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 Patients were analyzed independent of disease-modifying therapy.

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

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

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

7 Of those with MS, 11 received disease-modifying therapy.

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

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

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

11 time treated with high-to-moderate efficacy disease-modifying therapy.

12 top 10 causes of death for which there is no disease-modifying therapy.

13 ial design and catalysing the development of disease-modifying therapy.

14 on (OEF) than similar patients not receiving disease-modifying therapy.

15 disrupted employment, and had not received a disease-modifying therapy.

16 morbidity and mortality and lacks definitive disease-modifying therapy.

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

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

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

20 evalence of AD, there is a lack of effective disease modifying therapies.

21 eurodegenerative condition with no effective disease modifying therapies.

22 after unsuccessful treatment with first-line disease modifying therapies.

23 and patients had failed a median of 4 (2-7) disease modifying therapies.

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

25 of Alzheimer's disease and the evaluation of disease-modifying therapies.

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

27 urodegenerative disorder and lacks effective disease-modifying therapies.

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

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

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

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

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

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

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

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

36 neurodegenerative disorder without effective disease-modifying therapies.

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

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

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

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

41 is critical to identifying novel targets for disease-modifying therapies.

42 ibes current experimental approaches towards disease-modifying therapies.

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

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

45 ich will be essential for the development of disease-modifying therapies.

46 a leading cause of disability, there are no disease-modifying therapies.

47 disease and the ability to devise effective disease-modifying therapies.

48 k of one in 350 people and an unmet need for disease-modifying therapies.

49 nue to investigate the disease and potential disease-modifying therapies.

50 lower HTT are being actively investigated as disease-modifying therapies.

51 at a turning point, with increasing focus on disease-modifying therapies.

52 ymptomatic, underscoring the urgent need for disease-modifying therapies.

53 mains unknown, preventing the development of disease-modifying therapies.

54 ing the discovery of targeted biomarkers and disease-modifying therapies.

55 , monitoring and the development of targeted disease-modifying therapies.

56 g leukocytes are also primary targets for MS disease-modifying therapies.

57 t is an ineffective predictor of response to disease-modifying therapies.

58 may reveal novel targets for preventive and disease-modifying therapies.

59 nd to demonstrate target engagement of novel disease-modifying therapies.

60 ials and opportunities for developing future disease-modifying therapies.

61 There are no disease-modifying therapies.

62 ing about 5 million people worldwide with no disease-modifying therapies.

63 population and the availability of effective disease-modifying therapies.

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

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

66 is is a common inflammatory disorder with no disease-modifying therapies.

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

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

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

70 0001, adjusted for proportion of time on any disease-modifying therapy) across the 6-10 year follow-u

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

72 ring the healthcare system for the advent of disease-modifying therapies against AD is imperative.

73 y for targeting tau and neuroinflammation in disease-modifying therapy against Alzheimer's disease.

74 es that health behaviours, comorbidities and disease-modifying therapies all contribute to multiple s

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

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

77 ction with time adjusted by age, sex, use of disease-modifying therapies and steroids, and prior opti

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

79 Associations of these measures with disease-modifying therapy and overall mortality were ana

80 ader and safer benefits, complement existing disease-modifying therapies, and improve outcomes for in

81 DPN and painful DPN still lack disease-modifying therapies, and research on novel mecha

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

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

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

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

86 Currently, no disease-modifying therapies are available for this group

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

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

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

90 r which highly effective oral medications or disease-modifying therapies are lacking.

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

92 Disease-modifying therapies are urgently needed to preve

93 partitioned into tertiles with people on no disease modifying therapy as a reference.

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

95 Challenges include the identification of disease-modifying therapies as well as finding biomarker

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

97 There are currently no disease-modifying therapies available, but approaches th

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

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

100 gnosing CMT-SORD will become imperative when disease-modifying therapies become available.

101 As none of the disease-modifying therapies can cross the blood-brain ba

102 There is no cure for MS, but available disease-modifying therapies can lessen severity and dela

103 on fraction (HFpEF) is hindered by a lack of disease-modifying therapies capable of altering its dist

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

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

106 No disease-modifying therapies currently exist, and diagnos

107 With a dearth of disease-modifying therapy currently available for ALS pa

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

109 Despite the use of 'high efficacy' disease-modifying therapies, disease activity and clinic

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

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

112 e (SP) MS, and ACES and RAM rates under each disease-modifying therapy (DMT) were estimated.

113 c resonance imaging features, time receiving disease-modifying therapy (DMT), and time to first DMT.

114 ltiple sclerosis (MS) that are refractory to disease-modifying therapy (DMT).

115 Availability of new disease-modifying therapies (DMTs) and changes of therap

116 Disease-modifying therapies (DMTs) are critical for mana

117 Unlike RRMS, disease-modifying therapies (DMTs) did not impact rates

118 Disease-modifying therapies (DMTs) for Alzheimer's disea

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

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

121 y of evidence suggests inequitable access to disease-modifying therapies (DMTs) for multiple sclerosi

122 tween comorbidity and reduced persistence to disease-modifying therapies (DMTs) in multiple sclerosis

123 in relapsing-remitting MS (RRMS) and whether disease-modifying therapies (DMTs) influence GAP-43 conc

124 rding the effects of fetal exposure to novel disease-modifying therapies (DMTs).

125 ivity in measuring the successful outcome of disease-modifying therapies (DMTs).

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

127 he genetics of SMA led to the development of disease-modifying therapies, either transferring a healt

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

129 No disease-modifying therapy exists for the treatment of pa

130 mine agonists can improve motor symptoms, no disease-modifying therapy exists yet.

131 -protein thioesterase 1 (PPT1), for which no disease-modifying therapy exists.

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

133 atically lead to the discontinuation of this disease-modifying therapy (FINEARTS-HF Finerenone Trial

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

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

136 The use of MS disease modifying therapy for CIS varies among clinician

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

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

139 nement and development of GM1 as a potential disease modifying therapy for PD.

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

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

142 Disease-modifying therapies for Alzheimer's disease (AD)

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

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

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

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

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

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

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

150 There are no disease-modifying therapies for HD.

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

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

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

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

155 Currently, disease-modifying therapies for multiple sclerosis (MS)

156 Current disease-modifying therapies for multiple sclerosis have

157 or attention deficit/hyperactivity disorder, disease-modifying therapies for multiple sclerosis, hist

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

159 ical trials have indicated the potential for disease-modifying therapies for multiple system atrophy,

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

161 Identifying effective disease-modifying therapies for neurological diseases re

162 also assess the risks associated with using disease-modifying therapies for NMOSD during the course

163 s of sickle cell disease (SCD), there are no disease-modifying therapies for ongoing painful vaso-occ

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

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

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

167 An increasing number of highly effective disease-modifying therapies for people with multiple scl

168 A significant barrier to developing disease-modifying therapies for spinocerebellar ataxias

169 Current disease-modifying therapies for SSc predominantly target

170 elusive, perhaps contributing to the lack of disease-modifying therapies for tauopathies.

171 next decade will see the emergence of truly disease-modifying therapies for the first time.

172 d mechanisms need to be explored to identify disease-modifying therapies for the growing population o

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

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

175 Before the development of disease-modifying therapies for transthyretin amyloidosi

176 There are currently no definitive disease-modifying therapies for traumatic brain injury (

177 primate brain and may help develop effective disease-modifying therapies for treatment of AD and rela

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

179 en immunotherapy (AIT) is a well-established disease-modifying therapy for allergic rhinitis, yet the

180 ab has previously shown efficacy as a potent disease-modifying therapy for alleviating vaso-occlusive

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

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

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

184 After years of failed attempts to develop a disease-modifying therapy for Alzheimer's disease, consi

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

186 at the time of diagnosis who did not receive disease-modifying therapy for amyloidosis.

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

188 The development of potential disease-modifying therapy for BBS will require concurren

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

190 Although a disease-modifying therapy for classic late infantile neu

191 , SETTING, AND PARTICIPANTS: Topiramate as a Disease-Modifying Therapy for CSPN (TopCSPN) was a doubl

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

193 was safe and may potentially be an effective disease-modifying therapy for microvascular CED in human

194 ADs), there is still no clinically available disease-modifying therapy for osteoarthritis (OA).

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

196 together, these results highlight CLR01 as a disease-modifying therapy for PD and support further cli

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

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

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

200 ssess the potential of LRRK2 modulation as a disease-modifying therapy for PSP and related tauopathie

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

202 ing the potential of voxelotor to serve as a disease-modifying therapy for SCD.

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

204 -1 inhibition has the potential to provide a disease-modifying therapy for the treatment of Alzheimer

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

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

207 proteostatic axis, offer a realistic path to disease-modifying therapy for this once enigmatic condit

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

209 y different (P < .001): participants without disease-modifying therapy had the highest OEF (median 42

210 Currently, no cure or disease modifying therapy has been successfully develope

211 A major bottleneck to the discovery of disease-modifying therapies has been an incomplete under

212 efficient non-imaging screening methods and disease-modifying therapies has been challenging, but kn

213 g efficient nonimaging screening methods and disease-modifying therapies has been challenging, but kn

214 neurodegenerative disorders, development of disease-modifying therapies has proven challenging for m

215 The currently available MS disease modifying therapies have demonstrated to reduce

216 Disease-modifying therapies have also been used in combi

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

218 Although disease-modifying therapies have been efficacious for re

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

220 Novel, highly effective disease-modifying therapies have revolutionized multiple

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

222 nts with SCA who were grouped by therapy: no disease-modifying therapy, HU, or CTT.

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

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

225 ng the key hurdle of central distribution of disease modifying therapies in LSDs.

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

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

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

229 Disease-modifying therapies in clinical development may

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

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

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

233 ort-term and long-term effects of sequential disease-modifying therapies in phase 4 studies, cohort s

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

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

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

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

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

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

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

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

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

243 Oral treatment options for disease-modifying therapy in relapsing multiple sclerosi

244 ival and overall survival with comprehensive disease-modifying therapy in the control group of the EM

245 Current disease-modifying therapies increase SMN levels and dram

246 Currently, effective disease-modifying therapy is not available for ALS.

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

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

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

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

251 Clinical trials of disease-modifying therapies might usefully stratify pati

252 Discontinuation of disease-modifying therapy might be a reasonable option i

253 ians of the symptoms, systemic findings, and disease-modifying therapies most frequently associated w

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

255 e comparative study of 3 highly effective MS disease-modifying therapies, no increased risk of invasi

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

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

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

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

260 Disease-modifying therapy reinitiation within 1 month po

261 crucial to know if the short-term effects of disease-modifying therapies reported in randomised contr

262 Development of disease-modifying therapies requires a better understand

263 Despite the availability of disease-modifying therapies, scalable strategies for hea

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

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

266 Future disease-modifying therapies, should they be forthcoming,

267 any US Food and Drug Administration-approved disease-modifying therapies, some patients do not respon

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

269 the population to be reduced under effective disease-modifying therapy, suggesting that the identifie

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

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

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

273 urate detection of AD is crucial to plan for disease modifying therapies that could prevent or delay

274 and diabetes-induced dementia, there are no disease-modifying therapies that are able to prevent or

275 is an essential prerequisite for developing disease-modifying therapies that can prevent the onset o

276 for continued research to develop targeted, disease-modifying therapies that do not compromise norma

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

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

279 Disease-modifying therapies that mitigate pathophysiolog

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

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

282 Compared to no disease modifying therapy, the use of anti-CD20 monoclon

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

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

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

286 disorders into new diagnostic approaches and disease-modifying therapies to prevent disease or restor

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

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

289 visually stratified participants enrolled in disease-modifying therapy trials.

290 aggregate treatment effects of comprehensive disease-modifying therapy versus conventional therapy on

291 stress compared with patients not receiving disease-modifying therapy, we prospectively obtained bra

292 Concomitant disease-modifying therapies were allowed.

293 en ageing and MS, the safety and efficacy of disease-modifying therapies, when discontinuation of tre

294 young adults that is primarily treated with disease-modifying therapies which target the immune and

295 The development of disease-modifying therapies will necessitate monitoring

296 alancing risks with the expected efficacy of disease-modifying therapies will still be key for treatm

297 erosis are complex given the large number of disease-modifying therapies with diverse safety and effi

298 ransporter 2 inhibitors, as well as specific disease-modifying therapies with transthyretin stabilize

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

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