ライフサイエンスコーパス: disease-modifying

1 hibitors, are palliative and not shown to be 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 eted polyphenols for potential beneficial AD disease-modifying activities.

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

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

7 g system that has therapeutic potential as a disease-modifying agent for the injured peripheral nervo

8 te the beneficial profile of fingolimod as a disease-modifying agent in the management of patients wi

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

10 Disease-modifying agents also reduce the skeletal morbid

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

12 Currently no effective disease-modifying agents exist for the treatment of Alzh

13 ious food constituents have been proposed as disease-modifying agents for Alzheimer's disease (AD), d

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

15 affords the opportunity to assess potential disease-modifying agents in clinical trials.

16 Treatments are generally divided into disease-modifying agents or interventions that improve h

17 idently, there is still a need for effective disease-modifying agents to improve patient outcomes.

18 particularly relevant in trials of potential disease-modifying agents, which typically involve partic

19 l be important in the discovery of potential disease-modifying agents.

20 ing clinical trials, especially of potential disease-modifying agents.

21 incorporated into clinical trials to assess disease-modifying agents.

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

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

24 data suggest that lovastatin is potentially disease modifying and could be a viable prophylactic tre

25 , but allergen-specific immunotherapy may be disease modifying and therefore warrants further explora

26 CFTR function; these therapies promise to be disease modifying and to improve the lives of people wit

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

28 itis and an inadequate response to synthetic disease modifying anti-rheumatic drugs (DMARDs) from 35

29 deficits, thereby emerging as an interesting disease-modifying anti-Alzheimer drug candidate.

30 us, (+)- and (-)-7e emerge as very promising disease-modifying anti-Alzheimer drug candidates.

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

32 e toxins and may also be considered as novel disease-modifying anti-Parkinsonian agents, which are mu

33 t aggressive immunosuppression with biologic disease-modifying anti-rheumatic drugs (DMARDs), such as

34 d not previously received treatment with any disease-modifying anti-rheumatic drugs, were enrolled fr

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

36 thout methotrexate (a conventional synthetic disease-modifying antirheumatic drug [DMARD]), versus in

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

38 =33,324) and patients initiating nonbiologic disease-modifying antirheumatic drugs (DMARDs) (n=25,742

39 Adherence to disease-modifying antirheumatic drugs (DMARDs) and predn

40 previously received treatment with biologic disease-modifying antirheumatic drugs (DMARDs).

41 serious infection compared with traditional disease-modifying antirheumatic drugs (DMARDs).

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

43 positivity or self-reported validated use of disease-modifying antirheumatic drugs (DMARDs).

44 not achieve adequate and safe responses with disease-modifying antirheumatic drugs (DMARDs).

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

46 methotrexate therapy to a triple regimen of disease-modifying antirheumatic drugs (methotrexate, sul

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

48 gs (NSAIDs), glucocorticoids and traditional disease-modifying antirheumatic drugs before and during

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

50 ozygous carriers of this variant needed more disease-modifying antirheumatic drugs, and more patients

51 ients with established RA who were naive for disease-modifying antirheumatic drugs, matched healthy c

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

53 ntional, biological, and newz non-biological disease-modifying antirheumatic drugs.

54 ared with 58.7% (43.3%-79.7%; P=0.0025) with disease-modifying antirheumatic drugs.

55 risk of serious infections compared to other disease-modifying antirheumatic drugs.

56 harmacological inhibition of Nogo-A may be a disease-modifying approach in ALS.

57 them with BMP mimetics may provide a novel, disease-modifying approach to PAH therapy.

58 ndard drug therapy or for those who prefer a disease-modifying approach.

59 a GluN2B-NMDAR antagonist does not provide a disease-modifying benefit and could cause cognitive liab

60 This manuscript describes the significant disease modifying benefits associated with daily dosing

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

62 Disease-modifying biological agents and other drug regim

63 , making it a viable therapeutic target with disease-modifying capacity for the treatment of this dis

64 Previous drug screens aiming to identify disease-modifying compounds for Parkinson's disease have

65 .55; 1.42, 1.10-1.84, respectively), whereas disease-modifying drug (DMD) exposure reduced this risk

66 on rheumatologic diseases, there is still no disease-modifying drug for primary Sjogren's syndrome (p

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

68 uired for double-blind trials of a potential disease-modifying drug in PD.

69 s are needed for accurate multiple sclerosis disease-modifying drug monitoring and decision making in

70 To date, there is no disease-modifying drug to slow the neuronal degeneration

71 e while a patient is receiving an injectable disease-modifying drug, many physicians advocate therapy

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

73 tive commonly used interferon beta (IFNbeta) disease modifying drugs: Avonex (x1 weekly), Betaseron (

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

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

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

77 domised controlled trials (RCTs) of proposed disease-modifying drugs have failed to show positive res

78 Disease-modifying drugs have mostly failed as treatments

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

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

81 opriate outcomes to be assessed in trials of disease-modifying drugs.

82 olonged period in the absence of any ongoing disease-modifying drugs.

83 in monitoring the effects of investigational disease-modifying drugs.

84 to exert not only a symptomatic but also, a disease-modifying effect against AD.

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

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

87 p acutely after trauma may have a beneficial disease-modifying effect in subjects with acute TBI.

88 ese compounds have failed to have a reliable disease-modifying effect in subsequent clinical trials.

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

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

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

92 rio of MF, there is no clear indication of a disease-modifying effect.

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

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

95 ly relevant time point after injury can have disease-modifying effects in epilepsy.

96 2X7 receptor has anticonvulsant and possibly disease-modifying effects in experimental epilepsy.

97 he diseased brain, providing symptomatic and disease-modifying effects in Parkinson's disease.

98 n humans may have implications for potential disease-modifying effects of BCHE-modulating agents in t

99 Huntington's disease, even in the absence of disease-modifying effects.

100 unlikely to provide both anticonvulsant and disease-modifying effects.

101 Bank still remains to identify causative and disease modifying factors for this devastating disease.

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

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

104 wild plant pathosystems to determine whether disease-modifying fungi are common enough to be ecologic

105 enced by altering the expression profiles of disease-modifying genes.

106 nerative disease multiple sclerosis (MS) use disease-modifying immunosuppressive compounds but do not

107 eful in tracking disease progression and for disease-modifying intervention trials.

108 s, and the complex is a potential target for disease-modifying intervention.

109 ation is important for effectively designing disease modifying interventions.

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

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

112 A potential disease-modifying management change was made in 113 pati

113 therapies have not targeted the fundamental disease-modifying mechanisms and result in only modest i

114 ultaneously modulate multiple independent AD disease-modifying mechanisms and, as such, may contribut

115 Riluzole remains the only available disease-modifying medication and confers a survival adva

116 New disease-modifying medications are needed to prevent and

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

118 immune system, therefore, not only bring new disease modifying modalities to inflammatory diseases, b

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

120 tor 2 (S1PR2) as a sex- and strain-specific, disease-modifying molecule that regulates BBB permeabili

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

122 al targets in chondrocytes may lead to novel disease-modifying OA therapies.

123 sease will be critical to the development of disease-modifying or even preventative therapies.

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

125 the most compelling targets for a potential disease-modifying Parkinson's disease therapy.

126 t of novel therapeutics, and target specific disease-modifying pathways intrinsic to the ventricle.

127 n and targeting of the intrinsic fundamental disease-modifying pathways that culminate in HF.

128 luating the potential of LRRK2 inhibitors as disease-modifying PD therapies.

129 diagnosis of probable AD may be too late for disease modifying pharmacotherapy.

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

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

132 s relying on symptomatic medications without disease-modifying potential.

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

134 and whether extraduplication factors have a disease-modifying role.

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

136 t responders, risk prediction, and design of disease-modifying strategies.

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

138 rapy might prove to be an integral part of a disease-modifying strategy for treating atopic diseases.

139 currently under investigation as a potential disease-modifying strategy in people with PD.

140 and post-traumatic OA, and point to a novel disease-modifying strategy to therapeutically target the

141 ory, prognostic stratification and multisite disease-modifying studies in ALS.

142 peutic potential of utrophin modulation as a disease modifying therapeutic strategy for all DMD patie

143 ations in clinical trials involving putative disease-modifying therapeutic agents for Alzheimer disea

144 , accounting for a potential symptomatic and disease-modifying therapeutic benefit in the treatment o

145 lial-mediated clearance mechanisms may drive disease-modifying therapeutic benefit with BACE1 inhibit

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

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

148 /C pathologies, enabling us to propose novel disease-modifying therapeutic strategies.

149 a beta-secretase, is an attractive potential disease-modifying therapeutic strategy for Alzheimer's d

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

151 ort microtubule stabilisation as a promising disease-modifying therapeutic strategy for tauopathies l

152 hat the CNP/NPR-C pathway has potential as a disease-modifying therapeutic target for cardiovascular

153 have been established as targets of proposed disease-modifying therapeutic treatments of AD.

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

155 tool but also may enable the development of disease modifying therapeutics for AD.

156 Furthermore, development of disease-modifying therapeutics for AD has been hampered

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

158 ficient and cost-effective group for testing disease-modifying therapeutics.

159 t early intervention with neuroprotective or disease-modifying therapeutics.

160 ded as a principal target for development of disease-modifying therapeutics.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

197 The development of disease-modifying therapies will necessitate monitoring

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

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

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

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

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

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

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

205 urodegenerative disorder and lacks effective disease-modifying therapies.

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

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

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

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

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

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

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

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

214 neurodegenerative disorder without effective disease-modifying therapies.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

244 Patients were analyzed independent of disease-modifying therapy.

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

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

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

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

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

250 Clinical trials of disease-modifying treatment are feasible in patients wit

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

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

253 No disease-modifying treatment exists for the fatal neurode

254 unotherapy is the only allergen-specific and disease-modifying treatment for allergy.

255 n the hope of providing a desperately needed disease-modifying treatment for ALS patients, as well as

256 The findings suggest a potential disease-modifying treatment for epilepsy based on target

257 15, as a neuroprotective and neuroreparative disease-modifying treatment for MS.

258 An effective disease-modifying treatment for progressive multiple scl

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

260 ions, and therefore they might be suited for disease-modifying treatment of infectious arthritis.

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

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

263 Patients on disease-modifying treatment show increased abundances of

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

265 Development of novel disease-modifying treatment strategies for neurological

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

267 also established weight loss as an effective disease-modifying treatment, and further clinical trials

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

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

270 We cover management settings, disease-modifying treatment, vitamin D, respiratory mana

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

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

273 Several innovative disease-modifying treatments (DMTs) for relapsing-remitt

274 ngolimod compared with those receiving other disease-modifying treatments (empirical Bayes geometric

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

276 isease, and there are currently no effective disease-modifying treatments available.

277 As disease-modifying treatments emerge, it is critical to a

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

279 a overproduction and may ultimately serve as disease-modifying treatments for AD.

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

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

282 Currently there are no effective disease-modifying treatments for HD, although antidepres

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

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

285 concern, especially with the advent of more disease-modifying treatments in MS that affect T-cell-me

286 Translation into disease-modifying treatments is challenging, particularl

287 The effectiveness of new disease-modifying treatments may depend on the timely in

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

289 evelopment of novel symptomatic or, ideally, disease-modifying treatments, and to assess these therap

290 larification of the pathogenesis, leading to disease-modifying treatments.

291 nowledge may ultimately translate into novel disease-modifying treatments.

292 nt dementia for which there are currently no disease-modifying treatments.

293 cellent prognostic tool in MDS in the era of disease-modifying treatments.

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

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

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

297 Despite extensive R&D efforts, there are no diseases modifying treatments for AD available.

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

299 oimaging measures such as caudate atrophy in disease-modifying trials, we propose their use as (1) in

300 nt guidelines on rapid efficacy readouts for disease-modifying trials.