ライフサイエンスコーパス: disease-modifying

1 No current therapy for AD is disease-modifying.

2 Our findings provide new insights into the disease-modifying action of 12/15-LO pharmacological inh

3 e of PD that would be required to evaluate a disease-modifying action.

4 provide substantial clinical benefit, their disease-modifying activity is limited, and rational comb

5 available drugs has shown clear evidence of disease-modifying activity, even if some patients treate

6 protective immunity and inform the design of disease-modifying adjunctive therapies and next-generati

7 unds show promise for further development as disease modifying agents for the potential treatment of

8 ight the potential of this model for testing disease-modifying agents and show that results obtained

9 Although there are potent disease-modifying agents for its initial relapsing-remit

10 ressant drugs reduced and multiple sclerosis disease-modifying agents increased the likelihood of rel

11 The development of disease-modifying agents may be facilitated by the relat

12 tain these new classes of MTDLs as potential disease-modifying agents.

13 lopment that could usher in a novel class of disease-modifying agents.

14 iminishes the power of clinical trials using disease-modifying agents.

15 ening these individuals for trials involving disease-modifying agents.

16 apeutic potential as innovative and targeted disease-modifying agents.

17 With the potential development of new disease-modifying Alzheimer's disease (AD) therapies, si

18 In this Review, we focus on disease-modifying and symptomatic therapies under develo

19 A comprehensive framework for both disease-modifying and symptomatic treatment trials in RB

20 e prospect of a novel, rapidly translatable, disease-modifying, and neuroprotective treatment for Fri

21 owed particular potential for development as disease-modifying anti-Alzheimer's drugs, based on their

22 pression profiles were also determined after disease-modifying anti-rheumatic drug (DMARD) treatment

23 e needed for predicting the effectiveness of disease modifying antirheumatic drugs (DMARDs).

24 ed by a physician or by self-reported use of disease modifying antirheumatic drugs, were compared wit

25 ated permuted blocks; stratified by baseline disease-modifying antirheumatic drug use and C-reactive

26 le of protein citrullination, and serum from disease-modifying antirheumatic drug-naive early arthrit

27 , including 36 who were receiving biological disease-modifying antirheumatic drugs (bDMARDs).

28 ith stable background conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) in pati

29 rheumatoid arthritis refractory to biologic disease-modifying antirheumatic drugs (DMARDs) are uncle

30 premilast, at least 3 months of non-biologic disease-modifying antirheumatic drugs (DMARDs), or at le

31 rticipants to continue using any concomitant disease-modifying antirheumatic drugs (DMARDs).

32 nadequate response to conventional synthetic disease-modifying antirheumatic drugs (DMARDs).

33 id in combination with bDMARDs and synthetic disease-modifying antirheumatic drugs (sDMARDs) had the

34 eatment, and expanded therapeutic options of disease-modifying antirheumatic drugs have markedly impr

35 Biological, disease-modifying antirheumatic drugs were prescribed mo

36 paring the efficacy and safety of biological disease-modifying antirheumatic drugs within the same cl

37 a, were previously untreated with biological disease-modifying antirheumatic drugs, and had inadequat

38 med by physicians or by self-reported use of disease-modifying antirheumatic drugs, were compared wit

39 cterized clinical cohort of newly diagnosed, disease-modifying antirheumatic drugs-naive rheumatoid a

40 uccessful immunotherapy that may guide other disease-modifying approaches for type 1 diabetes.

41 The disease-modifying aspects of DBS at a cellular level are

42 Targeting ChRM3 may have disease-modifying benefits in childhood asthma.

43 n after device removal, suggesting potential disease-modifying benefits.

44 erived cells are therapeutic candidates with disease-modifying bioactivity, but their variable potenc

45 titative gait measures as outcomes in future disease-modifying clinical trials.

46 .55; 1.42, 1.10-1.84, respectively), whereas disease-modifying drug (DMD) exposure reduced this risk

47 application of an expanding armamentarium of disease-modifying drug and device therapies.

48 ions are yet to be developed, many promising disease-modifying drug candidates are currently under in

49 iscovery and limiting the likelihood of true disease-modifying drug candidates.

50 ar disintegrity, implying its potential as a disease-modifying drug for SSc.

51 ed to the continuous identification of novel disease-modifying drug targets and an increased apprecia

52 L may a useful measure to monitor effects in disease-modifying drug trials.

53 GBA or LRRK2 modifiers) and other potential disease modifying drugs provide cautious optimism that m

54 oduce different cytokines, and respond to MS disease modifying drugs.

55 mmon degenerative joint disease for which no disease-modifying drugs are currently available.

56 ive overview of the currently most promising disease-modifying drugs as well as potential drug delive

57 ng and to select patients for treatment when disease-modifying drugs become available.

58 Despite the wide prevalence, no FDA-approved disease-modifying drugs exist.

59 Because of the lack of significant disease-modifying drugs for neurodegenerative disorders,

60 ng candidates for the design of multi-target disease-modifying drugs for treatment of AD and/or simil

61 The analyses in patients treated with disease-modifying drugs identified the phosphorylation o

62 There is a need for disease-modifying drugs that can eradicate clonal hemato

63 ther restricted the development of targeted, disease-modifying drugs to help patients avoid long-term

64 ting the efficacy of multiple sclerosis (MS) disease-modifying drugs) at a genome-wide scale.

65 With the availability of a variety of novel disease-modifying drugs, gene addition and gene editing

66 ultiple sclerosis (MS) patients treated with disease-modifying drugs.

67 Thus, there is an unmet need for disease-modifying drugs.

68 Determining whether levodopa also has a disease-modifying effect could provide guidance as to wh

69 Defining a disease-modifying effect could radically change the way

70 An additional, disease-modifying effect has been suspected from studies

71 This disease-modifying effect is both antigen-specific and an

72 e normalized to control levels, indicating a disease-modifying effect of acidified water.

73 New evidence was published for the disease-modifying effect of allergen immunotherapy in te

74 ata support the putative neuroprotective and disease-modifying effect of STN-DBS in a mechanistically

75 related interstitial lung disease, elicits a disease-modifying effect on SSc vasculopathy, such as fo

76 evodopa in combination with carbidopa had no disease-modifying effect.

77 ion, suggesting a potential miR-23a-specific disease-modifying effect.

78 ence at week 80 implies that levodopa had no disease-modifying effect.

79 AIT reduces symptoms, but has also a disease-modifying effect.

80 ired to demonstrate that a ligand can have a disease-modifying effect.

81 drug delivery platform like this can elicit disease modifying effects as well as facilitate long-ter

82 on of dopaminergic therapies does not convey disease-modifying effects but does reduce disability.

83 These therapies are hypothesised to have disease-modifying effects by reducing the concentration

84 2X7 receptor has anticonvulsant and possibly disease-modifying effects in experimental epilepsy.

85 These results indicate disease-modifying effects of 4-AP beyond symptomatic the

86 e pathophysiology, course, and potential for disease-modifying effects of treatment.

87 neffective in one-third of patients and lack disease-modifying effects.

88 ffers an ideal system to monitor the role of disease-modifying factors over a long time.

89 ative relationships between the abundance of disease-modifying foliar fungi and disease severity in w

90 t strategy to upregulate the expression of a disease-modifying gene associated with congenital muscul

91 strates that in vivo AtN conversion may be a disease-modifying gene therapy to treat HD and other neu

92 ch has a broad applicability to a variety of disease-modifying genes and could serve as a therapeutic

93 To uncover stress-responsive disease-modifying genes, here we have carried out renal

94 presents a unique opportunity to learn about disease-modifying host factors from pediatric population

95 lingual immunotherapy (SCIT/SLIT)], the only disease-modifying intervention for allergic rhinitis (AR

96 esting that immunotherapies may be promising disease-modifying interventions against Alzheimer's dise

97 which patients may still respond to putative disease-modifying interventions.

98 essential for adequately powering trials of disease-modifying interventions.

99 cardiomyocytes from human infants with heart disease, modifying LMNB2 expression correspondingly alte

100 Multiple disease-modifying medications with regulatory approval t

101 The availability of multiple disease-modifying medications with regulatory approval t

102 for future simultaneous testing of multiple disease-modifying medicines in neurological medicine.

103 rgeting these dysfunction may offer a unique disease modifying method of therapeutic intervention in

104 ecent discoveries have identified underlying disease-modifying molecular aberrations contributing to

105 However, disease-modifying, neuroprotective treatments for glauco

106 he medial meniscus (DMM) used for evaluating disease-modifying OA targets are frequently performed on

107 (Q111/+) mice are a useful tool for modeling disease-modifying or neuroprotective strategies for dise

108 pharmacogenomics comes the hope for better, disease-modifying, or even curative, pharmacological and

109 Sprifermin is under investigation as a disease-modifying osteoarthritis drug.

110 treatment may merit further evaluation as a disease-modifying osteoarthritis drug.

111 itochondria are of interest for developing a disease-modifying PD therapeutic.

112 No disease-modifying pharmacologic treatments are available

113 estimated treatment effects of comprehensive disease-modifying pharmacological therapy (ARNI, beta bl

114 ate treatment effects of early comprehensive disease-modifying pharmacological therapy are substantia

115 Treatment with comprehensive disease-modifying pharmacological therapy was estimated

116 We previously investigated the disease-modifying potential of a microtubule-stabilising

117 kB signaling in the symptomatic efficacy and disease-modifying potential of STN DBS.

118 ibition of HbS polymerization and indicate a disease-modifying potential.

119 s that reduce network hyperexcitability have disease-modifying properties.

120 brain's major resident immune cells, provide disease-modifying regulation of the other major glial po

121 ese diseases and consider their potential as disease-modifying strategies in the era of precision med

122 iateness of current animal-models to develop disease-modifying strategies that can be translated to h

123 el for the assessment of neuroprotective and disease-modifying strategies.

124 restore its function as a novel and unifying disease-modifying strategy against these diseases.

125 ve and behavioral defects may be a promising disease-modifying strategy for FXS and other brain disor

126 ether these observations establish EYA3 as a disease-modifying target whose function in the pathophys

127 way are well-known, we hypothesized that new disease-modifying targets of SHH-MB might be identified

128 Gene therapy plays an important role in disease modifying therapeutic strategies.

129 larified aspects of disease management and a disease-modifying therapeutic drug is now available for

130 Cibinetide thus holds promise as novel disease-modifying therapeutic of inflammatory bowel dise

131 substantiated proof of effectiveness of this disease-modifying therapeutic option.

132 regulatory cells as targets for potentially disease-modifying therapeutic strategies is discussed.

133 Hence, inhibition of GCS represents a disease-modifying therapeutic strategy for GBA-related s

134 approach, as applied to SNCA, is a promising disease-modifying therapeutic strategy for PD and other

135 aminergic neurons and its possibility as the disease-modifying therapeutic target against PD have not

136 d modulation of GTPase activity as promising disease-modifying therapeutic targets.

137 fore substantial interneuron loss could be a disease-modifying therapeutic.

138 o AD drug development, the lack of effective disease-modifying therapeutics and the complexity of the

139 help guide the discovery and development of disease-modifying therapeutics for neurodegenerative dis

140 (s) is an urgent need for the development of disease-modifying therapeutics.

141 ed drug discovery towards the development of disease-modifying therapeutics.

142 ikely catalyze additional efforts to develop disease-modifying therapeutics.

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

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

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

146 eurodegenerative condition with no effective disease modifying therapies.

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

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

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

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

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

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

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

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

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

156 No disease-modifying therapies currently exist, and diagnos

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

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

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

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

161 There are no disease-modifying therapies for HD.

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

163 Identifying effective disease-modifying therapies for neurological diseases re

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

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

166 Current disease-modifying therapies for SSc predominantly target

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

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

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

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

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

172 Although disease-modifying therapies have been efficacious for re

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

174 Disease-modifying therapies in clinical development may

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

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

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

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

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

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

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

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

183 Concomitant disease-modifying therapies were allowed.

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

185 The development of disease-modifying therapies will necessitate monitoring

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

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

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

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

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

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

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

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

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

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

196 There are no disease-modifying therapies.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

230 0001, adjusted for proportion of time on any disease-modifying therapy) across the 6-10 year follow-u

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

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

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

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

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

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

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

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

239 tablished AD endophenotypes in a therapeutic disease-modifying time window after symptom onset.

240 d functional interference with RGMa may be a disease modifying treatment option.SIGNIFICANCE STATEMEN

241 ine in cognitive functions with no validated disease modifying treatment.

242 sNfL levels were lower under disease-modifying treatment (beta = 0.818, p = 0.003).

243 ogressive multiple sclerosis who were not on disease-modifying treatment and who had an Expanded Disa

244 Allergen immunotherapy is currently the only disease-modifying treatment available for allergic rhini

245 degenerative disorder with no symptomatic or disease-modifying treatment available.

246 For disease-modifying treatment clinical trials, the recomme

247 Despite this, no disease-modifying treatment currently exists, and numero

248 Licensed disease-modifying treatment focuses on amelioration of c

249 throughout life, providing a path towards a disease-modifying treatment for a syndromic neurodevelop

250 LS4326 support its clinical development as a disease-modifying treatment for ADPKD.

251 BACE1 inhibitors hold potential as agents in disease-modifying treatment for Alzheimer's disease.

252 n may confer broad therapeutic benefits as a disease-modifying treatment for atopic dermatitis and it

253 15, as a neuroprotective and neuroreparative disease-modifying treatment for MS.

254 There currently is no disease-modifying treatment for Wolfram syndrome, as the

255 clinical development of LRRK2 inhibitors as disease-modifying treatment in PD biomarkers for kinase

256 spread of tau, providing a novel target for disease-modifying treatment of AD and other tauopathies.

257 significant benefit of BChE inhibition for a disease-modifying treatment of AD.

258 ials evaluating LRRK2 kinase inhibition as a disease-modifying treatment principle in PD.

259 sease progression and evaluating preclinical disease-modifying treatment response.

260 Patients on disease-modifying treatment show increased abundances of

261 butes to cognitive impairment, but effective disease-modifying treatment strategies are missing.

262 Allergen-specific immunotherapy is a disease-modifying treatment that induces long-term T-cel

263 inically isolated syndrome) with and without disease-modifying treatment were compared to 35 healthy

264 revious multiple sclerosis diagnosis, use of disease-modifying treatment, and use of corticosteroids

265 hat allergen immunotherapy (AIT) is the only disease-modifying treatment, including prevention of the

266 monitoring of cysteamine, the only available disease-modifying treatment, is recommended.

267 or other treatment and who are not receiving disease-modifying treatment.

268 e failed, and there is currently no approved disease-modifying treatment.

269 s may be an effective symptomatic, but not a disease-modifying, treatment for AD related to apoE4, wh

270 The association between disease-modifying treatments (DMTs), and this conversion

271 eurodegenerative process, and no significant disease-modifying treatments are approved.

272 Currently, no disease-modifying treatments are available for these dis

273 Disease-modifying treatments are in development for Hunt

274 Despite this progress, no disease-modifying treatments exist for AD, an issue that

275 Despite this, no disease-modifying treatments exist with clear clinical b

276 There are no disease-modifying treatments for adult human neurodegene

277 compounds therefore represent potential new disease-modifying treatments for dementia.

278 INTRODUCTION: Among disease-modifying treatments for multiple sclerosis, nat

279 rogression are the cornerstone of developing disease-modifying treatments for neurodegenerative disea

280 In the course of developing disease-modifying treatments for neurodegenerative disor

281 or neurodegenerative disorders, there are no disease-modifying treatments for Parkinson's disease.

282 complications is needed in order to develop disease-modifying treatments for patients.

283 ion is an ideal study population for testing disease-modifying treatments for synucleinopathies, sinc

284 There are no disease-modifying treatments for this disease that affec

285 The majority of putative disease-modifying treatments in development for Alzheime

286 ented strategies may be useful for effective disease-modifying treatments in PSP.

287 ible therapeutic approach for developing new disease-modifying treatments of Parkinson's disease and

288 imer's disease in the United States, with no disease-modifying treatments to prevent or treat cogniti

289 re research will need to establish effective disease-modifying treatments, address whether patients'

290 ed in clinical trials of neuroprotective and disease-modifying treatments, improving trial design by

291 t on long-term disability with first-line MS disease-modifying treatments, which is clinically meanin

292 erative amyloidoses might help in developing disease-modifying treatments.

293 d by nucleotide expansions, and most have no disease-modifying treatments.

294 ypic severity and efficacy assessment of new disease-modifying treatments.

295 atest public health challenges, as many lack disease-modifying treatments.

296 ase duration, disease course, disability, or disease-modifying treatments.

297 inform future investigations into potential disease-modifying treatments.

298 lity, which could be of potential benefit in disease-modifying trials seeking a measurable response t

299 Sample size estimates for disease-modifying trials were calculated using a time-to

300 considered in evaluating outcomes in future disease-modifying trials, and support the search for pro