ライフサイエンスコーパス: multiple sclerosis

1 odels of acute graft-versus-host disease and multiple sclerosis.

2 w therapeutic targets for mitigating pain in multiple sclerosis.

3 id arthritis, celiac disease, psoriasis, and multiple sclerosis.

4 d susceptibility in an inflammatory model of multiple sclerosis.

5 intervene in demyelinating diseases such as multiple sclerosis.

6 n's syndrome, inflammatory bowel disease and multiple sclerosis.

7 nal factors are implicated in dysimmunity in multiple sclerosis.

8 large cohort of patients in early stages of multiple sclerosis.

9 ing of inflammation and neurodegeneration in multiple sclerosis.

10 tional conduction akin to muscle weakness in multiple sclerosis.

11 at is involved in several diseases including multiple sclerosis.

12 idence of dementia, Parkinson's disease, and multiple sclerosis.

13 metabolic, and genetic causes that can mimic multiple sclerosis.

14 ltured myeloid cells and in a mouse model of multiple sclerosis.

15 known as a clinically isolated syndrome) to multiple sclerosis.

16 cterized by oligodendrocyte death, including multiple sclerosis.

17 d chronic neurodegenerative diseases such as multiple sclerosis.

18 pproved for treatment of relapsing-remitting multiple sclerosis.

19 es in a proteomics study of a mouse model of multiple sclerosis.

20 B cells influence the pathogenesis of multiple sclerosis.

21 esis of many autoimmune disorders, including multiple sclerosis.

22 rophages in acute, relapsing and progressive multiple sclerosis.

23 ne fumarate as a treatment for patients with multiple sclerosis.

24 motif that is significantly associated with multiple sclerosis.

25 ncephalomyelitis, principal animal models of multiple sclerosis.

26 the failure in remyelination associated with multiple sclerosis.

27 ng its potential for alleviating symptoms in multiple sclerosis.

28 y used and safe formulation for treatment of multiple sclerosis.

29 treatment of chronic demyelinating injury in multiple sclerosis.

30 involved in demyelinating diseases, such as multiple sclerosis.

31 lly received a diagnosis of paediatric-onset multiple sclerosis.

32 and Drug Administration to treat refractory multiple sclerosis.

33 encephalomyelitis (EAE) and, ostensibly, in multiple sclerosis.

34 f 368 patients developed clinically definite multiple sclerosis.

35 tion is a critical impediment to recovery in multiple sclerosis.

36 ementia, but not with Parkinson's disease or multiple sclerosis.

37 ved for the treatment of relapsing-remitting multiple sclerosis.

38 s, which is the most-studied animal model of multiple sclerosis.

39 ualised relapse rates in relapsing-remitting multiple sclerosis.

40 cortical pathology or therapeutic effects in multiple sclerosis.

41 tive in neurodegenerative diseases including multiple sclerosis.

42 tionized the treatment of relapsing forms of multiple sclerosis.

43 hly effective and viable immunotherapies for multiple sclerosis.

44 iation was found with Parkinson's disease or multiple sclerosis.

45 s as significant predictors of conversion to multiple sclerosis.

46 and implicates vitamin D in the etiology of multiple sclerosis.

47 represent an environmental consideration in multiple sclerosis.

48 es of Parkinson's disease, and 9247 cases of multiple sclerosis.

49 data (in total 5776 eyes from patients with multiple sclerosis [1667 MSON eyes and 4109 MSNON eyes]

50 gastrointestinal-related illness (5 cases), multiple sclerosis (3 cases), sepsis (3 cases), and Lyme

51 1% of patients, with sarcoidosis (22.6%) and multiple sclerosis (4.6%) the most frequent systemic ass

52 elination and typical of relapsing-remitting multiple sclerosis, a complete neurological examination,

53 fficiency and tested their effect on risk of multiple sclerosis, a disease influenced by low vitamin

54 A subset will be diagnosed with multiple sclerosis, a life-long disorder.

55 omponents were related to ADHD in offspring: multiple sclerosis (adjusted odds ratio [OR] = 1.8; 95%

56 otes remyelination in a model of progressive multiple sclerosis ameliorating motor dysfunction.

57 isorders such as stroke, spinal cord injury, multiple sclerosis, amyotrophic lateral sclerosis (ALS),

58 trocytes are key players in the pathology of multiple sclerosis and can assume beneficial and detrime

59 as Alzheimer's disease, Parkinson's disease, multiple sclerosis and cardiovascular disease.

60 istinguishes neuromyelitis optica (NMO) from multiple sclerosis and causes characteristic immunopatho

61 differences between the eyes of people with multiple sclerosis and control eyes were found in the pe

62 subsequent conversion to clinically definite multiple sclerosis and disability.

63 ction due to retinal ganglion cell damage in multiple sclerosis and experimental autoimmune encephalo

64 ellular mechanism for pain and neuropathy in multiple sclerosis and IL-17 may act upstream of CaMKIIa

65 mplicated in numerous pathologies, including multiple sclerosis and its animal model experimental aut

66 In the autoimmune disease multiple sclerosis and its animal model, experimental au

67 tical role in autoimmune diseases, including multiple sclerosis and its animal model, experimental au

68 the status of cell-based therapies to treat multiple sclerosis and make consensus recommendations fo

69 is indicated for the treatment of relapsing multiple sclerosis and may exert therapeutic effects via

70 o supported by the clear distinction between multiple sclerosis and MOG antibody disease both conside

71 set of dysbiosis in the gut of patients with multiple sclerosis and neuromyelitis optica provides evi

72 In multiple sclerosis and neuromyelitis optica spectrum dis

73 in autoimmune disorders and cancers such as multiple sclerosis and non-Hodgkin's lymphomas.

74 ential therapeutic value of AhR agonists for multiple sclerosis and other autoimmune diseases.

75 levant clinical targets for the treatment of multiple sclerosis and other autoimmune disorders.

76 esponse might be of therapeutic relevance in multiple sclerosis and other demyelinating conditions.

77 he current status of therapy for progressive multiple sclerosis and outline prospects for the future.

78 nd has implications for vitamin D biology in multiple sclerosis and perhaps other autoimmune diseases

79 A TNFSF13B variant was associated with multiple sclerosis and SLE, and its effects were clarifi

80 lieve pain in human diseases such as cancer, multiple sclerosis, and fibromyalgia.

81 DR15 has also been associated with multiple sclerosis, and its component alleles have been

82 uding chronic obstructive pulmonary disease, multiple sclerosis, and stroke.

83 eneficial effects of exercise in people with multiple sclerosis, and the absence of a conceptual fram

84 h autoimmune diseases such as Crohn disease, multiple sclerosis, and ulcerative colitis and hereby el

85 ctivating factor (BAFF), was associated with multiple sclerosis as well as SLE.

86 assified data on eyes into healthy controls, multiple-sclerosis-associated optic neuritis (MSON), and

87 Comprehensive Longitudinal Investigation of Multiple Sclerosis at the Brigham and Women's Hospital.

88 second clinical attack (clinically definite multiple sclerosis) at months 36 and 60.

89 hirty-nine patients with relapsing remitting multiple sclerosis, at high risk of PML, were switched f

90 e demyelination and neurodegeneration in the multiple sclerosis brain and are thought to play a centr

91 g postmortem imaging and histopathology in 9 multiple sclerosis brain donors.

92 ntibody disease spontaneously separated from multiple sclerosis but overlapped with AQP4 antibody dis

93 f white matter integrity in paediatric-onset multiple sclerosis, but also show that even a single dem

94 a-1a in the treatment of relapsing-remitting multiple sclerosis, but its efficacy relative to more po

95 g sequelae in demyelinating diseases such as multiple sclerosis, but the underlying mechanisms of sec

96 ic injury and demyelinating diseases such as multiple sclerosis, causes impaired neural transmission

97 months from clinical onset in eight European multiple sclerosis centres were included in this retrosp

98 pants underwent randomization at 12 Canadian multiple sclerosis clinics; 72 participants were assigne

99 adults aged 20-50 years (about 4.4 million; multiple sclerosis cohort) and all adults aged 55-85 yea

100 The primary outcome was conversion to multiple sclerosis (diagnosed on the basis of the 2005 M

101 2010 McDonald and 2016 MAGNIMS criteria for multiple sclerosis diagnosis in a large multicentre coho

102 ld be considered during further revisions of multiple sclerosis diagnostic criteria.

103 IS to provide evidence to guide revisions of multiple sclerosis diagnostic criteria.

104 toimmune encephalomyelitis (a model of human multiple sclerosis) disease development when administere

105 from patients with typical CIS suggestive of multiple sclerosis done less than 3 months from clinical

106 al autoimmune encephalomyelitis, a model for multiple sclerosis, even in myelin regions that appear m

107 and transient altered mental status and late multiple sclerosis exacerbation in another patient.

108 lly isolated syndrome or relapsing-remitting multiple sclerosis (Expanded Disability Status Scale: me

109 been extended using an experimental model of multiple sclerosis [experimental autoimmune encephalomye

110 paralysis associated with a murine model of multiple sclerosis, experimental autoimmune encephalomye

111 a diagnosis of definite relapsing-remitting multiple sclerosis, exposure to one of the study therapi

112 iR-27 in T cells isolated from patients with multiple sclerosis facilitate disease progression by inh

113 s, Dawson's fingers, T1 hypointense lesions (multiple sclerosis), fluffy lesions and three lesions or

114 However, in participants with multiple sclerosis, fractional anisotropy decreased and

115 ty-matched patients with relapsing-remitting multiple sclerosis from the MSBase and six other cohorts

116 greatly increased accuracy in distinguishing multiple sclerosis from these disorders, but misdiagnosi

117 The change in the Multiple Sclerosis Functional Composite score (a composi

118 a main determinant of disease progression in multiple sclerosis; however, its underlying pathophysiol

119 parison of Alemtuzumab and Rebif Efficacy in Multiple Sclerosis I and II (CARE-MS I and II) trials we

120 present from the earliest clinical stages of multiple sclerosis; (ii) they occur independent of white

121 signed 732 patients with primary progressive multiple sclerosis in a 2:1 ratio to receive intravenous

122 ce (DIS) and time (DIT) for the diagnosis of multiple sclerosis in patients with clinically isolated

123 d May 2015 in a tertiary referral center for multiple sclerosis, in collaboration with several region

124 The efficacy of B cell depletion therapy in multiple sclerosis indicates their central pathogenic ro

125 Multiple sclerosis is a degenerative inflammatory diseas

126 Multiple sclerosis is a major cause of neurological disa

127 mmatory demyelination.SIGNIFICANCE STATEMENT Multiple sclerosis is a severe, chronic, demyelinating d

128 The diagnosis of multiple sclerosis is based on neurological symptoms and

129 A pathological hallmark of multiple sclerosis is the presence of leukocytes in the

130 One major challenge in multiple sclerosis is to understand the cellular and mol

131 tion transfer ratio gradient occurs early in multiple sclerosis, is clinically relevant, and may aris

132 FTY720/fingolimod, used for treatment of multiple sclerosis, is phosphorylated by nuclear sphingo

133 We examined multiple sclerosis lesions and other central nervous sys

134 Astrocytes in acute multiple sclerosis lesions have been shown previously to

135 Multiple sclerosis lymphocytes exhibit intrinsic capacit

136 In 2016, the Magnetic Resonance Imaging in Multiple Sclerosis (MAGNIMS) network proposed modificati

137 (c) mapping of lesions and immune cells in a multiple sclerosis mouse model.

138 lymphocytes are a key pathologic feature of multiple sclerosis (MS) and are becoming an important th

139 ies of retinal architecture in patients with multiple sclerosis (MS) and corresponding alterations in

140 fiber layer (RNFL) changes in patients with multiple sclerosis (MS) and healthy controls with a 5-ye

141 ed to play a key role in the pathogenesis of multiple sclerosis (MS) and its animal model, experiment

142 y player in inflammatory diseases, including multiple sclerosis (MS) and its animal model, experiment

143 al and dystonic tremor and tremor related to multiple sclerosis (MS) and midbrain lesions.

144 n from clinically isolated syndrome (CIS) to multiple sclerosis (MS) and MS activity and disability.

145 xicity in the development and progression of multiple sclerosis (MS) and of its mouse model experimen

146 s) play a crucial role in the progression of multiple sclerosis (MS) and other neurodegenerative dise

147 professions - continence advisors, urology, multiple sclerosis (MS) and spinal cord injury specialis

148 estimate long-term outcomes in patients with multiple sclerosis (MS) and to assign patients to indivi

149 Therefore, using multiple sclerosis (MS) as an example of a complex polyg

150 MicroRNAs (miRNAs) are promising multiple sclerosis (MS) biomarkers.

151 nal antibody, effectively inhibits relapsing multiple sclerosis (MS) but is associated with a high in

152 ect and quantify peripheral nerve lesions in multiple sclerosis (MS) by magnetic resonance neurograph

153 These drugs can delay multiple sclerosis (MS) diagnosis and slow down future d

154 otal clinical trials testing the efficacy of multiple sclerosis (MS) disease-modifying drugs) at a ge

155 t of a concurrent or subsequent diagnosis of multiple sclerosis (MS) from a population-based cohort (

156 Multiple sclerosis (MS) is a chronic demyelinating disea

157 Multiple sclerosis (MS) is a common autoimmune disease t

158 Multiple sclerosis (MS) is a disease that is characteriz

159 Multiple sclerosis (MS) is a neuroinflammatory, demyelin

160 Multiple Sclerosis (MS) is an autoimmune disease driving

161 Multiple sclerosis (MS) is an autoimmune disease of the

162 Multiple sclerosis (MS) is an autoimmune disease targeti

163 Multiple sclerosis (MS) is an autoimmune disorder where

164 Multiple sclerosis (MS) is an autoimmune inflammatory de

165 Multiple Sclerosis (MS) is an immune-mediated demyelinat

166 rocytes in MS and EAE.SIGNIFICANCE STATEMENT Multiple sclerosis (MS) is an inflammatory demyelinating

167 Multiple sclerosis (MS) is an inflammatory demyelinating

168 Multiple Sclerosis (MS) is an inflammatory demyelinating

169 Multiple sclerosis (MS) is caused by immune-mediated dam

170 Multiple sclerosis (MS) is multifocal by definition.

171 tivity of many autoimmune diseases including multiple sclerosis (MS) is temporarily suppressed by pre

172 BMP target Id2 are increased in demyelinated multiple sclerosis (MS) lesions.

173 limod is currently used for the treatment of multiple sclerosis (MS) little is known how S1P1 signali

174 recognised as an important early feature of multiple sclerosis (MS) pathology.

175 nical use for the treatment of spasticity in multiple sclerosis (MS) patients and to alleviate nausea

176 d in normal-appearing white matter (NAWM) of multiple sclerosis (MS) patients using PET.

177 cally isolated syndrome (pCIS) suggestive of multiple sclerosis (MS) patients.

178 ospinal fluid (CSF) and serum, obtained from Multiple Sclerosis (MS) patients.

179 The high female-to-male sex ratio of multiple sclerosis (MS) prevalence has continuously conf

180 ases of acute heart failure (AHF) related to multiple sclerosis (MS) relapses.

181 Despite continuous interest in multiple sclerosis (MS) research, there is still a lack

182 ability in inflammatory CNS diseases such as multiple sclerosis (MS) result from the translocation of

183 ological studies have shown that people with multiple sclerosis (MS) suffer from increased morbidity

184 ier (BBB) is a defining and early feature of multiple sclerosis (MS) that directly damages the centra

185 ssing speed (IPS) impairment associated with multiple sclerosis (MS) that might result from functiona

186 Ns) functional connectivity abnormalities in multiple sclerosis (MS) to explore their impact on balan

187 In multiple sclerosis (MS), a chronic inflammatory and dege

188 Pain is a common and severe symptom in multiple sclerosis (MS), a chronic inflammatory and demy

189 an established environmental risk factor for Multiple Sclerosis (MS), a chronic inflammatory and neur

190 ms that drive the development of progressive multiple sclerosis (MS), although inflammatory factors,

191 testinal bacteria impact the pathogenesis of multiple sclerosis (MS), an autoimmune disorder of the C

192 Multiple sclerosis (MS), and its animal model experiment

193 ible association between age at menarche and multiple sclerosis (MS), and results are conflicting.

194 esent with very similar clinical features to multiple sclerosis (MS), but the international diagnosti

195 , which occurs in the demyelinating disorder multiple sclerosis (MS), contributes to axonal dysfuncti

196 ymptoms occur frequently in individuals with multiple sclerosis (MS), either as the initial presentin

197 key substrate of irreversible disability in multiple sclerosis (MS), is a recognized feature of MS c

198 In the chronic inflammatory disease multiple sclerosis (MS), reports on lipoprotein level al

199 NT Pain is highly prevalent in patients with multiple sclerosis (MS), significantly reducing patients

200 high-impact neurological diseases including multiple sclerosis (MS), stroke, and Alzheimer's disease

201 lar volumetries in patients with progressive multiple sclerosis (MS), testing the contribution of cer

202 st function of CLEC12A in an animal model of multiple sclerosis (MS), we administered blocking antibo

203 ctor in multiple chronic diseases, including multiple sclerosis (MS), where the lowest and greatest r

204 cule array (Simoa) serum NfL (sNfL) assay in multiple sclerosis (MS).

205 remyelination, in the demyelinating disease multiple sclerosis (MS).

206 nt of several autoimmune diseases, including multiple sclerosis (MS).

207 a variety of neurological diseases, such as multiple sclerosis (MS).

208 and the prototypic neuroinflammatory disease multiple sclerosis (MS).

209 enesis of neuroinflammatory diseases such as multiple sclerosis (MS).

210 ys further disease activity in patients with multiple sclerosis (MS).

211 disease (PD), Huntington's disease (HD), and multiple sclerosis (MS).

212 -related brain connectivity in patients with multiple sclerosis (MS).

213 l outcomes in medical research, including in multiple sclerosis (MS).

214 that characterizes the demyelinating disease multiple sclerosis (MS).

215 odegeneration often precede symptom onset in multiple sclerosis (MS).

216 y/tropical spastic paraparesis (HAM/TSP) and multiple sclerosis (MS).

217 halomyelitis (EAE), an animal model of human multiple sclerosis (MS).

218 T-cell infiltration in an EAE mouse model of multiple sclerosis (MS).

219 treatment of demyelinating diseases such as multiple sclerosis (MS).SIGNIFICANCE STATEMENT Myelin lo

220 xample, were identified as a risk factor for Multiple Sclerosis (MS); however, the potential biologic

221 =4), other demyelinating syndromes (n=3) and multiple sclerosis (n=1).

222 TION: Among disease-modifying treatments for multiple sclerosis, natalizumab (NTZ) is highly effectiv

223 erative conditions affecting humans, such as multiple sclerosis, neuromyelitis optica spectrum disord

224 In multiple sclerosis, neuropathological studies have shown

225 (MRI) is widely used to diagnose and monitor multiple sclerosis, no imaging tools exist to predict th

226 Among patients with primary progressive multiple sclerosis, ocrelizumab was associated with lowe

227 ted conditions can be clearly separated from multiple sclerosis on conventional brain imaging, both i

228 One patient was diagnosed with multiple sclerosis, one with cortical dysplasia, one wit

229 a new paradigm by grafting healthy donor or multiple sclerosis patient lymphocytes in the demyelinat

230 nd management of relapse/remission cycles in multiple sclerosis patients by providing information cur

231 Multiple sclerosis patients exhibit a progressive axonal

232 Why remyelination fails or succeeds in multiple sclerosis patients remains largely unknown, mai

233 Tecfidera-treated stable relapsing-remitting multiple sclerosis patients using multiparametric flow c

234 hat mitochondrial biogenesis is deficient in Multiple Sclerosis patients, which could have implicatio

235 tant tool in the diagnosis and monitoring of multiple sclerosis patients.

236 easures of subsequent disease progression in multiple sclerosis patients.

237 ng cognitive deficits in primary-progressive multiple sclerosis (PP-MS) and to explore how they are a

238 d quality of life (QOL; based on the 54-item Multiple Sclerosis Quality of Life Scale score).

239 l leukoencephalopathy (PML) in patients with multiple sclerosis receiving natalizumab were stratified

240 PI was effective in vivo in a mouse model of multiple sclerosis, reducing clinical severity and weigh

241 represent a useful biomarker to distinguish multiple sclerosis relapse.

242 In multiple sclerosis, remyelination can fail despite abund

243 ce is a frequently used model in preclinical multiple sclerosis research.

244 elin loss in demyelinating disorders such as multiple sclerosis results in disability due to loss of

245 es, heart diseases, Alzheimer's disease, and multiple sclerosis revealed that autophagy and inflammas

246 The International Panel on Diagnosis of Multiple Sclerosis reviewed the 2010 McDonald criteria a

247 s a key role in the onset and progression of multiple sclerosis, rheumatoid arthritis, and breast can

248 l fluid of patients with relapsing remitting multiple sclerosis (RRMS) have higher replacement mutati

249 exosome transcriptome in relapsing-remitting multiple sclerosis (RRMS) patients and healthy controls

250 of disability that characterises progressive multiple sclerosis seems to result more from diffuse imm

251 which may be useful in classifying atypical multiple sclerosis, seronegative neuromyelitis optica sp

252 Twenty-one patients with multiple sclerosis (seven with secondary progressive dis

253 -0.374; P = .004 for RNFL thickness) and the Multiple Sclerosis Severity Score (R = -0.354; P = .007

254 rmal-appearing white matter of patients with multiple sclerosis showed a significant reduction of P2R

255 tic target in demyelinating diseases such as multiple sclerosis.SIGNIFICANCE STATEMENT In the present

256 rophy in patients with secondary progressive multiple sclerosis (SPMS).

257 Twenty-six early stage multiple sclerosis subjects (disease duration </=5 years

258 ickness did not differ significantly between multiple sclerosis subjects and controls.

259 g understanding of the immunopathogenesis of multiple sclerosis suggests that depleting B cells could

260 of PML in patients receiving natalizumab for multiple sclerosis, supporting yearly benefit-risk re-ev

261 re (Genetic and Environmental Risk Score for Multiple Sclerosis Susceptibility [GERSMS]) comprising a

262 r, and no more than 10 years since the first multiple sclerosis symptom.

263 ific oligoclonal bands allows a diagnosis of multiple sclerosis; symptomatic lesions can be used to d

264 Effective therapies for progressive multiple sclerosis that prevent worsening, reverse damag

265 pathological process in relapsing-remitting multiple sclerosis, the gradual accumulation of disabili

266 f CSPGs deposition in a progressive model of multiple sclerosis, the Theiler's murine encephalomyelit

267 n the cortex and white matter in early stage multiple sclerosis, their distribution in lesional and n

268 In established multiple sclerosis, tissue abnormality-as assessed using

269 tor in mouse models of chronic disease: from multiple sclerosis to autoimmune encephalomyelitis.

270 cial rehabilitation strategy for people with multiple sclerosis to manage symptoms, restore function,

271 assigned 821 and 835 patients with relapsing multiple sclerosis to receive intravenous ocrelizumab at

272 spinal cords of the EAE, the animal model of multiple sclerosis, to see if the expression of the IGF-

273 on beta in patients with relapsing-remitting multiple sclerosis treated for up to 5 years.

274 cognition and quality of life in progressive multiple sclerosis treatment trials.

275 in the long-term, and effective in treating multiple sclerosis tremor or other severe tremor disorde

276 r border [the VO lead]) for the treatment of multiple sclerosis tremor.

277 tive option for improving severe, refractory multiple sclerosis tremor.

278 B lymphotropic EBV is a major risk factor in multiple sclerosis, via as yet unclear mechanisms.

279 autoimmune encephalomyelitis animal model of multiple sclerosis was assessed.

280 Multiple sclerosis was discriminated from MOG antibody d

281 r placebo was continued until a diagnosis of multiple sclerosis was established or until 24 months af

282 The latitudinal gradient evident in multiple sclerosis was not seen in NMOSD.

283 rsion from a clinically isolated syndrome to multiple sclerosis was significantly lower with minocycl

284 urrently in advanced clinical development in multiple sclerosis, was equipotent in both assays (EC50

285 resentative signature genes in patients with multiple sclerosis, we find that TH1/17 cells have eleva

286 Using a model of multiple sclerosis, we show an impairment in trafficking

287 gnoses of dementia, Parkinson's disease, and multiple sclerosis were ascertained from provincial heal

288 classifiers between MOG antibody disease and multiple sclerosis were similar in adults and children,

289 atrophy associated with neurodegeneration in multiple sclerosis when measured with SD-OCT.

290 latter phenomenon seems to occur in vivo in multiple sclerosis, where it reflects the remission/rela

291 ls of hemophagocytic lymphohistiocytosis and multiple sclerosis, which are driven by foreign antigens

292 r trial (ReBUILD) in patients with relapsing multiple sclerosis with chronic demyelinating optic neur

293 mediated conditions were differentiated from multiple sclerosis with high accuracy.

294 e homeostatic microglial signature in active multiple sclerosis with restoration associated with dise

295 with the development of clinically definite multiple sclerosis within 2 years (magnetization transfe

296 eper in those developing clinically definite multiple sclerosis within 2 years compared to those who

297 Secondary outcomes included conversion to multiple sclerosis within 24 months after randomization

298 the difference in the risk of conversion to multiple sclerosis within 6 months after randomization w

299 erosis-associated optic neuritis (MSON), and multiple sclerosis without optic neuritis (MSNON).

300 T cells infiltrate the CNS in multiple sclerosis, yet little is known about T cell fun