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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

28 ability progression in patients with primary progressive multiple sclerosis.

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

30 better understanding of the pathogenesis of progressive multiple sclerosis.

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

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

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

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

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

36 ert neuroprotective effects in patients with progressive multiple sclerosis.

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

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

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

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

41 tial neuroprotective treatment for secondary progressive multiple sclerosis.

42 hogenetic mechanisms compared with secondary progressive multiple sclerosis.

43 tissue derived primarily from patients with progressive multiple sclerosis.

44 o neuroprotective in patients with secondary progressive multiple sclerosis.

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

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

47 89 cm3/year in those who developed secondary progressive multiple sclerosis, a difference of 2.09 cm3

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

75 Secondary progressive multiple sclerosis, for which no satisfactor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 Patients with secondary progressive multiple sclerosis involving the visual path

91 Progressive multiple sclerosis is associated with metabo

92 Progressive multiple sclerosis is characterised clinical

93 Clinical change in progressive multiple sclerosis may therefore occur witho

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

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

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

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

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

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

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

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

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

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

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

105 Secondary progressive multiple sclerosis patients showed considera

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 Patients with primary progressive multiple sclerosis underwent serial magnetic

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

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

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

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

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

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

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

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

152 Patients with secondary progressive multiple sclerosis who attended the National

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

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

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

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

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

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

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