ライフサイエンスコーパス: disease-modifying therapy

1 atients with sarcoidosis who were not taking disease modifying therapy.

2 ell surface has been highly anticipated as a disease modifying therapy.

3 ients may benefit from earlier initiation of disease-modifying therapy.

4 g steroids, and all had received <6 weeks of disease-modifying therapy.

5 ong duration, high cost of care, and lack of disease-modifying therapy.

6 vement who are thus candidates for potential disease-modifying therapy.

7 Patients were analyzed independent of disease-modifying therapy.

8 ity and mortality, despite aggressive use of disease-modifying therapy.

9 these 20 patients were undergoing first-line disease-modifying therapy.

10 tion will pave the way for major advances in disease modifying therapies.

11 ovided important clues in the development of disease modifying therapies.

12 ion of those at risk, and allow for targeted disease modifying therapies.

13 ase, which may be used in clinical trials of disease-modifying therapies.

14 for these tauopathies and clinical trials of disease-modifying therapies.

15 inhibitors to those treated with alternative disease-modifying therapies.

16 ibes current experimental approaches towards disease-modifying therapies.

17 ility gene for PD and a potential target for disease-modifying therapies.

18 atric symptoms, and contribute to monitoring disease-modifying therapies.

19 increasingly important with the prospect of disease-modifying therapies.

20 ecificity and will be critical in evaluating disease-modifying therapies.

21 g of disease progression, and development of disease-modifying therapies.

22 ians but will be critical for the success of disease-modifying therapies.

23 n PD are important for future development of disease-modifying therapies.

24 urodegenerative disorder and lacks effective disease-modifying therapies.

25 st obviously in the development of potential disease-modifying therapies.

26 gnostication and earlier access to potential disease-modifying therapies.

27 d prognostic decisions in clinical trials of disease-modifying therapies.

28 source from which to develop a new class of disease-modifying therapies.

29 nique opportunity for developing and testing disease-modifying therapies.

30 s that can identify a therapeutic window for disease-modifying therapies.

31 gnosis and for the successful development of disease-modifying therapies.

32 trials or targeted applications of tau-based disease-modifying therapies.

33 neurodegenerative disorder without effective disease-modifying therapies.

34 e disorder, for which there are no effective disease-modifying therapies.

35 be particularly important for the testing of disease-modifying therapies.

36 se for diagnostic purposes and evaluation of disease-modifying therapies.

37 Several disease-modifying therapies act on T regulatory cells an

38 einopathy will be highly valuable in testing disease-modifying therapies and dissecting the mechanism

39 rs to aid in the objective assessment of new disease-modifying therapies and identify new regions tha

40 d in importance with the availability of new disease-modifying therapies and will continue to do so a

41 There are no cures or disease-modifying therapies, and this may be due to our

42 birthday): death, first overt stroke, use of disease-modifying therapy, and hospitalizations for pain

43 , gender, race, ethnicity, disease duration, disease-modifying therapy, and length of follow-up, ever

44 Teriflunomide is an oral disease-modifying therapy approved for treatment of rela

45 reat to the world's aging population, yet no disease-modifying therapies are available.

46 Currently, many potential disease-modifying therapies are being developed and eval

47 otein tau, progranulin and TDP-43, potential disease-modifying therapies are being studied in animal

48 The currently available disease-modifying therapies are limited in their efficac

49 evious unilateral optic neuritis, and use of disease-modifying therapies as covariates.

50 ncy coupled with the absence of any approved disease-modifying therapies at present position AD as a

51 ies for dementia, and establishing effective disease modifying therapies based on amyloid or tau rema

52 e prognostic information will be critical if disease-modifying therapies become available.

53 There are currently no disease-modifying therapies capable of reducing alpha-sy

54 The search for true disease-modifying therapy continues and many clinical tr

55 is a difficult clinical problem for which no disease-modifying therapy currently exists.

56 ed natalizumab at once and initiated another disease modifying therapy (DMT) following the last natal

57 Discontinuation of injectable disease-modifying therapy (DMT) for multiple sclerosis (

58 been approved for clinical use, all existing disease-modifying therapies (DMTs) for MS modulate B-cel

59 latiramer acetate would be cost effective as disease-modifying therapies (DMTs) for multiple sclerosi

60 loss of neurologic function while receiving disease-modifying therapies during the 18 months before

61 Effective disease-modifying therapies exist for many diffuse, nonl

62 multiple sclerosis (MS) who receive approved disease-modifying therapies experience breakthrough dise

63 d holds potential to accelerate discovery of disease modifying therapies for LB PD, DLB, and related

64 ation is a compelling target for discovering disease modifying therapies for PD, DLB, and related syn

65 lity is currently the most important goal of disease modifying therapy for multiple sclerosis.

66 , e.g. with dantrolene, could be a potential disease modifying therapy for nGD.

67 MMP-13 inhibitor would therefore be a novel disease modifying therapy for the treatment of arthritis

68 ll as tau-focused drug discovery to identify disease-modifying therapies for AD and related tauopathi

69 derlying pathogenic mechanisms and effective disease-modifying therapies for Alzheimer's disease rema

70 -naive patients with MS had not received any disease-modifying therapies for at least 3 months before

71 Currently there are no effective disease-modifying therapies for chemotherapy-induced per

72 Currently, there are no available disease-modifying therapies for CMML, nor are there prec

73 However, the lack of disease-modifying therapies for diabetic DSP makes the i

74 There are no disease-modifying therapies for either FTD or NCL, in pa

75 her the development of specific cognitive or disease-modifying therapies for FXTAS.

76 There are no cures or disease-modifying therapies for HD.

77 ed to herald a new era in the development of disease-modifying therapies for MDS, but there have been

78 RECENT FINDINGS: A number of disease-modifying therapies for MS, including oral agent

79 ay represents a novel target for much needed disease-modifying therapies for MS.

80 oped in patients without any previous use of disease-modifying therapies for multiple sclerosis, prev

81 The evaluation of effective disease-modifying therapies for neurodegenerative disord

82 n provide novel targets for the discovery of disease-modifying therapies for PD and related neurodege

83 The development of disease-modifying therapies for PD has been hindered by

84 d in this study may be useful for monitoring disease-modifying therapies for PD.

85 eview evidence and best practice for current disease-modifying therapies for the treatment of systemi

86 elatively inaccessible organ, and we have no disease-modifying therapies for them.

87 s immunoglobulin (IVIG) is a frequently used disease-modifying therapy for a large spectrum of autoim

88 inst amyloid-beta (Abeta) holds promise as a disease-modifying therapy for Alzheimer disease (AD), it

89 these are promising compounds for developing disease-modifying therapy for Alzheimer's disease and re

90 al of amyloid-beta (Abeta) immunization as a disease-modifying therapy for Alzheimer's disease is lim

91 toxicity, which hold promise for developing disease-modifying therapy for amyloidoses.

92 e of the recent advances in the search for a disease-modifying therapy for amyotrophic lateral sclero

93 efine the potential of targeting PrP(C) as a disease-modifying therapy for certain AD-related phenoty

94 ggest that APC has promising applications as disease-modifying therapy for ischemic stroke and other

95 The development of disease-modifying therapy for Parkinson disease has been

96 nitive development of inosine as a potential disease-modifying therapy for PD.

97 ping urate-elevating strategies as potential disease-modifying therapy for PD.

98 er allergic diseases, has shown promise as a disease-modifying therapy for peanut allergy.

99 vestigated as a targeted immunomodulator and disease-modifying therapy for rheumatoid arthritis.

100 This article reviews recent progress in disease-modifying therapy for spondyloarthropathy, inclu

101 -1 inhibition has the potential to provide a disease-modifying therapy for the treatment of Alzheimer

102 These findings suggest that ivacaftor is a disease-modifying therapy for the treatment of cystic fi

103 There is no disease-modifying therapy for this condition and the mec

104 be further investigated as a potential novel disease-modifying therapy for treatment of Parkinson dis

105 Disease-modifying therapies have also been used in combi

106 f this disease has been transformed, and two disease-modifying therapies have been approved, worldwid

107 the promise, possibly in the near future, of disease-modifying therapies have made the characterizati

108 o are thrombocytopenic and unable to receive disease-modifying therapy have few treatment options.

109 Two disease-modifying therapies, hydroxyurea and long-term b

110 ease offers a window of opportunity in which disease-modifying therapies-ie, those aimed at delaying

111 phase I, II and III trials of new, putative disease modifying therapies in multiple sclerosis.

112 design of future studies assessing potential disease modifying therapies in patients with multiple sy

113 oth for diagnostic use and for evaluation of disease-modifying therapies in AD.

114 n urgent need for early biomarkers and novel disease-modifying therapies in Huntington's disease.

115 his pathway has the potential to lead to new disease-modifying therapies in multiple sclerosis and ot

116 entrally to assess the efficacy of potential disease-modifying therapies in PD.

117 alone should not be discounted as potential disease-modifying therapies in SMA.

118 ntific basis and current status of promising disease-modifying therapies in the discovery and develop

119 's disease can facilitate the development of disease-modifying therapies in the future.Dual Perspecti

120 to centre on hippocampal dysfunction and how disease-modifying therapies in this region can potential

121 the potential of targeting this pathway as a disease-modifying therapy in MS.

122 nergic degeneration are important for future disease-modifying therapy in Parkinson disease.

123 tudy to report benefits of an available oral disease-modifying therapy in patients with early multipl

124 tifies TIGAR as a promising novel target for disease-modifying therapy in PINK1-related PD.

125 rogressive disease treatment as adjuvant for disease-modifying therapy in RA.

126 Potential disease-modifying therapies may alter the time course of

127 mines clinical phenotypic expression and how disease-modifying therapies may best be developed and de

128 iduals because it is in this population that disease-modifying therapies may have the greatest chance

129 The focus of guidelines on disease-modifying therapies may not address the full spe

130 Potential disease-modifying therapies must be initiated early to m

131 siologically relevant screening platform for disease-modifying therapies of PD.

132 vastating illness and at present there is no disease modifying therapy or cure for it; and management

133 for 1 day and were monitored on any approved disease-modifying therapy, or no therapy thereafter.

134 ce for diagnosing, monitoring and developing disease modifying therapies, particularly for the early

135 We argue that disease modifying therapy should be considered for acute

136 Second, disease-modifying therapy should be used early in multip

137 We hypothesized that pDCs are inhibited by disease-modifying therapy such as interferon (IFN)-beta,

138 e sclerosis during treatment with injectable disease-modifying therapies, switching to natalizumab is

139 e, disease duration, previous treatment with disease-modifying therapy, T1 gadolinium-enhancing lesio

140 CM and ultimately assist in developing novel disease-modifying therapy, targeting interstitial fibros

141 f high relevance to the search for potential disease-modifying therapies that inhibit BACE1 to reduce

142 so BBB malfunction, and highlighting current disease-modifying therapies that may also have an effect

143 e treatment of steroid refractory cases with disease-modifying therapies that were originally designe

144 -dopaminergic features of the disease, and a disease-modifying therapy that slows or stops disease pr

145 Without disease-modifying therapies, the impact is profound for

146 The failure of clinical trials of candidate disease modifying therapies to slow disease progression

147 There is an unmet need for disease-modifying therapies to improve ambulatory functi

148 At present, there are no disease-modifying therapies to prevent PD progression.

149 There are currently no disease-modifying therapies to slow down or halt disease

150 The development of disease-modifying therapies will necessitate monitoring

151 cal diseases are often treated with a single disease-modifying therapy without understanding patient-

152 on is that treatment with multiple sclerosis disease-modifying therapy would seem reasonable.