerosis.

189 y generation of new myelin sheaths following demyelinating injury in the adult CNS.

190 into Gamt-deficient and wild-type mice with demyelinating injury reduced oligodendrocyte apoptosis,

191 resulted in delayed remyelination following demyelinating injury to the adult mouse corpus callosum.

192 e no efficient remyelination after a primary demyelinating insult if myelin clearance by microglia is

193 hormone (T3)-free window, with or without a demyelinating insult, provides a favorable environment f

194 earance and diminished remyelination after a demyelinating insult.

195 roptotic, and apoptotic cell death caused by demyelinating, ischemic, and traumatic injuries, implyin

196 n the remyelination of a focal, lysolecithin-demyelinated lesion in adult male mice.

197 ultiple sclerosis patient lymphocytes in the demyelinated lesion of nude mice spinal cord.

198 prevented motor and sensory dysfunction and demyelinating lesion formation.

199 f ET signaling prevented Notch activation in demyelinated lesions and accelerated remyelination.

200 etrograde degeneration was mainly related to demyelinated lesions and axonal loss in the white matter

201 tem cells can be mobilized for the repair of demyelinated lesions by inhibiting Gli1, identifying a n

202 endrocyte progenitor cells (OPCs) can repair demyelinated lesions by maturing into myelin-producing o

203 Many chronically demyelinated lesions have oligodendrocyte progenitor cel

204 ectin aggregate containing cuprizone-induced demyelinated lesions in male mice.

205 ted from the subventricular zone to populate demyelinated lesions in the forebrain but never enter he

206 oitin sulfate proteoglycan deposition around demyelinated lesions in the spinal cord of Theiler's mur

207 s CSPGs accumulation and astrogliosis around demyelinated lesions in the spinal cord of Theiler's mur

208 Focal demyelinated lesions in the white matter occurred at sit

209 xonal vesicular release or AMPA receptors in demyelinated lesions results in reduced remyelination.

210 produces cytolysis, leading to formation of demyelinated lesions with devastating consequences.

211 nimals resulted in selective colonization of demyelinated lesions, preferential differentiation into

212 eloid cell population at the edge of chronic demyelinated lesions.

213 d glutamate homeostasis has been reported in demyelinated lesions.

214 ed numbers of mature oligodendrocytes within demyelinated lesions.

215 All presented with cerebral demyelinating lesions and gadolinium enhancement.

216 r Th cells that can drive the development of demyelinating lesions are phenotypically diverse or aris

217 S autoimmunity characterized by inflammatory demyelinating lesions confined to optic nerves and spina

218 sulfate proteoglycans (CSPGs) accumulate at demyelinating lesions creating a nonpermissive environme

219 onounced acute axonal damage in inflammatory demyelinating lesions from children compared to adults.

220 We now report actively demyelinating lesions in patients with multiple sclerosi

221 Demyelinating lesions were induced in the rat spinal dor

222 Demyelinating lesions were not centered on the injection

223 ises the regenerative response to subsequent demyelinating lesions.

224 early axonal pathology outside inflammatory demyelinating lesions.

225 gene underlie autosomal dominant adult-onset demyelinating leukodystrophy (ADLD), a rare neurological

226 grammed cells has been evaluated in neonatal demyelinating models.

227 spectrum is broad and encompasses axonal and demyelinating motor and sensory neuropathies, including

228 reated with Inh X migrate extensively in the demyelinated mouse spinal cord and remyelinate axons.

229 activation were increased in myelinated and demyelinated MS hippocampi, mainly in the CA3/2 and CA1

230 s of DNA methyltransferase were increased in demyelinated MS hippocampus, while de-methylation enzyme

231 6 genes and hyper-methylation of 10 genes in demyelinated MS hippocampus.

232 The presence of myelinosomes in actively demyelinating MS lesions suggests that oligodendrocyte d

233 ially phosphorylated in astrocytes in active demyelinating MS lesions, as well as in cuprizone-induce

234 Chronically demyelinated multiple sclerosis (MS) lesions are frequen

235 ogen and the BMP target Id2 are increased in demyelinated multiple sclerosis (MS) lesions.

236 henotype described previously in chronically demyelinated multiple sclerosis lesions.

237 nctional and structural properties of single demyelinated neocortical L5 axons.

238 at peripheral nerve and their dynamics after demyelinating nerve injury.

239 e axonal degeneration observed in peripheral demyelinating neuropathies.

240 es proof of principle for treating inherited demyelinating neuropathies.

241 neuropathy, and some paraprotein-associated demyelinating neuropathies.

242 , implicating c-Jun as a potential player in demyelinating neuropathies.

243 ses myelin genes, and has been implicated in demyelinating neuropathies.

244 ed as HRs [95% CIs]) of chronic inflammatory demyelinating neuropathy (2.8; 1.6-5.1; P = .001), auton

245 n of OGT (OGT-SCKO mice) causes a tomaculous demyelinating neuropathy accompanied with progressive ax

246 athy does not meet morphological criteria of demyelinating neuropathy and therefore, might rather be

247 The OGT-SCKO mice develop tomaculous demyelinating neuropathy characterized by focal thickeni

248 common form of hereditary autosomal dominant demyelinating neuropathy known as Charcot-Marie-Tooth di

249 trodiagnostic classification into axonal and demyelinating neuropathy may not always accurately refle

250 ts with recurrent acute predominantly motor, demyelinating neuropathy with conduction block, and chro

251 for patients with acute predominantly motor, demyelinating neuropathy with conduction block, and seco

252 linical and electrophysiological evidence of demyelinating neuropathy.

253 Demyelinating optic nerve inflammation, termed optic neu

254 Acute demyelinating optic neuritis, a common feature of multip

255 , two had brainstem features mainly, two had demyelinating optic neuropathies and one had an unclear

256 th relapsing multiple sclerosis with chronic demyelinating optic neuropathy on stable immunomodulator

257 on with implications in axonal repair in CNS demyelinating pathologies.SIGNIFICANCE STATEMENT The dep

258 ther central nervous system disorders with a demyelinating pathology.media-1vid110.1093/brain/aww039_

259 Inherited demyelinating peripheral neuropathies are progressive in

260 a potential opportunity for the treatment of demyelinating peripheral neuropathies.

261 ie-Tooth disease type 4B1 (CMT4B1), a severe demyelinating peripheral neuropathy characterized by mye

262 sociated with Charcot-Marie-Tooth 1B (CMT1B) demyelinating peripheral neuropathy in human and mouse.

263 aged Prnp(ZH3/ZH3) mice developed a chronic demyelinating peripheral neuropathy, confirming the cruc

264 lly authentic model of CMT1X that develops a demyelinating peripheral neuropathy.

265 providing robust evidence that the profound demyelinating phenotype observed in the dorsal columns o

266 y sensitive to psychosine, thus leading to a demyelinating phenotype.

267 ssociation between CD and acute inflammatory demyelinating polyneuropathy (0.8; 0.3-2.1; P = .68).

268 thirds of patients with chronic inflammatory demyelinating polyneuropathy (CIDP) need long-term intra

269 of nerve hypertrophy in chronic inflammatory demyelinating polyneuropathy (CIDP), magnetic resonance

270 n reported as mimicking chronic inflammatory demyelinating polyneuropathy (CIDP).

271 tion indicated for a patient presenting with demyelinating polyneuropathy and concurrent papilledema.

272 were consistent with the acute inflammatory demyelinating polyneuropathy subtype of the Guillain-Bar

273 ropathy and variants of chronic inflammatory demyelinating polyneuropathy, account for a proportion o

274 ived from patients with chronic inflammatory demyelinating polyneuropathy, an autoimmune disease of t

275 uillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropath

276 uillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropath

277 rse myelitis, and 1 had chronic inflammatory demyelinating polyneuropathy.

278 %) with newly diagnosed chronic inflammatory demyelinating polyneuropathy.

279 Peripheral neuropathies included axonal and demyelinating polyradiculoneuropathies (n = 2), length-d

280 nd similar proportions of acute inflammatory demyelinating polyradiculoneuropathy (AIDP) (71.5% vs. 7

281 Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an inflam

282 fied from a cohort with chronic inflammatory demyelinating polyradiculoneuropathy (n=53) and Guillain

283 d in four patients with chronic inflammatory demyelinating polyradiculoneuropathy and in none of the

284 Because the pathogenicity and demyelinating properties of anti-MAG autoantibodies are

285 An imbalance between remyelinating and demyelinating rates underlies degenerative processes in

286 onstrate that administration of tamoxifen to demyelinated rats in vivo accelerates remyelination.

287 These cells are abundant in demyelinated regions of patients with multiple sclerosis

288 em myelinating glia, are found remyelinating demyelinated regions of the CNS.

289 utoreactive T-cell and microglial/macrophage demyelinating response is critical to effectively target

290 cells transition from axon myelination to a demyelinated state that supports neuronal survival and u

291 ssigned participants who had had their first demyelinating symptoms within the previous 180 days to r

292 Most children who experience an acquired demyelinating syndrome of the central nervous system wil

293 ti-AQP4 positive) or brainstem or multifocal demyelinating syndromes (7 cases, all anti-MOG positive)

294 QP4-IgG-negative optic neuritis (n=4), other demyelinating syndromes (n=3) and multiple sclerosis (n=

295 Atypical inflammatory demyelinating syndromes are rare disorders that differ f

296 Fifty-three participants with demyelinating syndromes eventually received a diagnosis

297 of 132 paediatric participants with acquired demyelinating syndromes followed for a median of 4.4 yea

298 tence of sexual dimorphism in the effects of demyelinating syndromes on normal-appearing white matter

299 in thickness was reduced and some axons were demyelinated, the majority of axons were wrapped by inta

300 Further, Nfasc140 is reexpressed in demyelinated white matter lesions of postmortem brain ti