ライフサイエンスコーパス: progressive multiple sclerosis

1 ogressive course from disease onset (primary progressive multiple sclerosis).

2 ging biomarker in future treatment trials of progressive multiple sclerosis.

3 th secondary-progressive and 28 with primary-progressive multiple sclerosis.

4 g candidate drug for patients with secondary progressive multiple sclerosis.

5 rations were higher in primary and secondary-progressive multiple sclerosis.

6 es, reminiscent of what is observed in human progressive multiple sclerosis.

7 th secondary-progressive and 20 with primary-progressive multiple sclerosis.

8 ert neuroprotective effects in patients with progressive multiple sclerosis.

9 trahydrocannabinol) might slow the course of progressive multiple sclerosis.

10 ffects of amiloride in patients with primary progressive multiple sclerosis.

11 rtem brain tissue from 26 cases with primary progressive multiple sclerosis.

12 most evident in participants with secondary progressive multiple sclerosis.

13 ased rate of clinical progression in primary progressive multiple sclerosis.

14 tial neuroprotective treatment for secondary progressive multiple sclerosis.

15 hogenetic mechanisms compared with secondary progressive multiple sclerosis.

16 tissue derived primarily from patients with progressive multiple sclerosis.

17 o neuroprotective in patients with secondary progressive multiple sclerosis.

18 y, in chronic active and inactive lesions in progressive multiple sclerosis.

19 cord in patients with primary and secondary progressive multiple sclerosis.

20 e conditions such as Alzheimer's disease and progressive multiple sclerosis.

21 is, and chronically in primary and secondary progressive multiple sclerosis.

22 n brain samples from patients with secondary progressive multiple sclerosis.

23 disease and the more diffuse degeneration of progressive multiple sclerosis.

24 onstrate a treatment effect of GA on primary progressive multiple sclerosis.

25 ility accrual and earlier onset of secondary progressive multiple sclerosis.

26 system, with a phenotype similar to chronic progressive multiple sclerosis.

27 n abnormalities are present in patients with progressive multiple sclerosis.

28 (MBP) in the reconstituted immune system in progressive multiple sclerosis.

29 te that causes major disability in secondary progressive multiple sclerosis.

30 or the axonal loss associated with secondary progressive multiple sclerosis.

31 the phenotype is similar to that of chronic progressive multiple sclerosis.

32 loss in both arms of this study of secondary progressive multiple sclerosis.

33 ing multiple sclerosis and 20 with secondary progressive multiple sclerosis.

34 as also shown to be efficacious in secondary progressive multiple sclerosis.

35 ut in 20 patients with primary and secondary progressive multiple sclerosis.

36 uppressive drug, in the treatment of chronic progressive multiple sclerosis.

37 processes might contribute to development of progressive multiple sclerosis.

38 lts that are relevant for people living with progressive multiple sclerosis.

39 m to improve processing speed in people with progressive multiple sclerosis.

40 worsening of disability in individuals with progressive multiple sclerosis.

41 lapsing multiple sclerosis and non-relapsing progressive multiple sclerosis.

42 ssociated with increased hazard of secondary progressive multiple sclerosis.

43 D1003 cannot be recommended for treatment of progressive multiple sclerosis.

44 a higher probability of developing secondary progressive multiple sclerosis.

45 tinct from relapsing-remitting and secondary progressive multiple sclerosis.

46 specific therapies for patients with primary progressive multiple sclerosis.

47 he art of potential measures able to predict progressive multiple sclerosis.

48 s have not been clearly shown in people with progressive multiple sclerosis.

49 ing speed might be attainable in people with progressive multiple sclerosis.

50 proved treatments for nonrelapsing secondary progressive multiple sclerosis.

51 rehabilitation and exercise in patients with progressive multiple sclerosis.

52 ons over time were associated with secondary progressive multiple sclerosis.

53 or for many neurologic conditions, including progressive multiple sclerosis.

54 ultiple sclerosis including active secondary progressive multiple sclerosis.

55 ity outcomes over 12 months in patients with progressive multiple sclerosis.

56 icroglia/macrophages in acute, relapsing and progressive multiple sclerosis.

57 erosis, but has not been assessed in primary progressive multiple sclerosis.

58 icacy of fingolimod in patients with primary progressive multiple sclerosis.

59 , a well-established animal model of primary progressive multiple sclerosis.

60 did not slow disease progression in primary progressive multiple sclerosis.

61 relapsing-remitting multiple sclerosis, and progressive multiple sclerosis.

62 No treatments have been approved for primary progressive multiple sclerosis.

63 sures could lead to effective treatments for progressive multiple sclerosis.

64 emains of neural plasticity in patients with progressive multiple sclerosis.

65 and have yet to be applied in early primary progressive multiple sclerosis.

66 and perspectives from trials in progress in progressive multiple sclerosis.

67 ability progression in patients with primary progressive multiple sclerosis.

68 g drugs have mostly failed as treatments for progressive multiple sclerosis.

69 better understanding of the pathogenesis of progressive multiple sclerosis.

70 ubstantially reduced the hazard of secondary progressive multiple sclerosis [0.76 (0.73, 0.79)] and r

71 e 25-65 years, clinical diagnosis of primary progressive multiple sclerosis, 1 year or more of diseas

72 versus 44.75 +/- 3.10, P < 0.01) and primary-progressive multiple sclerosis (46.99 +/- 3.78 versus 45

73 89 cm3/year in those who developed secondary progressive multiple sclerosis, a difference of 2.09 cm3

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

75 tients with relapsing-remitting or secondary progressive multiple sclerosis, all of whom were experie

76 Swiss National Science Foundation, Progressive Multiple Sclerosis Alliance, Biogen, Celgene

77 creased motor function in people with severe progressive multiple sclerosis, although not to the degr

78 ol tone promotes remyelination in a model of progressive multiple sclerosis ameliorating motor dysfun

79 from relapsing-remitting phase to secondary progressive multiple sclerosis among all patients was 39

80 graphical variation in the risk of secondary progressive multiple sclerosis, an advanced form of mult

81 Thirty patients with secondary progressive multiple sclerosis and 17 healthy control su

82 fied independent MRI predictors of secondary progressive multiple sclerosis and Expanded Disability S

83 em brain tissue from 20 cases with secondary progressive multiple sclerosis and five age-matched heal

84 lerosis, compared with patients with primary progressive multiple sclerosis and healthy subjects.

85 eatment of relapsing, remitting, and primary progressive multiple sclerosis and Huntington's disease.

86 High-dose therapy has been used in progressive multiple sclerosis and in myasthenia gravis

87 with higher concentrations seen in secondary-progressive multiple sclerosis and in patients with grea

88 een identified as a key feature of secondary progressive multiple sclerosis and may contribute to the

89 vity predict clinical progression in primary progressive multiple sclerosis and may qualify as a long

90 del and may be effective in the treatment of progressive multiple sclerosis and other neurodegenerati

91 be promising to modulate immunopathology in progressive multiple sclerosis and other neuroinflammato

92 summarise the current status of therapy for progressive multiple sclerosis and outline prospects for

93 controlled superiority trial of people with progressive multiple sclerosis and severe mobility impai

94 the operationalized definition of secondary progressive multiple sclerosis and the Swedish decision

95 disability or walking speed in patients with progressive multiple sclerosis and thus, in addition to

96 o the presence of spinal cord MRI lesions in progressive multiple sclerosis and to investigate the re

97 n abnormalities who met criteria for primary progressive multiple sclerosis and whose son died at age

98 r relapsing-remitting or relapsing secondary progressive multiple sclerosis), and one or more of the

99 th relapsing remitting and 28 with secondary progressive multiple sclerosis, and 38 healthy control s

100 apsing remitting multiple sclerosis, six had progressive multiple sclerosis, and all patients had con

101 isease duration), 13 subjects with secondary progressive multiple sclerosis, and in 17 age-matched he

102 ngs in patients with long-standing, chronic, progressive multiple sclerosis, and the noninflammatory

103 Given the profound burden of progressive multiple sclerosis, and the recent developme

104 lopment in relapsing-remitting and secondary progressive multiple, sclerosis, and this usually correl

105 linical and pathological features of primary progressive multiple sclerosis are antibody-mediated and

106 were independently associated with secondary progressive multiple sclerosis at 15 years.

107 splantation (HSCT) is in clinical trials for progressive multiple sclerosis based on the rationale th

108 ications for the design of future studies of progressive multiple sclerosis, because lower than expec

109 Significantly, analysis of secondary progressive multiple sclerosis brain tissue also reveale

110 urodegeneration, similar to that seen in the progressive multiple sclerosis brain.

111 to estimate the cumulative risk of secondary progressive multiple sclerosis by country of residence (

112 estigated cytokine profiles in patients with progressive multiple sclerosis by using intracytoplasmic

113 Finally, expansion of the concept of progressive multiple sclerosis, by including an assessme

114 al cortical lesions of post-mortem secondary progressive multiple sclerosis cases relative to control

115 (coefficient = -0.51, P < 0.01) and primary-progressive multiple sclerosis (coefficient = -0.38, P <

116 (i) are abnormal in patients with secondary progressive multiple sclerosis compared with healthy con

117 transfer ratio were greater in the secondary progressive multiple sclerosis compared with relapsing r

118 ion was lower in the patients with secondary progressive multiple sclerosis, compared with patients w

119 oss within areas of demyelination in primary progressive multiple sclerosis could explain high levels

120 recombinant antibodies derived from primary progressive multiple sclerosis CSF recapitulates the pat

121 ly, removal of immunoglobulin G from primary progressive multiple sclerosis CSF via filtration or imm

122 n cerebral volume of patients with secondary progressive multiple sclerosis did not differ from that

123 hemispheric brain slices of 23 patients with progressive multiple sclerosis directly after autopsy, a

124 (1)H MRS as a viable means of characterizing progressive multiple sclerosis disease status and paves

125 to establish measures capable of identifying progressive multiple sclerosis early in the disease cour

126 ound in the meninges of cases with secondary progressive multiple sclerosis exhibiting tertiary lymph

127 Secondary progressive multiple sclerosis, for which no satisfactor

128 s aged 18-65 years with primary or secondary progressive multiple sclerosis from 27 UK neurology or r

129 ng, 84 secondary progressive, and 73 primary progressive multiple sclerosis) from 13 clinical sites.

130 itting, 39 secondary progressive, 31 primary progressive multiple sclerosis) from eight sites.

131 ars, had a diagnosis of primary or secondary progressive multiple sclerosis fulfilling the revised In

132 lly low in primary progressive and secondary progressive multiple sclerosis groups versus controls.

133 n both the relapsing remitting and secondary progressive multiple sclerosis groups.

134 An effective disease-modifying treatment for progressive multiple sclerosis has not yet been identifi

135 bstantial proportion of cases with secondary progressive multiple sclerosis have extensive inflammati

136 ge between primary progressive and secondary progressive multiple sclerosis have not been reported.

137 The lack of therapies for progressive multiple sclerosis highlights the need to un

138 with early relapsing-remitting and secondary progressive multiple sclerosis; (ii) assess the spinal c

139 randomly assigned 732 patients with primary progressive multiple sclerosis in a 2:1 ratio to receive

140 scular and meningeal inflammation in primary progressive multiple sclerosis in order to understand th

141 were safely given to patients with secondary progressive multiple sclerosis in our study.

142 aluated differences in the risk of secondary progressive multiple sclerosis in relation to latitude a

143 The frequency of progressive multiple sclerosis in the paediatric onset m

144 in inflammation and perilesional activity in progressive multiple sclerosis in vivo.

145 ned participants with nonrelapsing secondary progressive multiple sclerosis, in a 2:1 ratio, to recei

146 thways in the cervical cord of early primary progressive multiple sclerosis, in the absence of extens

147 applies to all subgroups except for primary progressive multiple sclerosis, in which none of these m

148 Patients with secondary progressive multiple sclerosis involving the visual path

149 Progressive multiple sclerosis is associated with metabo

150 Progressive multiple sclerosis is characterised clinical

151 onal pathobiology in patients with secondary progressive multiple sclerosis is insufficient to mitiga

152 In a phase 2 trial of patients with primary progressive multiple sclerosis, laquinimod also did not

153 Clinical change in progressive multiple sclerosis may therefore occur witho

154 Therapeutic strategies for primary progressive multiple sclerosis might need different appr

155 sease (TMEV-IDD) is a mouse model of chronic-progressive multiple sclerosis (MS) characterized by Th1

156 sis of clinical and genetic heterogeneity in progressive multiple sclerosis (MS) has hindered the sea

157 Primary progressive multiple sclerosis (MS) has long been recogn

158 Primary progressive multiple sclerosis (MS) is a demyelinating a

159 Progressive multiple sclerosis (MS) is characterized by

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

161 ates of worsening and evolution to secondary progressive multiple sclerosis (MS) may be substantially

162 olated a panel of T-cell clones from chronic progressive multiple sclerosis (MS) patients that are ca

163 significantly decreased in long-term active progressive multiple sclerosis (MS) patients.

164 There were 21 patients with rapidly progressive multiple sclerosis (MS) treated on a phase 1

165 out mechanisms that drive the development of progressive multiple sclerosis (MS), although inflammato

166 ular cerebellar volumetries in patients with progressive multiple sclerosis (MS), testing the contrib

167 encephalomyelitis (EAE), a model of primary progressive multiple sclerosis (MS).

168 to be the predominant cause of disability in progressive multiple sclerosis (MS).

169 izumab was not shown to modify disability in progressive multiple sclerosis (MS).

170 ing-remitting multiple sclerosis (n=664), or progressive multiple sclerosis (n=141) were included in

171 ceramide levels in the CSF of patients with progressive multiple sclerosis not only impaired mitocho

172 Among patients with primary progressive multiple sclerosis, ocrelizumab was associat

173 ion criteria included a diagnosis of primary progressive multiple sclerosis or a diagnosis of seconda

174 ay evolve to a progressive course (secondary progressive multiple sclerosis) or as having a progressi

175 ients with relapsing-remitting and secondary progressive multiple sclerosis (p<=0.026), but it was si

176 remitting, secondary progressive and primary progressive multiple sclerosis (p<=0.042).

177 cesses driving the build-up of disability in progressive multiple sclerosis (P-MS) have not been full

178 d in the central nervous system (CNS) during progressive multiple sclerosis (P-MS).

179 cruited 20 relapsing-remitting, 15 secondary progressive multiple sclerosis participants and 11 age-m

180 mab on this outcome in patients with primary progressive multiple sclerosis participating in the phas

181 ammation are neuropathological correlates of progressive multiple sclerosis pathology.

182 ression is increased in the CSF of naive and progressive multiple sclerosis patients and post-mortem

183 fraction and between relapsing-remitting and progressive multiple sclerosis patients for all metrics

184 sing a novel mouse model that CSF of primary progressive multiple sclerosis patients is unique in its

185 Secondary progressive multiple sclerosis patients showed considera

186 Development of therapies to benefit progressive multiple sclerosis patients will require a b

187 tic factor and therapeutic target in primary progressive multiple sclerosis patients', by Malhotra et

188 s the pathological findings in relapsing and progressive multiple sclerosis patients.

189 the relapsing phase, have little benefit for progressive multiple sclerosis patients.

190 cacious in relapsing-remitting and secondary progressive multiple sclerosis patients.

191 f key long-term outcomes including secondary progressive multiple sclerosis, physical disability and

192 Progressive multiple sclerosis (PMS) causes slow accumul

193 Therapeutic development in progressive multiple sclerosis (PMS) has been hampered b

194 Progressive multiple sclerosis (PMS) involves a persiste

195 Progressive multiple sclerosis (PMS) is an immune-initia

196 erobic exercise (EX) to improve cognition in progressive multiple sclerosis (PMS) remains limited.

197 n identified in brain lesions of people with progressive multiple sclerosis (PMS).

198 contributes to the disability of people with progressive multiple sclerosis (PMS).

199 cross groups and representative of a primary progressive multiple sclerosis population (48% women, me

200 rks underlying cognitive deficits in primary-progressive multiple sclerosis (PP-MS) and to explore ho

201 spinal cord damage in patients with primary progressive multiple sclerosis (PP-MS) provides insights

202 multiple sclerosis (RR-MS; n = 52), primary progressive multiple sclerosis (PP-MS; n = 21), other in

203 or ocrelizumab, treatment options in primary progressive multiple sclerosis (PPMS) are lacking.

204 cell (iPSC) lines from patients with primary progressive multiple sclerosis (PPMS) failed to promote

205 Longitudinal imaging studies of primary progressive multiple sclerosis (PPMS) have shown signifi

206 reatment (DMT) in people affected by primary progressive multiple sclerosis (PPMS) is limited.

207 tients with a confirmed diagnosis of primary progressive multiple sclerosis (PPMS) is uncertain.

208 e unique clinical characteristics of primary progressive multiple sclerosis (PPMS) pose particular di

209 brain atrophy in the early stages of primary progressive multiple sclerosis (PPMS), affecting both gr

210 ical disability, a disorder known as primary-progressive multiple sclerosis (PPMS).

211 esonance imaging (MRI) parameters in primary progressive multiple sclerosis (PPMS).

212 lapsing multiple sclerosis (RMS) and primary progressive multiple sclerosis (PPMS).

213 c real-world cohort of patients with primary progressive multiple sclerosis (PPMS).

214 solated syndrome (RIS) who evolve to primary progressive multiple sclerosis (PPMS).

215 Some studies comparing primary and secondary progressive multiple sclerosis (PPMS, SPMS) report simil

216 cts have been approved for the management of progressive multiple sclerosis, primarily for people who

217 ume were studied in 23 patients with primary progressive multiple sclerosis (primary progressive MS)

218 primary progressive compared with secondary progressive multiple sclerosis raise the question as to

219 parallel-group study, patients with primary progressive multiple sclerosis recruited across 148 cent

220 ran and Canada had higher risks of secondary progressive multiple sclerosis relative to the other stu

221 The absence of treatments for progressive multiple sclerosis represents a major unmet

222 une encephalomyelitis mouse model of chronic progressive multiple sclerosis results in striking rever

223 on 11 years), and 27 patients with secondary progressive multiple sclerosis (secondary progressive MS

224 ccumulation of disability that characterises progressive multiple sclerosis seems to result more from

225 The evidence suggests that treatment of progressive multiple sclerosis should be based on a comb

226 a-1b (IFNbeta-1b) in patients with secondary progressive multiple sclerosis (SP multiple sclerosis) h

227 ossly unaffected white matter from secondary progressive multiple sclerosis (SP-MS) patients is heavi

228 People severely impaired with progressive multiple sclerosis spend much of their day s

229 mice remained weak and, as in patients with progressive multiple sclerosis, spinal cord atrophy had

230 Patients with secondary progressive multiple sclerosis (SPMS) are lacking effici

231 on brain atrophy and disability in secondary progressive multiple sclerosis (SPMS) are mediated by re

232 tatus Scale (EDSS), development of secondary-progressive multiple sclerosis (SPMS), brain T2-lesion v

233 ng-remitting multiple sclerosis to secondary progressive multiple sclerosis (SPMS), characterized by

234 vastatin (80 mg) versus placebo in secondary progressive multiple sclerosis (SPMS), the adjusted diff

235 ting multiple sclerosis (RRMS) and secondary progressive multiple sclerosis (SPMS), which in part is

236 tting multiple sclerosis (RRMS) or secondary progressive multiple sclerosis (SPMS).

237 ole brain atrophy in patients with secondary progressive multiple sclerosis (SPMS).

238 In primary progressive multiple sclerosis, striatum and pallidum sh

239 y shown no effect of relapse frequency among progressive multiple sclerosis subtypes, here we examine

240 t-mortem spinal cord of patients affected by progressive multiple sclerosis, suggesting that pharmaco

241 In secondary progressive multiple sclerosis, T2* in normal-appearing

242 Effective therapies for progressive multiple sclerosis that prevent worsening, r

243 e that for relapsing-remitting and secondary progressive multiple sclerosis, the combination of tripl

244 For people with progressive multiple sclerosis, the poor response to cur

245 In participants with nonrelapsing secondary progressive multiple sclerosis, the risk of disability p

246 in lesions from post-mortem of patients with progressive multiple sclerosis to identify the target pr

247 xpands the differential diagnosis of primary progressive multiple sclerosis to include proteolipid pr

248 h relapsing-remitting or relapsing secondary progressive multiple sclerosis to receive 3 mg of intrav

249 A 78-year-old man with progressive multiple sclerosis treated with ocrelizumab

250 y assessing cognition and quality of life in progressive multiple sclerosis treatment trials.

251 Patients with primary progressive multiple sclerosis underwent serial magnetic

252 ride in a cohort of 14 patients with primary progressive multiple sclerosis using magnetic resonance

253 Secondary progressive multiple sclerosis was identified as per cli

254 In chronic brain lesions of patients with progressive multiple sclerosis, we demonstrate an increa

255 In patients with primary progressive multiple sclerosis, we observed a significan

256 Patients with progressive multiple sclerosis were eligible for inclusi

257 14, 2018, and April 2, 2022, 311 people with progressive multiple sclerosis were enrolled and 284 (91

258 undred and twenty three cases with secondary progressive multiple sclerosis were examined for the pre

259 A total of 943 patients with primary progressive multiple sclerosis were randomized to GA or

260 Patients aged 18-65 years with secondary progressive multiple sclerosis were randomly assigned (1

261 6, 2015, and April 28, 2017, 285 people with progressive multiple sclerosis were screened for eligibi

262 afety and efficacy of ocrelizumab in primary progressive multiple sclerosis were shown in the phase 3

263 Twenty-four patients with secondary progressive multiple sclerosis were studied psychophysic

264 sion expansion and disability progression in progressive multiple sclerosis, whereas those lining gra

265 t of several neurologic conditions including progressive multiple sclerosis, which is represented by

266 studies devoted solely to these symptoms in progressive multiple sclerosis, which translates to few

267 Patients with secondary progressive multiple sclerosis who attended the National

268 t the findings in 60 patients with secondary progressive multiple sclerosis who had monthly brain MRI

269 d patients (aged 25-65 years) with secondary progressive multiple sclerosis who were not on disease-m

270 ty in both primary progressive and secondary progressive multiple sclerosis with a common plaque-cent

271 extensive collection of cases with secondary progressive multiple sclerosis with a wide age range and

272 Furthermore, cases with primary progressive multiple sclerosis with extensive meningeal

273 was performed on 718 patients with secondary progressive multiple sclerosis with follow-up of up to 3

274 ingle-cell data from Alzheimer's disease and progressive multiple sclerosis with our pipeline, we fin

275 g-remitting multiple sclerosis and secondary progressive multiple sclerosis with relapses) were rando

276 Data from 21 patients with primary progressive multiple sclerosis within 6 years of disease

277 iple sclerosis have little or no efficacy in progressive multiple sclerosis without inflammatory lesi

278 ltiple sclerosis or a diagnosis of secondary progressive multiple sclerosis without relapse.