ライフサイエンスコーパス: RRMS

1 RRMS may start years prior to clinical presentation, and

2 RRMS relaxing-remitting MS patients had lower WM white m

3 RRMS was characterized by autoantibodies to heat shock p

4 tting MS (RRMS; mean age: CIS: 31.4 +/- 9.0; RRMS: 33.0 +/- 8.7 years; mean disease duration: CIS: 7.

5 1106 RRMS patients were randomised 1:1 to receive once-daily

6 e global RNA profile of serum exosomes in 19 RRMS patients (9 in relapse, 10 in remission) and 10 HC.

7 We conducted a retrospective study in 192 RRMS patients treated with IFNbeta-1b.

8 Furthermore, low-BMI (BMI </= 23 kg/m(2)) RRMS patients show increased levels of small HDL (sHDL),

9 atus Scale (median, min-max): CIS: 1, 0-3.5; RRMS: 1.25, 0-4) with 3.0T magnetic resonance imaging.

10 dated using qPCR on an independent set of 50 RRMS patients, 51 SPMS patients, and 32 HCs.

11 Thirteen trials including >13,500 RRMS patients were included in the meta-analysis.

12 in reaction with an independent cohort of 63 RRMS patients (33 in relapse, 30 in remission) and 32 HC

13 the majority of patients with highly active RRMS over an average seven-year follow-up.

14 efficacy and safety of alemtuzumab in active RRMS.

15 e for inducing sustained remission of active RRMS and was associated with improvements in neurologic

16 In addition, RRMS, SPMS, and PPMS were characterized by unique patter

17 We compared outcomes for all RRMS patients switching from natalizumab due to JC virus

18 tion of CD8(low)CD4(-) cells in both CIS and RRMS in the absence of treatment as well as suggestive e

19 Similarities between untreated CIS and RRMS subjects extend to broader immunological profiles:

20 hsa-miR-145 differentiated RRMS from HCs and RRMS from SPMS.

21 y of miRNAs differentiated SPMS from HCs and RRMS from SPMS.

22 It was different in RRMS versus SPMS, and RRMS versus HCs, and showed an association with EDSS and

23 ons (SPMS 1.4 (1.8) per person per year, and RRMS 1.1 (1.0)), and none arose de novo, or from previou

24 nhancing lesions on brain MRI scans for both RRMS studies.

25 ive lesions were found in patients with both RRMS and SPMS.

26 re similar for relapsing-remitting MS cases (RRMS), those developing primary-progressive MS (PPMS) sc

27 patients to one of two diagnosis categories, RRMS or other neurological disease, with 87% accuracy by

28 ave multifocal disease at onset, and develop RRMS by follow-up.

29 -based statistical classifier for diagnosing RRMS that provides a high degree of diagnostic capabilit

30 MS from SPMS, and hsa-miR-145 differentiated RRMS from HCs and RRMS from SPMS.

31 hsa-miR-454 differentiated RRMS from SPMS, and hsa-miR-145 differentiated RRMS from

32 t the brain MRI criteria for differentiating RRMS from NMOSD are sensitive and specific for all pheno

33 mab improves ambulatory function in disabled RRMS subjects and may have efficacy in disabled SPMS sub

34 hat begins as a relapsing-remitting disease (RRMS) and is followed by a progressive phase (SPMS).

35 stribution criteria were able to distinguish RRMS with a sensitivity of 90.9% and with a specificity

36 que autoantibody patterns that distinguished RRMS, secondary progressive (SPMS), and primary progress

37 treatment-naive patients with active, early RRMS were randomly assigned in a 1:1:1 ratio to receive

38 ve MS plaques predominate in acute and early RRMS and are the likely substrate of clinical attacks.

39 rs in the pivotal trial of IM IFNbeta-1a for RRMS was conducted.

40 chanisms of action of the approved drugs for RRMS provide a strong foundation for understanding the p

41 g Administration approval as a treatment for RRMS.

42 ted amyotrophic lateral sclerosis (ALS) from RRMS subjects, but were not different between SPMS and A

43 We found that memory and naive B cells from RRMS and secondary progressive MS patients exhibited a s

44 he study was performed on blood samples from RRMS patients enrolled in the CARE-MS II clinical trial,

45 In RRMS patients, IFN-beta nonresponders had higher IL-17F

46 In RRMS, lesion accumulation rate was associated with GCIP

47 In RRMS, the treatment effect on brain atrophy is correlate

48 poprotein levels and function are altered in RRMS patients, especially in low-BMI patients, which may

49 expressed in RRMS and SPMS versus HCs and in RRMS versus SPMS.

50 rain (and additionally GM and WM) atrophy in RRMS increased incrementally with step-wise refinement t

51 ted for 62% of the variance in GM atrophy in RRMS, but there were no significant predictors of GM atr

52 gnificantly correlated with decreased CMT in RRMS (r = -0.295; p = 0.015), but not in CIS (r = 0.032;

53 ol of structural RNAs, are also deficient in RRMS.

54 r atrophy indicate that mechanisms differ in RRMS and SPMS.

55 It was different in RRMS versus SPMS, and RRMS versus HCs, and showed an ass

56 ects in structural RNA surveillance exist in RRMS and establish a causal link between Ro60 and La pro

57 ating miRNAs are differentially expressed in RRMS and SPMS versus HCs and in RRMS versus SPMS.

58 NA category were differentially expressed in RRMS patients versus HC: hsa-miR-122-5p, hsa-miR-196b-5p

59 iR-92) that were differentially expressed in RRMS versus SPMS also differentiated amyotrophic lateral

60 croRNAs (miRNAs) differentially expressed in RRMS.

61 nts) comparing directly INFbeta versus GA in RRMS.

62 ivity is becoming a viable treatment goal in RRMS; we therefore aimed to assess the effects of cladri

63 ammonis (CA) 1 region of the hippocampus in RRMS with further worsening of CA1 loss and extension in

64 ear cells was also significantly impaired in RRMS.

65 ssemination in time on MRI) and increased in RRMS patients in two clinically relevant networks subser

66 We observed smaller LDL in RRMS patients compared to healthy controls and to progre

67 reduced CD40-mediated P65 phosphorylation in RRMS patients, suggesting that reducing CD40-mediated p-

68 e more destructive pathological processes in RRMS patients.

69 ting exosomes have a distinct RNA profile in RRMS.

70 red capacity of Treg cells to proliferate in RRMS correlates with the clinical state of the subject,

71 as significantly decreased during relapse in RRMS.

72 important measure of therapeutic response in RRMS.

73 efects in surveillance of structural RNAs in RRMS exemplified by elevated levels of poly(A) + Y1-RNA,

74 across the brain was greater in SPMS than in RRMS.

75 significantly more abnormal in SPMS than in RRMS.

76 all published randomized clinical trials in RRMS lasting at least 2 years and including as endpoints

77 y have prognostic value, over many years, in RRMS.

78 ability Status Scale score >/=3.5, including RRMS subjects from the phase 3 AFFIRM and SENTINEL trial

79 ase compared with relapsing-remitting males (RRMS) and female MS subjects, with increased levels of C

80 an disease duration: CIS: 7.2 +/- 15 months; RRMS: 8.0 +/- 6.5 years, Expanded Disability Status Scal

81 fecal microbiota in relapsing remitting MS (RRMS) (n = 31) patients to that of age- and gender-match

82 ppocampal volumes in relapsing remitting MS (RRMS) and secondary progressive MS (SPMS) patients and c

83 Patients with relapsing-remitting MS (RRMS) or clinically isolated syndrome (CIS) with disease

84 ic acid plasma in 10 relapsing-remitting MS (RRMS) patients, 9 secondary progressive MS (SPMS) patien

85 (SPMS) patients, 12 relapsing-remitting MS (RRMS) patients, and 14 matched healthy controls underwen

86 acute monophasic and relapsing-remitting MS (RRMS) were active.

87 es, 36 patients with relapsing-remitting MS (RRMS), and 27 patients with secondary progressive MS (SP

88 38) in patients with relapsing-remitting MS (RRMS), compared with patients with chronic progressive M

89 reated subjects with relapsing-remitting MS (RRMS).

90 y remissions, called relapsing-remitting MS (RRMS).

91 me (CIS) and 69 with relapsing-remitting MS (RRMS; mean age: CIS: 31.4 +/- 9.0; RRMS: 33.0 +/- 8.7 ye

92 .67; p < 0.001) than relapsing-remitting MS (RRMS; r = 0.33; p = 0.007).

93 e MS [SPMS], 27 with relapsing remitting MS [RRMS]) and 30 healthy volunteers, genetically stratified

94 (AC), 47 HAM/TSP, 74 relapsing-remitting MS [RRMS], 17 secondary progressive MS [SPMS], and 40 primar

95 n with 70% of SPMS sera compared with 25% of RRMS sera (P < 0.001).

96 ostic biochemical motif in the antibodies of RRMS patients, which may offer insight into the disease

97 he hyperphosphorylation of P65 in B cells of RRMS patients at levels similar to healthy donor control

98 e activity (clinical and/or radiological) of RRMS.

99 d that the endogenous IFN-beta from serum of RRMS patients induced a significantly lower IFN-inducibl

100 estigation of ponesimod for the treatment of RRMS is under consideration.

101 e and effective regimen for the treatment of RRMS, providing the convenience of fewer sc injections p

102 ere are nine approved drugs for treatment of RRMS.

103 treatment of clinically isolated syndrome or RRMS males with a high-expresser genotype might slow or

104 219 patients with paediatric RRMS or CIS were enrolled.

105 ubsets and its contribution to the prolonged RRMS suppression following alemtuzumab-induced lymphocyt

106 n independent cohort of relapsing-remitting (RRMS) samples.

107 progressive (SPMS) and relapsing-remitting (RRMS) subgroups.

108 relapsing-remitting MS multiple sclerosis ( RRMS relaxing-remitting MS ) patients, and 12 secondary

109 t of relapsing-remitting multiple sclerosis (RRMS) and AQP4-ab NMOSD patients and also assessed their

110 s in relapsing remitting multiple sclerosis (RRMS) and other inflammatory diseases.

111 for relapsing-remitting multiple sclerosis (RRMS) are only partly effective -- breakthrough disease

112 with relapsing remitting multiple sclerosis (RRMS) as compared to healthy control individuals.

113 with relapsing-remitting multiple sclerosis (RRMS) because of altered interleukin-2 (IL-2) secretion

114 with relapsing remitting multiple sclerosis (RRMS) have higher replacement mutation frequencies than

115 tive relapsing-remitting multiple sclerosis (RRMS) in Europe, which in phase II and III studies demon

116 y in relapsing-remitting multiple sclerosis (RRMS) is not well understood, but induction of apoptosis

117 with relapsing-remitting multiple sclerosis (RRMS) or secondary progressive multiple sclerosis (SPMS)

118 e in relapsing-remitting multiple sclerosis (RRMS) patients and healthy controls (HC).

119 from relapsing-remitting multiple sclerosis (RRMS) patients exhibited enhanced proliferation with CD4

120 tive relapsing-remitting multiple sclerosis (RRMS) patients who are stable on natalizumab switch to o

121 the relapsing-remitting multiple sclerosis (RRMS) population, 30-50% of MS patients are non-responsi

122 with relapsing-remitting multiple sclerosis (RRMS) showed that short-course oral treatment with cladr

123 with relapsing-remitting multiple sclerosis (RRMS) to assess the drug's safety, efficacy, and pharmac

124 with relapsing-remitting multiple sclerosis (RRMS), alemtuzumab reduced relapse rate and the risk of

125 for relapsing-remitting multiple sclerosis (RRMS), but no published randomised trials have directly

126 y in relapsing-remitting multiple sclerosis (RRMS), oral laquinimod slowed disability and brain atrop

127 with relapsing-remitting multiple sclerosis (RRMS), TRANSFORMS, fingolimod showed greater efficacy on

128 for relapsing-remitting multiple sclerosis (RRMS).

129 and relapsing-remitting multiple sclerosis (RRMS).

130 with relapsing-remitting multiple sclerosis (RRMS).

131 with relapsing-remitting multiple sclerosis (RRMS).

132 s in relapsing-remitting multiple sclerosis (RRMS).

133 with relapsing-remitting multiple sclerosis (RRMS).

134 for relapsing-remitting multiple sclerosis (RRMS).

135 n in relapsing-remitting multiple sclerosis (RRMS).

136 Compared to HC, CIS and (even more so) RRMS patients demonstrated significantly reduced CMT.

137 rituximab compared with fingolimod in stable RRMS patients who switch from natalizumab due to JC viru

138 re inactive in patients with SPMS (35%) than RRMS (23%), but active lesions were found in all patient

139 er year was greater in SPMS (1.6 (1.9)) than RRMS (0.8 (1.9)) (Mann-Whitney p=0.039).

140 ervative threshold, lower diffusivities than RRMS patients in distinct cerebral associative, commissu

141 ation appears to be more common in SPMS than RRMS.

142 For the RRMS studies, an open-label phase I study found that rit

143 ly isolated syndromes patients converting to RRMS to 14-fold normal in SPMS.

144 We applied our method to RRMS, an autoimmune disease that is notoriously difficul

145 ndary progressive MS was reduced relative to RRMS relaxing-remitting MS in WM white matter , GM gray

146 s neuromyelitis optica, a disease similar to RRMS.

147 d as being reduced in frequency in untreated RRMS subjects (P = 0.0002), and this observation was con

148 lood whose frequency is altered in untreated RRMS subjects.

149 are three distinct populations of untreated RRMS subjects and that these distinct phenotypic categor

150 loring treatment to individual patients with RRMS and altering treatment in patients with breakthroug

151 ness to IFN-beta therapy among patients with RRMS and, furthermore, that such differential patterns o

152 proposed strategies to monitor patients with RRMS being treated with DMDs, outline approaches to iden

153 allel-group, open-label study, patients with RRMS diagnosed with the McDonald criteria who had had at

154 Thirty-six patients with RRMS from referral centers were screened; 25 were enroll

155 We found that patients with RRMS have increased serum and cerebrospinal fluid Th17 (

156 levels in natalizumab-treated patients with RRMS in clinical practice.

157 clinical trial of HDIT/HCT for patients with RRMS who experienced relapses with loss of neurologic fu

158 Patients with RRMS with at least 1 documented relapse in the 12 months

159 placebo-controlled study, 249 patients with RRMS, aged 18-65 years, were eligible to be assigned equ

160 coveries on human samples from patients with RRMS, NMO, psoriasis, rheumatoid arthritis, systemic lup

161 different leukocyte subsets of patients with RRMS.

162 phalomyelitis (EAE) but not in patients with RRMS.

163 r ongoing and future trials in patients with RRMS.

164 -1a with glatiramer acetate in patients with RRMS.

165 f pathogenic Th17 cytokines in patients with RRMS.

166 7F concentration in the serum of people with RRMS is associated with nonresponsiveness to therapy wit

167 27 people with RRMS, and 22 with SPMS were included in this study.

168 ononuclear cells obtained from subjects with RRMS and cell lines.