ライフサイエンスコーパス: PPMS

1 PPMS can be applied to both newly produced and publicly

2 PPMS prevalence (11.7%) and onset age (mean +/- standard

3 sphingolipids in healthy controls (n = 10), PPMS (n = 27), and RMS (n = 17) patients before and afte

4 234 PPMS patients were identified from a population-based co

5 Using 2:1 randomization, 439 PPMS patients received two 1,000 mg intravenous rituxima

6 post-hoc, MRI-blinded analysis evaluated 732 PPMS randomised to OCR (488) or PBO (244).

7 investigated cognitive and MRI change in 99 PPMS patients from five European centres for 2 years.

8 ual should be considered before amalgamating PPMS and SPMS in clinical trials.

9 PN1 comprised 10 hubs in HCs, RRMS and PPMS but did not include the right thalamus in SPMS.

10 In addition, RRMS, SPMS, and PPMS were characterized by unique patterns of reactivity

11 to demonstrate its efficacy, we have applied PPMS to publicly available scRNA-seq data generated from

12 ed to two other population- and clinic-based PPMS cohorts.

13 thylation of the 1q21.1 locus, controlled by PPMS-specific genetic variations and influencing the exp

14 As from single-cell RNA-sequencing datasets (PPMS).

15 PMS: 64% fulfilled the criteria for definite PPMS, 35% for probable PPMS, and only 1% for possible PP

16 In definite PPMS, evidence of intrathecal synthesis of immunoglobuli

17 ical, or neuroimaging features differentiate PPMS and SPMS; both are characterized by imaging finding

18 rosis (MS) have primary progressive disease (PPMS).

19 ion of MRI markers capable of distinguishing PPMS from RRMS and predicting the evolution of RRMS to S

20 an be detected over a 1-year period in early PPMS.

21 of 56 MS patients with a diagnosis of either PPMS (n = 16), relapsing-remitting MS (n = 20), or benig

22 reatment with rapamycin, which then enhanced PPMS NPC support for oligodendrocyte (OL) differentiatio

23 For PPMS vignettes, females were more likely to be correctly

24 In PPMS, we found hypermethylation of the 1q21.1 locus, con

25 lipid with significantly lower abundance in PPMS patients with a rapidly deteriorating disease cours

26 We compared disability accrual in PPMS and operationally diagnosed SPMS in the internation

27 Additionally, in PPMS patients C16 glucosylceramide levels correlated wit

28 Results showed the following in PPMS: 1) CD4(+)/CEACAM-1(+), CD4(+)/TIM-3(+), CD8(+)/TIM

29 This could however not be found in PPMS.

30 k analysis further implicates these genes in PPMS brain processes.

31 Expression of cellular senescence genes in PPMS NPCs was found to be reversible by treatment with r

32 sphingolipids measured herein was higher in PPMS (17.2 ng/mL) and RMS (17.6 ng/mL) when compared wit

33 ct of reducing the accumulation of aT2-LV in PPMS in the DBP period and was related to CDP-EDSS in OL

34 with ocrelizumab in RMS patients but not in PPMS patients.

35 eat shock proteins that were not observed in PPMS or SPMS.

36 Higher NfL Z-scores predicted CDW only in PPMS participants (1.236 (1.092 to 1.399), p=0.001).

37 an active inflammatory disease phenotype in PPMS patients.

38 nical presentation, and disease processes in PPMS could start decades prior to first apparent progres

39 ffect of rituximab on disease progression in PPMS appears to be marginal.

40 Disability progression in PPMS is variable and influenced by age at onset.

41 CEACAM-1 expression is reduced in PPMS; this exacerbates MBP-specific inflammatory T cell

42 ebo-controlled OLYMPUS study of rituximab in PPMS, we found that the presence of CSF-restricted IgM O

43 edictive power models for clinical trials in PPMS.

44 ssociation between a common NR1H3 variant in PPMS patients and loss of function for the encoded prote

45 or >=2 spinal cord lesions performed well in PPMS diagnosis when combined with dissemination in time/

46 ently under consideration, performed well in PPMS diagnosis.

47 does not ameliorate disability worsening in PPMS, in general.

48 Based on user input, PPMS can profile pri-miRNAs at cell-type resolution.

49 l fluid (CSF) and serum samples from a large PPMS patient cohort, and related to clinical and imaging

50 The 2017 McDonald PPMS criteria was the gold standard against which the 20

51 years especially in primary progressive MS (PPMS) are not fully understood.

52 sclerosis (RRMS) and primary progressive MS (PPMS) for historical, rather than biological, reasons.

53 pwPMS with primary progressive MS (PPMS) or secondary progressive MS (SPMS) with at least o

54 S), those developing primary-progressive MS (PPMS) scored a significant 4.6 to 6.9 IQ points lower th

55 ximab in adults with primary progressive MS (PPMS) through 96 weeks and safety through 122 weeks.

56 nges associated with primary progressive MS (PPMS) using a cross-tissue (blood and post-mortem brain)

57 elapsing MS (RMS) or primary progressive MS (PPMS) who were initiating anti-CD20 treatment.

58 itting MS (RRMS), 28 primary progressive MS (PPMS), 36 secondary progressive (SPMS) and 51 healthy co

59 le sclerosis (RRMS), primary progressive MS (PPMS), stroke, Parkinson disease, and epilepsy.

60 ular, is impaired in primary progressive MS (PPMS).

61 iated mouse model of primary progressive MS (PPMS).

62 ssive MS (SPMS), and primary-progressive MS (PPMS).

63 ones in persons with primary progressive MS (PPMS).

64 8) and patients with primary progressive MS (PPMS, n = 19) and either a rapid (PPMS-P, n = 9) or slow

65 ve MS [SPMS], and 40 primary progressive MS [PPMS]) from C1 to T10.

66 udy cohort were patients with a diagnosis of PPMS and at least 3 years of Expanded Disability Status

67 A diagnosis of PPMS based on high fulfillment of modified RRMS DIS crit

68 ion must be documented before a diagnosis of PPMS is made.) Three levels of diagnostic certainty have

69 Diagnosis of PPMS is more challenging than diagnosis of RRMS.

70 tive cerebrospinal fluid, for a diagnosis of PPMS.

71 aracteristics in the preprogressive phase of PPMS were indistinguishable from CIS/MS.

72 ere differentially abundant in the plasma of PPMS patients compared to controls and their levels corr

73 ating in a European natural history study of PPMS: 64% fulfilled the criteria for definite PPMS, 35%

74 F IgM OCB may be a biomarker for a subset of PPMS patients with more active inflammatory disease, who

75 ] and 2 white matter columns) are typical of PPMS.

76 1) in the RIS group were comparable to other PPMS populations (p > 0.05).

77 for probable PPMS, and only 1% for possible PPMS.

78 criteria for definite PPMS, 35% for probable PPMS, and only 1% for possible PPMS.

79 progressive (SPMS), and primary progressive (PPMS) MS from both healthy controls and other neurologic

80 and serum NfL (sNfL) levels in a prospective PPMS cohort and matched healthy controls.

81 essive MS (PPMS, n = 19) and either a rapid (PPMS-P, n = 9) or slow (PPMS-NP, n = 10) disease course

82 Inclusion required PPMS or SPMS with onset at age >=18 years since 1995.

83 s in primary progressive multiple sclerosis (PPMS) are lacking.

84 with primary progressive multiple sclerosis (PPMS) failed to promote oligodendrocyte progenitor cell

85 s of primary progressive multiple sclerosis (PPMS) have shown significant changes in MR measures over

86 d by primary progressive multiple sclerosis (PPMS) is limited.

87 s of primary progressive multiple sclerosis (PPMS) is uncertain.

88 s of primary progressive multiple sclerosis (PPMS) pose particular diagnostic difficulties, both in e

89 s of primary progressive multiple sclerosis (PPMS), affecting both grey and white matter (GM and WM).

90 with primary progressive multiple sclerosis (PPMS).

91 e to primary progressive multiple sclerosis (PPMS).

92 ial, progressive form of multiple sclerosis (PPMS).

93 n as primary-progressive multiple sclerosis (PPMS).

94 s in primary progressive multiple sclerosis (PPMS).

95 and primary progressive multiple sclerosis (PPMS).

96 nd secondary progressive multiple sclerosis (PPMS, SPMS) report similar ages at onset of the progress

97 and either a rapid (PPMS-P, n = 9) or slow (PPMS-NP, n = 10) disease course based on worsening disab

98 identified patients evaluated for suspected PPMS at 5 European centers.

99 eria when applied to patients with suspected PPMS.

100 In the PPMS study, rituximab delayed time to confirmed disease

101 A proteomic analysis of the PPMS NPC secretome identified high-mobility group box-1

102 the 1q21.1 locus potentially contributing to PPMS pathogenesis.

103 f subjects with RIS that evolved directly to PPMS were compared to those that developed a relapsing d

104 esions and being male predicted evolution to PPMS.

105 Subjects with RIS evolve to PPMS at the same frequency as expected from general MS p

106 Subjects who evolved to PPMS had more spinal cord lesions (100%) before symptoma

107 RIS evolved to PPMS more commonly in men (p = 0.005) and at an older ag

108 event consistent with CIS/MS, 15 evolved to PPMS).

109 Relative to PPMS, SPMS had older age at onset of the progressive pha

110 Median time to PPMS was 3.5 years (range, 1.6-5.4).

111 h neuroaxonal degeneration seems to underlie PPMS, the pathogenesis and the extent to which immune-me

112 and slower disability accrual in SPMS versus PPMS.

113 Included patients comprised 1872 with PPMS (47% men; 50% with activity) and 2575 with SPMS (32

114 8) included 41 patients with RMS and 27 with PPMS enrolled at diagnosis (age, 40 years [range, 20-61

115 acy and safety of ocrelizumab in adults with PPMS (ORATORIO) trial.

116 A total of 282 patients were diagnosed with PPMS using the 2017 McDonald criteria, and 40 with alter

117 review of their considerable experience with PPMS.

118 f change within and between individuals with PPMS.

119 e [EDSS] score, 0-5.5), and 31 patients with PPMS (mean [SD] age, 44.9 [7.4] years; 15 [48%] female a

120 We followed 81 patients with PPMS (mean disease duration 5.9 years) over 2.7 years on

121 In patients with PPMS and those with relapse-onset MS, location of lesion

122 A total of 141 patients with PPMS from 18 European MS centres were included.

123 on disability worsening among patients with PPMS stratified by different disability trajectories.

124 We identified patients with PPMS that started DMT or were never treated during the o

125 Forty-one patients with PPMS were followed prospectively for 5 years.

126 From a total of 3298 patients with PPMS, 2633 were excluded because they did not meet the e

127 with disability progression in patients with PPMS, being CHI3L1 findings less dependent on the inflam

128 at inflammation also occurs in patients with PPMS, may contribute to long-term disability, and may be

129 sues and iPS-derived NPCs from patients with PPMS.

130 elapse-onset multiple sclerosis, people with PPMS are older at onset and a higher proportion are men.

131 Thirty-one subjects with PPMS within 5 years of symptom onset were studied at bas