ライフサイエンスコーパス: levodopa

1 ed with PD patients with stable responses to levodopa.

2 onia and a dramatic long-lasting response to levodopa.

3 son's disease who have motor fluctuations on levodopa.

4 ly, differences in the long-term response to levodopa.

5 o alleviated dyskinetic behaviors induced by levodopa.

6 ed-release, capsule formulation of carbidopa-levodopa.

7 1) compared with immediate-release carbidopa-levodopa.

8 etrahydropyridine (MPTP) and dyskinetic with levodopa.

9 e abnormalities with STN stimulation but not levodopa.

10 patients were on or off the dopamine prodrug levodopa.

11 ration compared with that achieved with oral levodopa.

12 awal of levodopa and after administration of levodopa.

13 aphy twice, after taking and withdrawal from levodopa.

14 ase as well as in the therapeutic effects of levodopa.

15 ate have had a pregraft history of long-term levodopa.

16 ure for 9 weeks prior to introducing chronic levodopa.

17 or function compared to dopamine agonists or levodopa.

18 ear to affect the antiparkinsonian action of levodopa.

19 ral self-paced joystick movements ON and OFF levodopa.

20 ion of cotemporaneous bursts were reduced by levodopa.

21 ts of citalopram were stronger than those of levodopa.

22 ope in patients with Parkinson's disease OFF levodopa (-0.20 degrees /cycle, P = 0.002).

23 el imaging techniques (6-[fluoride-18]fluoro-levodopa [(18)F-DOPA] PET-CT and glucagon-like peptide 1

24 e conversion with extended-release carbidopa-levodopa, 23 (5%) of 450 patients withdrew because of ad

25 er) was determined on dyskinesias induced by levodopa (5 mg/kg twice daily by oral gavage) in 1-methy

26 We found that levodopa-a synthetic precursor of dopamine-increases res

27 ct changes in striatal dopamine levels after levodopa administration and relate these to motor respon

28 ydroxydopamine lesioned model of PD, chronic levodopa administration induced characteristic dyskinesi

29 patients, and PIGD patients before and after levodopa administration.

30 tergic transmission in motor areas following levodopa administration.

31 he exhibition of involuntary movements after levodopa administration.

32 at model to examine whether pregraft chronic levodopa affected graft efficacy and/or graft-induced dy

33 may combine to explain the addictive use of levodopa after loss of midbrain dopamine neurons in some

34 2% (SD 14.91) for extended-release carbidopa-levodopa and 29.79% (15.81) for immediate-release carbid

35 tly seated following overnight withdrawal of levodopa and after administration of levodopa.

36 This patient received levodopa and benserazide (200 and 50 mg, respectively) f

37 ddress gait disorders that respond poorly to levodopa and conventional DBS targets.

38 Strong evidence supports using levodopa and dopamine agonists for motor symptoms at all

39 se and motor fluctuations who were receiving levodopa and other antiparkinsonian drugs.

40 Levodopa and other dopaminergic treatments have not had

41 siology via aberrant processing of exogenous levodopa and release of dopamine as false neurotransmitt

42 combined accumulation of dopamine precursor levodopa and serotonin precursor 5-hydroxytryptophan.

43 to a number of factors including the dose of levodopa and the duration of its use.

44 tinal pigment epithelial (RPE) cells produce levodopa and their transplantation into the striatum mig

45 years; 11 females) received a single dose of levodopa and then performed a task in which they had to

46 al lesions were then challenged with l-dopa (levodopa) and various dopamine receptor agonists, and re

47 monotherapy, (2) acute coadministration with levodopa, and (3) chronic coadministration for 1 month.

48 tients treated with dopamine agonists and/or levodopa, and age- and education- matched neurologically

49 tment of Parkinson's disease, as adjuncts in levodopa based therapy, or for the treatment of schizoph

50 Grafted monkeys were also challenged with levodopa but did not show any greater responses to these

51 rolled, crossover study in 21 PD patients on levodopa but no agonists, we acquired pulsed arterial sp

52 te), and had symptoms that responded to oral levodopa but were insufficiently controlled by optimised

53 response of CaMKIIalpha-D2R interactions to levodopa can alleviate levodopa-induced dyskinesia.

54 patients allocated to immediate-release oral levodopa-carbidopa (difference -1.91 h [95% CI -3.05 to

55 ents allocated to the immediate-release oral levodopa-carbidopa group (seven [21%] serious), mainly a

56 We aimed to assess efficacy and safety of levodopa-carbidopa intestinal gel delivered continuously

57 h (SE 0.65) for 35 patients allocated to the levodopa-carbidopa intestinal gel group compared with a

58 ses 35 (95%) of 37 patients allocated to the levodopa-carbidopa intestinal gel group had adverse even

59 dopa plus placebo intestinal gel infusion or levodopa-carbidopa intestinal gel infusion plus oral pla

60 :1) to treatment with immediate-release oral levodopa-carbidopa plus placebo intestinal gel infusion

61 Continuous delivery of levodopa-carbidopa with an intestinal gel offers a promi

62 Most patients benefit dramatically from levodopa/carbidopa, often with further improvement with

63 rary to the model predictions, we found that levodopa caused an increase in the force exerted only in

64 of parkinsonism that is poorly responsive to levodopa, cerebellar ataxia and corticospinal dysfunctio

65 Following levodopa challenge, 5 mg eltoprazine caused a significan

66 an 30, which improved by 33% or more after a levodopa challenge.

67 y and efficacy of opicapone as an adjunct to levodopa compared with placebo or entacapone in patients

68 ort cue trials and when co-administered with levodopa, counteracted levodopa-induced deficits.

69 ysicians to individually tailor the existing levodopa daily regimen, by potentially reducing the tota

70 t demonstration of the benefit of continuous levodopa delivery in a double-blind controlled study.

71 mprovement in motor ratings during infusion, levodopa did not alter learning performance or network a

72 tle in the past decade and include carbidopa/levodopa, dopamine agonists, and monoamine oxidase type

73 use, including both dopamine agonist use and levodopa dosage.

74 ks of open-label immediate-release carbidopa-levodopa dose adjustment followed by 6 weeks of open-lab

75 eks of open-label extended-release carbidopa-levodopa dose conversion.

76 men, by potentially reducing the total daily levodopa dose, increasing the dosing interval, and ultim

77 , the expression of which is correlated with levodopa dose, many of which are under the control of ac

78 Identical levodopa doses induced markedly higher striatal synaptic

79 its including decreased off-time and reduced levodopa dosing frequency.

80 fluctuations may be managed by modifying the levodopa dosing regimen or by adding several other medic

81 In the 'OFF' state withdrawn from levodopa, dyskinetic and non-dyskinetic patients had sim

82 (UPDRS item 4) (1.94 [1.33-2.82]), a higher levodopa equivalent daily dose (1.63 [1.09-2.43]), and m

83 , education, disease duration, language, and levodopa equivalent daily dose.

84 ied Parkinson's Disease Rating Scale scores, levodopa equivalent dose, and global Pittsburgh Sleep Qu

85 he independent variable, with adjustment for levodopa equivalent dose, sex, age, disease duration, MD

86 n, UPDRS III scores off and on medication or levodopa equivalent doses between the two techniques.

87 isease, rates of pre-existing depression and Levodopa equivalent doses of anti-Parkinson's medication

88 se duration and severity and daily intake of levodopa equivalent units.

89 However, almost all patients receiving levodopa eventually develop debilitating involuntary mov

90 agonist buspirone prior to levodopa reduced levodopa-evoked striatal synaptic dopamine increases and

91 dyskinesias received 200mg fast-acting oral levodopa following prolonged withdrawal from their norma

92 opa, one group of parkinsonian rats received levodopa for 4 weeks prior to grafting.

93 Levodopa further impaired performance on short cue durat

94 g-term treatment with the dopamine precursor levodopa gradually induces involuntary "dyskinesia" move

95 mization by an average of 5.2 letters in the levodopa group and by 3.8 letters in the placebo group (

96 and only 12% in the Parkinson's disease OFF levodopa group.

97 Although levodopa had no effect in controls, it acquired 2 promin

98 For several decades, the dopamine precursor levodopa has been the primary therapy for Parkinson's di

99 Dopaminergic therapies such as levodopa have provided benefit for millions of patients

100 ase (PD), and the subsequent introduction of levodopa have revolutionalized the field of PD therapeut

101 ical gamma reactivity should occur following levodopa if the latter restores a more physiological pat

102 Levodopa improved consistent micrographia accompanied by

103 Levodopa improves consistent micrographia by restoring t

104 rmulation versus immediate-release carbidopa-levodopa in patients with Parkinson's disease and motor

105 and efficacy of tozadenant as an adjunct to levodopa in patients with Parkinson's disease who have m

106 ntrolled trial of opicapone as an adjunct to levodopa in patients with Parkinson's disease with end-o

107 upport safinamide as an effective adjunct to levodopa in patients with PD and motor fluctuations to i

108 is sensitive to long-term administration of levodopa in PD rats.

109 , nor interactions between movement type and levodopa in the STN, nor in the coherence between STN an

110 iological interaction analysis revealed that levodopa increased effective connectivity between the po

111 tion of dopaminergic input by treatment with levodopa increased the damping of oscillatory activity (

112 low level of dopamine sufficient to cause a levodopa-independent continuous form of diphasic dyskine

113 In parallel, levodopa induced an increase in CaMKIIalpha-D2R interact

114 anxiety, obsessive-compulsive disorders, and levodopa induced dyskinesia in Parkinson's disease.

115 thological feature, possibly associated with levodopa induced dyskinesias, or is primarily physiologi

116 sioned 6-hydroxydopamine rats that developed levodopa-induced abnormal involuntary movements (AIMs) a

117 co-administered with levodopa, counteracted levodopa-induced deficits.

118 This novel, levodopa-induced difference in the neural responses betw

119 logy, few neuroimaging studies have examined levodopa-induced differences in neural activation betwee

120 Levodopa-induced dyskinesia (LID) develops after repeate

121 Medical treatment of levodopa-induced dyskinesia (LID) in Parkinson disease (

122 Levodopa-induced dyskinesia (LID) is a persistent behavi

123 Effective medical management of levodopa-induced dyskinesia (LID) remains an unmet need

124 Here we show that levodopa-induced dyskinesia in hemiparkinsonian rats is

125 sion of the prevailing hypothesis that links levodopa-induced dyskinesia to an altered sensitivity to

126 ed not only with motor side-effects, such as levodopa-induced dyskinesia, but also behavioural side-e

127 a-D2R interactions to levodopa can alleviate levodopa-induced dyskinesia.

128 neurons and reverses aberrant plasticity in levodopa-induced dyskinesia.

129 Levodopa-induced dyskinesias (LIDs) are the most common

130 ale scores in those Parkinson's disease with levodopa-induced dyskinesias (n = 12), correlated with l

131 Levodopa-induced dyskinesias are a common complication o

132 Although levodopa-induced dyskinesias could be elicited postopera

133 have been associated with the development of levodopa-induced dyskinesias in animal models of Parkins

134 rtical connectivity as a neural signature of levodopa-induced dyskinesias in humans.

135 Nicotine pretreatment reduced peak and total levodopa-induced dyskinesias in levodopa-naive monkeys o

136 eural mechanisms underlying the emergence of levodopa-induced dyskinesias in vivo are still poorly un

137 Levodopa-induced dyskinesias occur in up to 80% of patie

138 ighly effective at preventing development of levodopa-induced dyskinesias, and GID-like behaviors occ

139 n revealed that patients who later developed levodopa-induced dyskinesias, but not patients without d

140 n patients with Parkinson's disease who have levodopa-induced dyskinesias, has been extended to the t

141 on in parkinsonian patients with and without levodopa-induced dyskinesias.

142 icated in the development and maintenance of levodopa-induced dyskinesias.

143 determine whether nicotine treatment reduced levodopa-induced dyskinesias.

144 ia connectivity that herald the emergence of levodopa-induced dyskinesias.

145 namic causal modelling was applied to assess levodopa-induced modulation of effective connectivity be

146 ividual dyskinesia severity was predicted by levodopa-induced modulation of striato-cortical feedback

147 otor disability, activities of daily living, levodopa-induced motor complications (as assessed with t

148 .001), activities of daily living (P<0.001), levodopa-induced motor complications (P<0.001), and time

149 advanced Parkinson's disease who have severe levodopa-induced motor complications.

150 licits involuntary movements, referred to as levodopa-induced peak-of-dose dyskinesias.

151 ep brain stimulation (n = 14) or intravenous levodopa infusion (n = 14).

152 e studied the subjects during an intravenous levodopa infusion titrated to achieve a motor response e

153 was conducted before and during intravenous levodopa infusion; the pace and extent of movement was c

154 n the putamen and primary motor cortex after levodopa intake during movement suppression.

155 on-making tasks, following either placebo or levodopa intake in a double blind within-subject protoco

156 The scan was continued for 45 minutes after levodopa intake or until dyskinesias emerged.

157 ), placebo, or entacapone (200 mg with every levodopa intake) for 14-15 weeks.

158 After levodopa intake, the PIGD patients had significantly inc

159 Immediately before and after levodopa intake, we performed fMRI, while patients produ

160 ty emerged during the first 20 minutes after levodopa intake.

161 ew extended release formulation of carbidopa/levodopa (IPX066), safinamide which inhibits MAO-B, dopa

162 role allows levodopa to be delayed, but once levodopa is added to the drug regimen the usual course o

163 replacement prior to introduction of chronic levodopa is highly effective at preventing development o

164 ost important limiting factor for the use of levodopa is the emergence of motor complications.

165 Levodopa is the most effective medical treatment for Par

166 Although levodopa is the most effective medication available for

167 Levodopa is the most effective therapy for Parkinson's d

168 Levodopa is the most potent of the dopaminergic drugs.

169 inson's disease using the dopamine precursor levodopa is unfortunately limited by gradual development

170 The optimization of levodopa is, in most cases, the most powerful therapeuti

171 out causing dyskinesia and, as an adjunct to levodopa, it improves motor function without worsening d

172 By boosting dopamine levels using levodopa (l-DOPA) as human subjects made economic decisi

173 ced dyskinesia (LID) develops after repeated levodopa (l-DOPA) exposure in Parkinson disease patients

174 l sensitization that develops after repeated levodopa (l-DOPA) exposure in Parkinson disease patients

175 A clinical trial of levodopa (L-DOPA) in AS is ongoing, although the underly

176 The dopamine precursor levodopa (L-DOPA) increased the task-based learning rate

177 Levodopa (L-DOPA) is widely used for symptomatic managem

178 reversals would occur on haloperidol than on levodopa (l-DOPA) or placebo.

179 Restoration of dopamine transmission by levodopa (L-DOPA) relieves motor symptoms of PD but ofte

180 Dopamine replacement with levodopa (L-DOPA) represents the mainstay of Parkinson's

181 Levodopa (L-dopa) therapy in PD patients has been shown

182 ent of PD involves chronic administration of Levodopa (l-DOPA) which is a pro-oxidant and may disrupt

183 certain catecholamines viz., dopamine (DA), levodopa (l-Dopa), epinephrine (EP) and norepinephrine (

184 armacological dopamine (DA) replacement with Levodopa [L-dihydroxyphenylalanine (L-DOPA)] is the gold

185 iO(2) nanoparticles for the determination of levodopa (LD) and carbidopa (CD) was described.

186 d the metabolic and neurovascular effects of levodopa (LD) therapy for Parkinson's disease (PD).

187 The dopamine precursor levodopa led to a dose-dependent (inverted U-shape) pers

188 Plasma levodopa levels were determined with and without nalbuph

189 nti-PD effect of levodopa or changing plasma levodopa levels.

190 Treatment with levodopa limited this evolution leading to a relative in

191 double-blind with extended-release carbidopa-levodopa (mean 3.6 doses per day [SD 0.7]) had greater r

192 ouble-blind with immediate-release carbidopa-levodopa (mean 5.0 doses per day [1.2]).

193 .79% (15.81) for immediate-release carbidopa-levodopa (mean difference -5.97, 95% CI -9.05 to -2.89;

194 hioneine, and significantly higher levels of levodopa metabolites and biliverdin than those of normal

195 Extended-release carbidopa-levodopa might be a useful treatment for patients with P

196 A second levodopa-naive group was grafted, and the grafts were al

197 ak and total levodopa-induced dyskinesias in levodopa-naive monkeys over an 8-week period, with a dec

198 tients allocated immediate-release carbidopa-levodopa), nausea (six [3%] vs three [2%]), and falls (s

199 The present study evaluated the effects of levodopa, nicotine and the nicotinic acetylcholine recep

200 ormance was assessed after administration of levodopa, nicotine ditartrate, or SIB-1553A and after ad

201 nesia that persists even after withdrawal of levodopa (off-medication dyskinesia).

202 The effects of levodopa on both local and distant synchronization at 60

203 with PD and suggest that negative effects of levodopa on cognition may be amenable to correction with

204 ibitor citalopram and the dopamine precursor levodopa on decisions to inflict pain on oneself and oth

205 finger movements and of the dopamine prodrug levodopa on induced power in the contralateral primary m

206 To investigate the effect of pregraft levodopa, one group of parkinsonian rats received levodo

207 ) without compromising the anti-PD effect of levodopa or changing plasma levodopa levels.

208 Sixteen weeks of oral levodopa or placebo administered 3 times daily while pat

209 rmeability, following separate injections of levodopa or saline.

210 has been associated with greater dosages of levodopa or short-acting DAs.

211 amic nucleus stimulation (p < 0.005) but not levodopa (p = 0.25).

212 asts for a few days, which is not related to levodopa pharmacokinetics.

213 Their pharmacotherapy included oral levodopa plus benserazide or carbidopa in a regimen that

214 ended-release or immediate-release carbidopa-levodopa plus matched placebos.

215 striato-cortical connectivity in response to levodopa produces an aberrant reinforcement signal produ

216 The implantation of such levodopa-producing cells can concurrently decrease the e

217 k activity by striatal implantation of human levodopa-producing retinal pigment epithelial (hRPE) cel

218 by early disease onset, moderate response to levodopa, rapid progression leading to loss of autonomy

219 Extended-release carbidopa-levodopa reduced daily off-time by, on average, an extra

220 arm aversion for both self and others, while levodopa reduced hyperaltruism.

221 receptor type 1A agonist buspirone prior to levodopa reduced levodopa-evoked striatal synaptic dopam

222 lly, administration of the dopamine prodrug, levodopa, reduced the frequency and duration of periods

223 talopram enhancing behavioral inhibition and levodopa reducing slowing related to being responsible f

224 s reflected in the long-duration response to levodopa, reinterpreted here as the correction of aberra

225 c therapy, and strategies to delay and treat levodopa-related motor complications and nonmotor Parkin

226 ne agonists) may be initiated first to avoid levodopa-related motor complications.

227 Although levodopa remains the most effective oral pharmacotherapy

228 subjects and trials (p = 0.01), although the levodopa response was not significant.

229 D who may have PD on the basis of a positive levodopa response, clinical progression, imaging and/or

230 se were reviewed to determine the pattern of levodopa response.

231 These include fluctuating levodopa responses and involuntary movements and posture

232 cant dissociation of vasomotor and metabolic levodopa responses was seen in the striatum/globus palli

233 tase deficiency (SRD) is an under-recognized levodopa-responsive disorder.

234 ated families who presented with adult-onset levodopa-responsive dystonia-parkinsonism, pyramidal sig

235 nsideration of SRD not only in patients with levodopa-responsive motor disorders, but also in patient

236 atients aged 30-75 years who had progressive levodopa-responsive Parkinson's disease and an overnight

237 In variants of PSP presenting with levodopa-responsive Parkinsonism, as well as pure akines

238 eatures of the disease: an age-dependent and levodopa-responsive slowness of movement associated with

239 A 55-year-old levodopa-responsive woman with PD received bilateral put

240 rogression, early postural instability, poor levodopa responsiveness and symmetric involvement) were

241 It is well established that long-term levodopa results in a plethora of long-lasting neurochem

242 ence of benefits for galantamine, modafinil, levodopa, rotigotine, clozapine, duloxetine, clonazepam,

243 Thus, increasing dopamine levels with levodopa selectively boosted striatal and substantia nig

244 in parkinsonian rats, preexposure to chronic levodopa significantly reduces behavioral and neurochemi

245 -like behaviors occur regardless of pregraft levodopa status.

246 altered motor behaviors in response to acute levodopa tests, including different types of abnormal in

247 While levodopa therapy alleviates basal ganglia dysfunction in

248 ings reported in patients with PD undergoing levodopa therapy and other symptomatic interventions.

249 While levodopa therapy for Parkinson's disease (PD) may effect

250 tion resembles the long-duration response to levodopa therapy in its slow buildup of improvement afte

251 d-of-dose motor fluctuations associated with levodopa therapy in patients with Parkinson disease (PD)

252 picapone compared with placebo as adjunct to levodopa therapy in patients with PD experiencing end-of

253 rs4680 polymorphism modulated the effect of levodopa therapy on planning-related activations in the

254 The motor complications associated with levodopa therapy, namely, fluctuations in motor response

255 disadvantages of delaying the initiation of levodopa therapy, the role of dopamine agonists, particu

256 parkinsonian features, and do not respond to levodopa therapy.

257 Following levodopa this feature became significantly more pronounc

258 OFF levodopa, this link with acceptance was weakened.

259 sts such as pramipexole or ropinirole allows levodopa to be delayed, but once levodopa is added to th

260 dopaminergic and nondopaminergic actions) in levodopa-treated patients with motor fluctuations.

261 dose-finding clinical trial of tozadenant in levodopa-treated patients with Parkinson's disease who h

262 nificant reduction in mean daily off-time in levodopa-treated patients with PD and motor fluctuations

263 Istradefylline (40mg/day) was studied in levodopa-treated PD subjects experiencing prominent wear

264 We studied 24 patients with levodopa-treated, moderate to advanced Parkinson's disea

265 In addition, cessation of levodopa treatment after acquisition of the motor skill

266 The addition of opicapone 50 mg to levodopa treatment in patients with Parkinson's disease

267 Although levodopa treatment in the Parkinson's disease patients d

268 enigmatic long-duration response to chronic levodopa treatment is a manifestation of rescued motor l

269 Levodopa treatment is the major pharmacotherapy for Park

270 Chronic levodopa treatment leads to the appearance of dyskinesia

271 ver, motor complications uniquely related to levodopa treatment may emerge that may be difficult to m

272 rk alterations were not seen with open-label levodopa treatment or during disease progression.

273 nic kainic acid lesion of the STN or chronic levodopa treatment reliably suppressed the giant GABAerg

274 Older age at diagnosis and poorer levodopa treatment response were the other factors assoc

275 der age at diagnosis, male sex, poor initial levodopa treatment response, and postural instability an

276 re acquired in each animal before initiating levodopa treatment, and again following the period of da

277 mice, together with the beneficial effect of levodopa treatment, strongly suggest that dysfunction of

278 egulated in direct pathway SPNs upon chronic levodopa treatment.

279 of a parkinsonian lesion followed by chronic levodopa treatment.

280 hese power peaks increased with movement and levodopa treatment.

281 ations in the primary motor cortex following levodopa treatment.

282 s that are typically associated with chronic levodopa treatment.

283 Tx3(-/-) is dramatic and can be rescued with levodopa treatment.

284 letion, which are reduced by apomorphine and levodopa treatments.

285 D and PSP are akinesia and rigidity that are levodopa unresponsive, although there has been evidence

286 a variable combination of autonomic failure, levodopa-unresponsive parkinsonism, cerebellar ataxia an

287 ed propensity for falls are interrelated and levodopa-unresponsive symptoms in patients with Parkinso

288 (18)F-levodopa-uptake PET did not change after treatment with

289 atients allocated extended-release carbidopa-levodopa vs two [1%] of 192 patients allocated immediate

290 Treatment with levodopa was associated with worsening, whereas treatmen

291 Nalbuphine coadministered with levodopa was well tolerated and did not cause sedation.

292 Levodopa was well tolerated during aDBS and led to furth

293 with Parkinson's disease who were receiving levodopa were enrolled and treated at 44 sites in 15 cou

294 No serious adverse effects from levodopa were reported during treatment.

295 te hypersensitivity of preSMA and putamen to levodopa, which heralds the failure of neural networks t

296 idual amblyopia after patching therapy, oral levodopa while continuing to patch 2 hours daily does no

297 duration 9.4 years +/- 2.5) both OFF and ON levodopa while they had to decide whether to engage in a

298 an sites among patients with PD treated with levodopa who experienced at least 1 hour of troublesome

299 d patients with moderate to severe PD taking levodopa who were experiencing motor fluctuations.

300 B permeability are simultaneously induced by levodopa within areas of active microvascular remodeling