ライフサイエンスコーパス: multiple sclerosis

1 rosis including active secondary progressive multiple sclerosis.

2 ed for optimal cortical lesion assessment in multiple sclerosis.

3 encephalomyelitis (EAE), an animal model of multiple sclerosis.

4 c encephalomyelitis (EAE), a murine model of multiple sclerosis.

5 ronmental risk factor for the development of multiple sclerosis.

6 lds promise as a new therapeutic strategy in multiple sclerosis.

7 over 12 months in patients with progressive multiple sclerosis.

8 imer's disease, autism spectrum disorder and multiple sclerosis.

9 ive nature of demyelinating diseases such as multiple sclerosis.

10 mal and becomes inefficient in the course of multiple sclerosis.

11 apeutically advantageous in the treatment of multiple sclerosis.

12 ly beneficial in autoimmune diseases such as multiple sclerosis.

13 this drug will probably not be continued in multiple sclerosis.

14 are almost always affected to some degree in multiple sclerosis.

15 hylphenidate for the treatment of fatigue in multiple sclerosis.

16 control disease activity in a mouse model of multiple sclerosis.

17 e were found in Mexican patients with NMO or multiple sclerosis.

18 ent of what is observed in human progressive multiple sclerosis.

19 t in participants with secondary progressive multiple sclerosis.

20 c encephalomyelitis, a mouse model for human multiple sclerosis.

21 such as Alzheimer's disease and progressive multiple sclerosis.

22 l and earlier onset of secondary progressive multiple sclerosis.

23 2) relaxometry and proton density mapping in multiple sclerosis.

24 ular architectural changes characteristic of multiple sclerosis.

25 clerosis, and demyelinating diseases such as multiple sclerosis.

26 es major disability in secondary progressive multiple sclerosis.

27 d one human TCR isolated from a patient with multiple sclerosis.

28 resent a novel remyelinating therapeutic for multiple sclerosis.

29 be recommended for treatment of progressive multiple sclerosis.

30 utoimmune diseases, including candidemia and multiple sclerosis.

31 The microbiome plays an important role in multiple sclerosis.

32 ogression remains an important unmet need in multiple sclerosis.

33 n a phase 3 trial of patients with relapsing multiple sclerosis.

34 encephalomyelitis (EAE), the mouse model of multiple sclerosis.

35 tment to ameliorate ambulatory disability in multiple sclerosis.

36 tential measures able to predict progressive multiple sclerosis.

37 isease of the CNS that serves as a model for multiple sclerosis.

38 autoimmune encephalomyelitis (EAE) model of multiple sclerosis.

39 a light damage mouse model and in humans for multiple sclerosis.

40 rial is underway, in patients with relapsing multiple sclerosis.

41 effective treatment for relapsing-remitting multiple sclerosis.

42 ng to CNS pathology in EAE and, potentially, multiple sclerosis.

43 herapeutic targets for disability accrual in multiple sclerosis.

44 om radiologically isolated syndrome (RIS) to multiple sclerosis.

45 limod were tested in patients with relapsing multiple sclerosis.

46 ropriately in the diagnosis and follow-up of multiple sclerosis.

47 Parkinson's disease, Alzheimer's disease and multiple sclerosis.

48 neurologic conditions, including progressive multiple sclerosis.

49 wo phase 3 trials of patients with relapsing multiple sclerosis.

50 utics that include DMF, for the treatment of multiple sclerosis.

51 ts identify candidate therapeutic targets in multiple sclerosis.

52 untington disease, 2.2 (95% CI, 1.9-2.6) for multiple sclerosis, 1.7 (95% CI, 1.6-1.7) for head injur

53 Astrocytes contribute to the pathogenesis of multiple sclerosis(2), but little is known about the het

54 evance of this glial barrier system in human multiple sclerosis active lesions.

55 Patients with primary progressive multiple sclerosis aged 18-55 years who had an Expanded

56 ents (age = 54.2 +/- 9.6) with long-standing multiple sclerosis and 48 healthy controls (age = 50.8 +

57 Cortical lesions represent a hallmark of multiple sclerosis and are proposed as a predictor of di

58 anisms common to RA and other IMDs including multiple sclerosis and asthma, in turn distinguishing th

59 as wider implications for disorders, such as multiple sclerosis and CNS injury.SIGNIFICANCE STATEMENT

60 Multiple sclerosis and experimental autoimmune encephalo

61 or the treatment of rheumatoid arthritis and multiple sclerosis and is re-emerging as an attractive t

62 lammatory conditions within the CNS, such as multiple sclerosis and its animal model, experimental au

63 utic intervention to slow the progression of multiple sclerosis and its ocular manifestations, is sti

64 Here we report the analysis of astrocytes in multiple sclerosis and its preclinical model experimenta

65 tine had a sudden death (primary cause) with multiple sclerosis and obesity listed as secondary cause

66 ty to several neurological diseases, such as multiple sclerosis and Parkinson's disease.

67 during development or in adulthood, such as multiple sclerosis and peripheral neuropathies, lead to

68 nic inflammatory autoimmune diseases such as multiple sclerosis and rheumatoid arthritis.

69 al autoimmune encephalitis, a mouse model of multiple sclerosis and thus support our conclusion that

70 r walking speed in patients with progressive multiple sclerosis and thus, in addition to the potentia

71 effort to develop therapeutic modalities for multiple sclerosis and, indeed, has provided insight in

72 matic brain injury, Alzheimer's disease, and multiple sclerosis, and evaluated for their diagnostic p

73 such as amyotrophic lateral sclerosis (ALS), multiple sclerosis, and Parkinson's disease, peripheral

74 Given the profound burden of progressive multiple sclerosis, and the recent development of effect

75 e been remarkably successful in treatment of multiple sclerosis, and they have shown promise in clini

76 diagnostic (clinically isolated syndrome for multiple sclerosis, another condition with cognitive abn

77 ly collect patient data that are specific to multiple sclerosis as part of routine clinical care.

78 phrenia (HC-clinically isolated syndrome for multiple sclerosis BAC = 56.7%).

79 maging was applied using 3T MRI ex vivo in 3 multiple sclerosis brain samples and in vivo in a prospe

80 mmon primary trigger for atherosclerosis and multiple sclerosis but suggest that an excess burden of

81 tion therapies will be ready for people with multiple sclerosis, but there is a real sense of hope th

82 lly, expansion of the concept of progressive multiple sclerosis, by including an assessment of cognit

83 Relapses in multiple sclerosis can result in irreversible nervous sy

84 The score was applied to 85 multiple sclerosis cases (46 females, age range 39 to 84

85 d cerebral small vessel disease is higher in multiple sclerosis cases that die at younger ages compar

86 n and inflammation) was characterized in the multiple sclerosis cases.

87 es of myoneural junction, Parkinson disease, multiple sclerosis, central nervous system infections, m

88 more than 33 were recruited at two academic multiple sclerosis centres in the USA.

89 in cancer, CNS infection (viral and fungal), multiple sclerosis, cerebral ischemia, and cerebral mala

90 ological diseases including Crohn's disease, multiple sclerosis, chronic lymphocytic leukemia, veno-o

91 r comorbidities have a deleterious impact on multiple sclerosis clinical outcomes but it is unclear w

92 lled trial done at 90 academic and community multiple sclerosis clinics across 13 countries.

93 From the Amsterdam multiple sclerosis cohort, 133 patients (age = 54.2 +/-

94 vessel disease is stronger in patients with multiple sclerosis compared with control subjects; and (

95 and white matter lesions from patients with multiple sclerosis corroborate the function of this path

96 , Sjogren syndrome, coronary artery disease, multiple sclerosis, cystic fibrosis, asthma, cancer, neu

97 Effective biomarkers for multiple sclerosis diagnosis, assessment of prognosis, a

98 tic resonance imaging (MRI) is essential for multiple sclerosis diagnostics but is conventionally not

99 brain slices of 23 patients with progressive multiple sclerosis directly after autopsy, at 3 T, using

100 measures capable of identifying progressive multiple sclerosis early in the disease course.

101 d myocarditis while taking amantadine, and a multiple sclerosis exacerbation requiring hospital admis

102 In multiple sclerosis, exacerbation of symptoms with rising

103 Here, we use a mouse model for multiple sclerosis, experimental autoimmune encephalomye

104 te were not superior to placebo in improving multiple sclerosis fatigue and caused more frequent adve

105 with each other and placebo in patients with multiple sclerosis fatigue.

106 ventional MRI identified enhanced lesions in multiple sclerosis from images from unenhanced multipara

107 We identified patients with multiple sclerosis from two longitudinal prospective stu

108 econdary progressive, 31 primary progressive multiple sclerosis) from eight sites.

109 iagnosis of primary or secondary progressive multiple sclerosis fulfilling the revised International

110 ng summary statistics from the International Multiple Sclerosis Genetics Consortium (IMSGC) meta-anal

111 bral small vessel disease scores and, in the multiple sclerosis group, the relationship between multi

112 The treatment of multiple sclerosis has been transformed by the successfu

113 In recent years, new imaging findings for multiple sclerosis have been described, and new evidence

114 s for disease-modifying therapy in relapsing multiple sclerosis have substantially increased over the

115 5 years of age who had rheumatoid arthritis, multiple sclerosis, hepatitis C, psoriasis, psoriatic ar

116 der's disease, Alzheimer's disease, hypoxia, multiple sclerosis, hereditary spastic paraplegia, and o

117 ribed medications for alleviating fatigue in multiple sclerosis; however, the evidence supporting the

118 elapsing-remitting and secondary progressive multiple sclerosis; (ii) assess the spinal cord lesion s

119 d efficacy of MD1003 in progressive forms of multiple sclerosis in a larger, more representative pati

120 eukin-4 (IL-4) suppresses the development of multiple sclerosis in a murine model of experimental aut

121 eins, OSM and HGF, were also associated with multiple sclerosis in comparison to healthy controls.

122 Minocycline reduced conversion to multiple sclerosis in patients with a clinically isolate

123 dministration for the treatment of relapsing multiple sclerosis including active secondary progressiv

124 loci for multiple immune diseases, including multiple sclerosis, inflammatory bowel disease, and alle

125 Multiple sclerosis is a chronic inflammatory disease cha

126 Multiple sclerosis is a chronic inflammatory disease of

127 Multiple sclerosis is a chronic, demyelinating disease o

128 ting CNS autoimmunity.SIGNIFICANCE STATEMENT Multiple sclerosis is an autoimmune neuroinflammatory di

129 Currently, studying mitochondrial changes in multiple sclerosis is hampered by a paucity of non-invas

130 ology in patients with secondary progressive multiple sclerosis is insufficient to mitigate neuroaxon

131 Chronic disability in multiple sclerosis is linked to neuroaxonal degeneration

132 imer's disease, autism spectrum disorder and multiple sclerosis is significantly elevated.

133 The identification of progression in multiple sclerosis is typically retrospective.

134 her these connections are equally damaged in multiple sclerosis is unknown, as is their relevance for

135 -approved immunomodulatory drug for treating multiple sclerosis, is an agonist of sphingosine-1-phosp

136 2 trial of patients with primary progressive multiple sclerosis, laquinimod also did not reach the pr

137 ked ultrashort echo time signal reduction in multiple sclerosis lesions and a smaller reduction in no

138 itriol) by the hydroxylase enzyme CYP27B1 In multiple sclerosis lesions, the tyrosine kinase MerTK ex

139 s burden of cerebral small vessel disease in multiple sclerosis may explain the link between vascular

140 currently used in the clinical management of multiple sclerosis, may represent as a potential candida

141 erations in schizophrenia, bipolar disorder, multiple sclerosis, mild cognitive impairment, dementia,

142 Patients diagnosed with multiple sclerosis, minimum 1-year exposure to treatment

143 s and axonal damage in chronic and relapsing multiple sclerosis models.

144 se III trial in 215 paediatric patients with multiple sclerosis (MS) (10 to <18 years), fingolimod ad

145 Patients with multiple sclerosis (MS) (aged 10-<18 years) were randomi

146 eronegative with unknown MOG-Ab-serostatus), multiple sclerosis (MS) (n=69), optic neuritis (n=5) and

147 Multiple sclerosis (MS) - an autoimmune disease of the C

148 Brain-infiltrating leukocytes contribute to multiple sclerosis (MS) and autoimmune encephalomyelitis

149 tory responses is critical for understanding multiple sclerosis (MS) and for developing successful im

150 -kappaB) is activated in oligodendrocytes in multiple sclerosis (MS) and its animal model experimenta

151 nervous system (CNS) in the pathogenesis of multiple sclerosis (MS) and its animal model, experiment

152 eterminant of brain inflammation, notably in multiple sclerosis (MS) and its experimental autoimmune

153 B-cell depletion in patients with relapsing multiple sclerosis (MS) and primary progressive MS has l

154 iest brain changes detected in patients with multiple sclerosis (MS) and the degree of thalamic atrop

155 Clinical outcomes in multiple sclerosis (MS) are highly variable.

156 tive medicines that promote remyelination in multiple sclerosis (MS) are making the transition from l

157 edications with regulatory approval to treat multiple sclerosis (MS) are unable to prevent inflammato

158 + inner plexiform layer (GCIPL) thinning in multiple sclerosis (MS) attributable to normal aging inc

159 ease-modifying therapies have revolutionized multiple sclerosis (MS) care.

160 n understanding how autoimmune diseases like multiple sclerosis (MS) contribute to variations in huma

161 Recent advances in multiple sclerosis (MS) diagnostic criteria have expande

162 New treatments for multiple sclerosis (MS) focused on B cells have created

163 ic success of B cell-targeting approaches in multiple sclerosis (MS) has intensified research into th

164 Epidemiological research in multiple sclerosis (MS) has mainly been performed in soc

165 disease-modifying therapies for people with multiple sclerosis (MS) have recently gained marketing a

166 es have suggested differences in the rate of multiple sclerosis (MS) in individuals of European ances

167 Multiple sclerosis (MS) is a chronic autoimmune disease

168 Multiple sclerosis (MS) is a chronic autoimmune disease

169 Multiple sclerosis (MS) is a chronic demyelinating disea

170 Multiple sclerosis (MS) is a heterogeneous inflammatory

171 Multiple sclerosis (MS) is a neurological disease with a

172 Multiple sclerosis (MS) is an autoimmune disease charact

173 Multiple sclerosis (MS) is an autoimmune disease charact

174 Multiple sclerosis (MS) is an autoimmune inflammatory de

175 Multiple sclerosis (MS) is an autoimmune inflammatory di

176 Multiple sclerosis (MS) is an inflammatory demyelinating

177 Multiple sclerosis (MS) is an inflammatory, demyelinatin

178 Disability in multiple sclerosis (MS) is considered primarily a result

179 r a role of microglia in the pathogenesis of multiple sclerosis (MS) is growing.

180 The pathology of progressive multiple sclerosis (MS) is poorly understood.

181 The unmet medical need of patients with multiple sclerosis (MS) is the inexorable loss of CNS my

182 Multiple sclerosis (MS) is the most common human demyeli

183 The accurate recognition of multiple sclerosis (MS) lesions is challenged by the hig

184 pair of inflamed, demyelinated lesions as in multiple sclerosis (MS) necessitates the clearance of ch

185 ch as in white matter lesion segmentation of multiple sclerosis (MS) patients.

186 is a widely used method for the diagnosis of multiple sclerosis (MS) that is essential for the detect

187 Healthy volunteers and participants with multiple sclerosis (MS) underwent MRI between November 2

188 In multiple sclerosis (MS), a subset of chronic active whit

189 Here, we investigate propionic acid (PA) in multiple sclerosis (MS), an autoimmune and neurodegenera

190 L-1beta, which is abundantly produced during multiple sclerosis (MS), arthritis (RA), and osteoarthri

191 ype is the strongest genetic risk factor for multiple sclerosis (MS), but our understanding of how it

192 grey matter damage since the early stages of multiple sclerosis (MS), but whether the cerebrospinal f

193 promote remyelination is a high priority for multiple sclerosis (MS), due to their potential for neur

194 mune diseases, including relapsing-remitting multiple sclerosis (MS), in which increased IFN response

195 orme (GBM), traumatic brain injuries (TBIs), multiple sclerosis (MS), intracerebral hemorrhage (ICH),

196 Background In multiple sclerosis (MS), knowledge about how spinal cord

197 autoimmune encephalomyelitis (EAE) model of multiple sclerosis (MS), no one has yet examined the imp

198 seases like psoriasis, Crohn's disease (CD), multiple sclerosis (MS), rheumatoid arthritis (RA), and

199 In multiple sclerosis (MS), Th17 cells are critical drivers

200 During the natural course of multiple sclerosis (MS), the brain is exposed to aging a

201 nal loss, which are pathological features of multiple sclerosis (MS), the most common disabling neuro

202 velopment and in demyelinating diseases like multiple sclerosis (MS), where failure of remyelination

203 of T cell-mediated autoimmunity that mimics multiple sclerosis (MS).

204 n and are key players in the pathogenesis of multiple sclerosis (MS).

205 treatment of autoimmune diseases, including multiple sclerosis (MS).

206 specially during autoimmune diseases such as Multiple Sclerosis (MS).

207 imens, healthy volunteers, and patients with multiple sclerosis (MS).

208 ntly nominated as a susceptibility locus for multiple sclerosis (MS).

209 s for several autoimmune diseases, including multiple sclerosis (MS).

210 autoimmune encephalomyelitis (EAE) model of multiple sclerosis (MS).

211 r the symptomatic treatment of patients with multiple sclerosis (MS).

212 is a common and devastating manifestation of multiple sclerosis (MS).

213 axons, is a feature of progressive forms of multiple sclerosis (MS).

214 permanent drug-free remission in people with multiple sclerosis (MS).

215 TY720 is a treatment for relapsing remitting multiple sclerosis (MS).

216 plays an important part in the pathology of multiple sclerosis (MS).

217 key issues in the management of people with multiple sclerosis (MS).

218 encephalomyelitis (EAE), an animal model of multiple sclerosis (MS).

219 d is associated with cognitive disability in multiple sclerosis (MS).

220 tibodies is a highly effective treatment for multiple sclerosis (MS).

221 ies of worsening disability in patients with multiple sclerosis (MS).

222 ections revealing topological alterations in multiple sclerosis (MS).

223 encephalomyelitis (EAE), an animal model of multiple sclerosis (MS).

224 s a central role in explaining disability in multiple sclerosis (MS): Lesion-induced damage in the la

225 stem B cells have several potential roles in multiple sclerosis (MS): secretors of proinflammatory cy

226 nly thought to represent disease activity in multiple sclerosis (MS); it is desirable to develop meth

227 ory SNPs, called dSNPs, were associated with multiple sclerosis (MS, 4,888 cases and 10,395 controls)

228 ohort prospective study of 560 patients with multiple sclerosis (MS, n = 147), rheumatoid arthritis (

229 dinal study included patients (n = 212) with multiple sclerosis (MS; n = 418 eyes), 59 healthy contro

230 t-mortem brain material from a subset of the multiple sclerosis (n = 42; age range 39-84 years, media

231 Among patients with multiple sclerosis, ofatumumab was associated with lower

232 therapies in patients more than 3 years from multiple sclerosis onset.

233 The etiology of CNS diseases including multiple sclerosis, Parkinson's disease and amyotrophic

234 elapsing-remitting, 15 secondary progressive multiple sclerosis participants and 11 age-matched healt

235 sition and inflammation, are key features of multiple sclerosis pathology outside the classic demyeli

236 or of cerebral small vessel disease or worse multiple sclerosis pathology.

237 gies in both the acute and chronic phases of multiple sclerosis pathophysiology.

238 itively correlated with macular thickness in multiple sclerosis patients (r = 0.49, P = 0.01) but not

239 es and in vivo in a prospective cohort of 71 multiple sclerosis patients and 21 age/sex-matched healt

240 l study involved population-based samples of multiple sclerosis patients and age-, race-, and gender-

241 A majority of multiple sclerosis patients experience visual impairment

242 Multiple sclerosis patients had, relative to controls, l

243 macular sensitivity of control subjects and multiple sclerosis patients in decibels was 18.2 +/- 0.4

244 experiments on two datasets corresponding to multiple sclerosis patients treated with interferon are

245 Among the key criteria for the multiple sclerosis patients were diagnosis by the McDona

246 measured by microperimetry was decreased in multiple sclerosis patients with normal visual acuity an

247 nd therapeutic target in primary progressive multiple sclerosis patients', by Malhotra et al. (doi:10

248 uent remyelination.SIGNIFICANCE STATEMENT In multiple sclerosis patients, demyelination progresses wi

249 city by millions of stroke, brain injury and multiple sclerosis patients, many of whom are also under

250 t for spasticity in stroke, brain injury and multiple sclerosis patients, who are often undergoing co

251 d portions to explain physical disability in multiple sclerosis patients, with a predominant impact o

252 of the mechanism of action of fingolimod in multiple sclerosis patients.

253 veness of natalizumab in relapsing-remitting multiple sclerosis patients.

254 Therapeutic development in progressive multiple sclerosis (PMS) has been hampered by a lack of

255 on beta-1a (IFN beta-1a) in paediatric-onset multiple sclerosis (PoMS).

256 a confirmed diagnosis of primary progressive multiple sclerosis (PPMS) is uncertain.

257 ted inflammatory symptoms in mouse models of multiple sclerosis, psoriasis, and asthma.

258 s of autoimmune diseases (such as arthritis, multiple sclerosis, psoriasis, inflammatory bowel diseas

259 Gait impairments in persons with multiple sclerosis (pwMS) leading to decreased ambulatio

260 Data from two multiple sclerosis registries, MSBase (multinational) an

261 The extent of multiple sclerosis-related pathology (focal demyelinatio

262 le sclerosis group, the relationship between multiple sclerosis-related pathology and both vascular s

263 croperimetry in the detection of subclinical multiple sclerosis-related retinal damage and visual dys

264 rk had a reduced efficiency and integrity in multiple sclerosis relative to healthy controls (both P

265 oad and physical disability in patients with multiple sclerosis remains modest.

266 t pathogenic conditions in humans, including multiple sclerosis, rheumatoid arthritis, type-I diabete

267 Y) treatment response in relapsing-remitting multiple sclerosis (RRMS) are lacking.

268 The transition from relapsing-remitting multiple sclerosis (RRMS) to secondary progressive MS (S

269 an be distinguished from relapsing-remitting multiple sclerosis (RRMS).

270 Subjects with relapsing-remitting multiple sclerosis showed a greater predominance of spin

271 ) Programme, an MRC and NIHR partnership, UK Multiple Sclerosis Society, and US National Multiple Scl

272 Multiple Sclerosis Society, and US National Multiple Sclerosis Society.

273 ge connections are more severely affected by multiple sclerosis-specific damage than short-range conn

274 ve both grey and white matter from the early multiple sclerosis stages and occur mostly independent f

275 a range of neurological conditions including multiple sclerosis, stroke, and epilepsy, and has also b

276 n lesion development that may differ between multiple sclerosis subtypes.

277 mental autoimmune encephalomyelitis model of multiple sclerosis, TAGAP deficient mice develop signifi

278 We identified astrocytes in EAE and multiple sclerosis that were characterized by decreased

279 , we have discovered, using a mouse model of multiple sclerosis, that the transfusion of autologous r

280 lination and remyelination in the context of multiple sclerosis, the mechanisms mediating demyelinati

281 des of action introduced to the treatment of multiple sclerosis, the question of how to select and se

282 In autoimmune diseases such as multiple sclerosis, the TCR erroneously recognizes self-

283 ons regarding optimal sequence and timing of multiple sclerosis therapy.

284 In the patient with multiple sclerosis, this sign appeared earlier than the

285 we randomly assigned patients with relapsing multiple sclerosis to receive subcutaneous ofatumumab (2

286 ase 4-AP is already licensed for symptomatic multiple sclerosis treatment, we performed a retrospecti

287 In multiple sclerosis, treatment start or switch is prompte

288 manifest fully and clinically the effect of multiple sclerosis treatments ('therapeutic lag') on cli

289 Multiple sclerosis treatments (n = 4) had the greatest i

290 onstrated correlations with brain atrophy in multiple sclerosis using magnetic resonance imaging, a n

291 The prevalence of cognitive impairment in multiple sclerosis varies across the lifespan and might

292 icity of combined CSF and plasma markers for multiple sclerosis were 85.7% and 73.5%, respectively.

293 ficacy of ocrelizumab in primary progressive multiple sclerosis were shown in the phase 3 ORATORIO tr

294 odes of action in the treatment of relapsing multiple sclerosis, which are exhibited by minocycline a

295 associated with autoimmune diseases such as multiple sclerosis, which has no curative treatment.

296 demyelination in normal-appearing tissue in multiple sclerosis, which is associated with both cognit

297 neurologic conditions including progressive multiple sclerosis, which is represented by substantial

298 crossover, double-blind trial, patients with multiple sclerosis who reported fatigue and had a Modifi

299 aged 25-65 years) with secondary progressive multiple sclerosis who were not on disease-modifying tre

300 s (aged >=18 years) with relapsing-remitting multiple sclerosis, with at least 6 years of follow-up s