ライフサイエンスコーパス: demyelinating

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

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

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

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

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

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

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

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

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

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

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

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

17 ts 2 (SH3TC2) gene cause autosomal recessive demyelinating Charcot-Marie-Tooth neuropathy.

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

19 atments for acutely symptomatic inflammatory demyelinating CNS lesions.

20 lls that mediate ongoing inflammation in the demyelinating CNS.

21 nctional deficits underlying diseases with a demyelinating component.

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

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

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

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

26 e in OL regeneration and remyelination under demyelinating conditions.

27 elitis are considered central nervous system demyelinating conditions.

28 ic relevance in multiple sclerosis and other demyelinating conditions.

29 MOG antibody disease both considered primary demyelinating conditions.

30 tance when understanding myelin assembly and demyelinating conditions.

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

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

33 6 transgene (IL-6 Tg) develop a TMEV-induced demyelinating disease accompanied by an increase in vira

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

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

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

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

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

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

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

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

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

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

44 differentiation and induce remyelination in demyelinating disease models.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

60 Multiple sclerosis is an inflammatory, demyelinating disease of the CNS of presumed autoimmune

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

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

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

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

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

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

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

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

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

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

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

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

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

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

75 onfirmed central nervous system inflammatory demyelinating disease who had undergone either diagnosti

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

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

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

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

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

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

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

83 with TMEV induces the development of chronic demyelinating disease, which is considered a relevant in

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

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

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

87 accelerating myelin clearance and improving demyelinating disease.

88 susceptibility of mice to the development of demyelinating disease.

89 icrocystic macular edema is not specific for demyelinating disease.

90 gression in a secondary progressive model of demyelinating disease.

91 ts the potential for cell-based treatment of demyelinating disease.

92 ovement disorders, psychiatric features, and demyelinating disease.

93 lammatory and proliferative genes to promote demyelinating disease.

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

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

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

97 ent neuron-supportive programme in inherited demyelinating disease?

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

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

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

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

102 CNS repair following lesions associated with demyelinating diseases are still unresolved.

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

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

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

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

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

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

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

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

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

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

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

114 In demyelinating diseases such as multiple sclerosis, disru

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

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

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

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

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

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

121 ically useful as immunomodulatory agents for demyelinating diseases through a novel mechanism involvi

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

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

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

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

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

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

128 mportant role in the pathogenesis underlying demyelinating diseases.

129 xonal degeneration that occurs in peripheral demyelinating diseases.

130 ying pathogenesis in autoimmune inflammatory demyelinating diseases.

131 e development of multiple sclerosis or other demyelinating diseases.

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

133 ral nervous system inflammatory and acquired demyelinating diseases.

134 nt diagnoses of multiple sclerosis and other demyelinating diseases.

135 al relationship between qHPV vaccination and demyelinating diseases.

136 ferentiation in multiple sclerosis and other demyelinating diseases.

137 development of multiple sclerosis and other demyelinating diseases.

138 aluate their roles and clinical relevance in demyelinating diseases.

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

140 A class II genes in chronic inflammatory and demyelinating diseases.

141 e for oligodendrogenesis and remyelinaton in demyelinating diseases.

142 PCs) offer a promising approach for treating demyelinating diseases.

143 and adhesion and has direct implications for demyelinating diseases.

144 may provide new avenues in the treatment of 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 sorders, and conversely patients with NMO or demyelinating disorders with atypical symptoms (eg, dysk

160 y develop concurrent or separate episodes of demyelinating disorders, and conversely patients with NM

161 bolic diseases, and traumatic brain injury), demyelinating disorders, and infectious brain lesions.

162 enues for treatment of neurodegenerative and demyelinating disorders.

163 s may be beneficial in neuroinflammatory and demyelinating disorders.

164 ew strategies for promoting myelin repair in demyelinating disorders.

165 promising new approach for the treatment of demyelinating disorders.

166 new therapeutic avenue for the treatment of demyelinating disorders.

167 a primary goal for regenerative medicine in demyelinating disorders.

168 at promote functional myelin regeneration in demyelinating disorders.

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

170 tion contributes to remyelination failure in demyelinating disorders.

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

172 nflammatory neuropathy with mixed axonal and demyelinating electrophysiology.

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

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

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

176 blocks OPC recruitment, which with repeated demyelinating episodes contributes to permanent remyelin

177 ut compared with anti-NMDAR encephalitis the demyelinating episodes required more intensive therapy a

178 ole of cholesterol in promoting repair after demyelinating episodes.

179 Patients with a first clinical demyelinating event </=75 days before screening were ran

180 with an initial central nervous system (CNS) demyelinating event (a clinically isolated syndrome), co

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

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

183 primary progressive (PP)-MS; n=6) MS; first demyelinating event (FDE; n=82); and unaffected controls

184 were obtained within 4 months of the initial demyelinating event and at 6, 12 and 24 months.

185 Patients with a first demyelinating event between January 1, 2010, and April 1

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

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

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

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

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

191 sclerosis (MS) present with a first clinical demyelinating event.

192 rsion in individuals experiencing an initial demyelinating event.

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

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

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

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

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

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

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

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

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

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

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

204 earance and diminished remyelination after a demyelinating insult.

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

206 prevented motor and sensory dysfunction and demyelinating lesion formation.

207 oligodendrocyte differentiation following a demyelinating lesion, however, the endogenous sources of

208 Other less common mechanism being demyelinating lesion, mass effect, infection, hemorrhage

209 acid (ACPD), was therefore injected into the demyelinating lesion.

210 All presented with cerebral demyelinating lesions and gadolinium enhancement.

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

212 s delayed significantly in response to focal demyelinating lesions compared with wild-type animals.

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

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

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

216 ination were identical among multiple active demyelinating lesions from the same individual, but diff

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

218 Demyelinating lesions were induced in the rat spinal dor

219 Demyelinating lesions were not centered on the injection

220 junction or within the gray matter, causing demyelinating lesions within cortical areas.

221 ssion in healthy control brain in all active demyelinating lesions, remyelinated lesions, and peripla

222 ia consisted of the presence of early active demyelinating lesions--required for immunopattern classi

223 ises the regenerative response to subsequent demyelinating lesions.

224 R4.1 immunoreactivity is retained or lost in demyelinating lesions.

225 early axonal pathology outside inflammatory demyelinating lesions.

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

227 that NPCs transplanted into an inflammatory demyelinating microenvironment participate directly in t

228 yelination within the cuprizone diet-induced demyelinating model.

229 grammed cells has been evaluated in neonatal demyelinating models.

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

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

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

233 e conclusion that netrin-1 expression within demyelinating MS plaques blocks OPC recruitment, which w

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

235 elin sheath is a common pathology underlying demyelinating neurological diseases from Multiple Sclero

236 ision in the classification of axonal versus demyelinating neuropathies to include the new category o

237 es proof of principle for treating inherited demyelinating neuropathies.

238 neuropathy, and some paraprotein-associated demyelinating neuropathies.

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

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

241 e axonal degeneration observed in peripheral demyelinating neuropathies.

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

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

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

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

246 Neurophysiology showed demyelinating neuropathy in four patients and axonal neu

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

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

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

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

251 mouse model exhibit severe muscle weakness, demyelinating neuropathy, failed muscle regeneration and

252 linical and electrophysiological evidence of demyelinating neuropathy.

253 mild clinical phenotype comprising myopathy; demyelinating neuropathy; premature ovarian failure; sho

254 Demyelinating optic nerve inflammation, termed optic neu

255 Acute demyelinating optic neuritis, a common feature of multip

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

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

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

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

260 Inherited demyelinating peripheral neuropathies are progressive in

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

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

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

264 h differential phenotypes in the most common demyelinating peripheral neuropathy, CMT1A.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

280 %) with newly diagnosed chronic inflammatory demyelinating polyneuropathy.

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

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

283 Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an inflam

284 atients with aggressive chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) shows autoan

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

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

287 th JC virus (JCV) may lead to development of demyelinating progressive multifocal leukoencephalopathy

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

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

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

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 m (CNS) autoantibodies in childhood-acquired demyelinating syndromes (ADS).

295 MS) or other acquired central nervous system demyelinating syndromes (CNS ADS) could have a significa

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

297 Atypical inflammatory demyelinating syndromes are rare disorders that differ f

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

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

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