ライフサイエンスコーパス: methylphenidate

1 ve been correlated with orally administrated methylphenidate.

2 hanced by treatment with the psychostimulant methylphenidate.

3 l reversal with a single therapeutic dose of methylphenidate.

4 ed with increasing feeding doses up to 25 mM methylphenidate.

5 ep deprivation; both after placebo and after methylphenidate.

6 of an injection of placebo or 0.5 mg/kg i.v. methylphenidate.

7 al treatment with a titrated regimen of oral methylphenidate.

8 binding and D2/3 receptor binding following methylphenidate.

9 complete loss of hydrolytic activity toward methylphenidate.

10 uterized sustained attention task after oral methylphenidate (0.5 mg/kg) and placebo administration i

11 medications amphetamine (0.1-1.0 mg/kg) and methylphenidate (1.0-10 mg/kg) were then determined; in

12 In Experiment 2, oral methylphenidate (1.5 mg/kg) and vehicle (water) were eva

13 Single doses of oral methylphenidate (20 mg) or placebo were administered at

14 The effects of methylphenidate (40 mg) were assessed using functional m

15 e compared the dopamine increases induced by methylphenidate (a drug that increases dopamine by block

16 Administration of methylphenidate (a psychostimulant drug used to treat AD

17 ion, we examined their response to a dose of methylphenidate, a common and effective treatment for at

18 that adolescent treatment with the stimulant methylphenidate, a dopamine (DAT) and norepinephrine (NE

19 ared with the effect of osmotic-release oral methylphenidate, a long-acting methylphenidate preparati

20 n performed the task twice, with and without methylphenidate, a norepinephrine-dopamine reuptake inhi

21 tion and impulsive behavior were reversed by methylphenidate, a psychostimulant commonly used for the

22 Methylphenidate, a psychostimulant drug used to treat AD

23 These results suggest that methylphenidate acts by modulating functional brain netw

24 These results suggest that methylphenidate acts by modulating strength in functiona

25 Methylphenidate (adjusted mean, 16.2) was superior to pl

26 Methylphenidate administration into the prelimbic, media

27 vement of response inhibition seen following methylphenidate administration is due to its influence o

28 Short-term methylphenidate administration reduced an abnormally str

29 ase using [(11)C]raclopride paired with oral methylphenidate administration.

30 Methylphenidate also improved cognition, functional stat

31 eural mechanisms by which stimulants such as methylphenidate ameliorate attention deficit hyperactivi

32 ts of Psychotropic Drugs on Developing Brain-Methylphenidate) among ADHD referral centers in the grea

33 gh 64 years with dispensed prescriptions for methylphenidate, amphetamine, or atomoxetine at baseline

34 as four comparison subjects who did not use methylphenidate, amphetamines, or atomoxetine.

35 d 50 participants were randomized to receive methylphenidate and 49 to placebo.

36 least 18 hours following their last dose of methylphenidate and again 120 minutes after a 0.4-mg/kg

37 Conversely, methylphenidate and amphetamine are both used clinically

38 The stimulants methylphenidate and amphetamine are used to treat childr

39 Thus, methylphenidate and amphetamine at therapeutic blood/pla

40 ficacy was stronger for the extended-release methylphenidate and amphetamine class stimulant medicati

41 vidence supports the use of extended-release methylphenidate and amphetamine formulations, atomoxetin

42 Both methylphenidate and amphetamine modulate extracellular c

43 The catecholamine agonists methylphenidate and atomoxetine effectively treat attent

44 opping, while the clinically effective drugs methylphenidate and atomoxetine enhanced stopping abilit

45 However, few have compared the effects of methylphenidate and atomoxetine on brain function in ADH

46 Our data show that the inhibitory effects of methylphenidate and atomoxetine on social play are media

47 CONCLUSIONS Treatment with methylphenidate and atomoxetine produces symptomatic imp

48 We have previously shown that methylphenidate and atomoxetine, drugs widely used for t

49 were observed under placebo were reduced by methylphenidate and atomoxetine, respectively, but neith

50 een with the commonly used ADHD therapeutics methylphenidate and atomoxetine.

51 us, our results show differential effects of methylphenidate and cocaine on neuronal adaptation in sp

52 ur analysis revealed that the selectivity of methylphenidate and desipramine for DAT and SERT, respec

53 ior to and after 12 months of treatment with methylphenidate and in 11 controls who were also scanned

54 re dopamine increases induced by intravenous methylphenidate and in 24 of the cocaine abusers, we als

55 methylphenidate, and placebo (Comparison of Methylphenidate and Psychotherapy in Adult ADHD Study Tr

56 lucidate the neural systems-level effects of methylphenidate and suggest that short-term methylphenid

57 The psychostimulant methylphenidate and the non-stimulant atomoxetine are us

58 To investigate the association between methylphenidate and the risk of suicide attempts.

59 was found for a positive association between methylphenidate and treatment-emergent mania among patie

60 ultitracer PET with (18)F-FDG, (11)C-d-threo-methylphenidate, and (11)C-raclopride.

61 vivo concentrations of the neuroactive drug, methylphenidate, and a metabolite in the heads of the fr

62 n for psychostimulant drugs such as cocaine, methylphenidate, and amphetamine.

63 hibitors, such as tricyclic antidepressants, methylphenidate, and cocaine.

64 proach by measuring the kinetics of cocaine, methylphenidate, and desipramine binding to SERT and DAT

65 of group psychotherapy, clinical management, methylphenidate, and placebo (Comparison of Methylphenid

66 enile prefrontal cortex is supersensitive to methylphenidate, and the accepted therapeutic range for

67 o produced slight reductions in the rates of methylphenidate- and food-reinforced responding, these e

68 d whether the dopamine increases elicited by methylphenidate are associated with long-term clinical r

69 ter inhibitors such as dextroamphetamine and methylphenidate are effective for increasing arousal and

70 The CNS stimulants modafinil and methylphenidate are recommended for the treatment of can

71 drugs, such as cholinesterase inhibitors and methylphenidate, are used as treatments for the cognitiv

72 harmacokinetic, and clinical ADR profiles of methylphenidate, aripiprazole, and risperidone, and of k

73 vels of nervousness and appetite loss in the methylphenidate arm.

74 es during a 1-year period when combined with methylphenidate as compared with placebo.

75 study of the stop signal task, we show that methylphenidate (as compared with placebo) robustly decr

76 e curve analysis, there was no evidence that methylphenidate, as compared with placebo, improved the

77 siology to show that acute administration of methylphenidate, as well as a selective dopamine transpo

78 Is treatment with methylphenidate associated with benefits or harms for ch

79 olled, cross-over design of the influence of methylphenidate, atomoxetine, and citalopram on error aw

80 lind cross-over design after single doses of methylphenidate, atomoxetine, and placebo in functional

81 This was a cohort study of new users of methylphenidate based on administrative data from a five

82 bipolar disorder who initiated therapy with methylphenidate between 2006 and 2014.

83 bipolar disorder who initiated therapy with methylphenidate between 2006 and 2014.

84 als aged 6 to 25 years who were treated with methylphenidate between January 1, 2001, and December 31

85 A single dose of methylphenidate, but not atomoxetine or citalopram, sign

86 all, these results indicate that cocaine and methylphenidate can increase or decrease DA neurotransmi

87 methylphenidate and suggest that short-term methylphenidate can, at least transiently, remodel abnor

88 during periods when patients were exposed to methylphenidate compared with nonexposed periods.

89 In the striatum, the methylphenidate condition differed significantly from pl

90 cortex and inferior parietal lobe during the methylphenidate condition for errors made with versus wi

91 tute a potentially viable mechanism by which methylphenidate could facilitate control of behavior in

92 therapeutic equivalent dose (0.75 mg/kg) of methylphenidate decreases the hyperactivity and increase

93 Combined treatment with citalopram and methylphenidate demonstrated an enhanced clinical respon

94 al and care must be taken in comparing (11)C-methylphenidate-derived assessment of DD with that obtai

95 investigate the characteristics of the (11)C-methylphenidate-derived quantification of DAT in rodents

96 ion, with similar responses to drugs such as methylphenidate, dexamphetamine, and atomoxetine, and ps

97 tive functioning, although augmentation with methylphenidate did not offer additional benefits.

98 Thus, atomoxetine, unlike methylphenidate, does not enhance vulnerability to cocai

99 Methylphenidate dose was 5 mg every 2 hours as needed up

100 ncipal components analysis (PCA) showed that methylphenidate dramatically affected both the distribut

101 ich also remained for a subgroup analysis of methylphenidate effects alone.

102 We tested methylphenidate effects relative to placebo in functiona

103 sease did have some fatigue improvement with methylphenidate (eg, in patients with stage III or IV di

104 It also provides preliminary evidence that methylphenidate-elicited dopamine increases in prefronta

105 Furthermore, methylphenidate exposure increased expression of DeltaFo

106 ers, such as L-DOPA for Parkinson's disease, methylphenidate for attention-deficit/hyperactivity diso

107 Recent trends in the high usage of methylphenidate for both therapeutic and nontherapeutic

108 oped to evaluate the efficacy of long-acting methylphenidate for improving cancer-related fatigue and

109 biomarkers in individualized treatment with methylphenidate for patients with cocaine dependence.

110 ently completed, placebo-controlled study of methylphenidate for preschool ADHD identified some age-r

111 and after the administration of a stimulant (methylphenidate), for measurement of striatal dopamine D

112 was associated with therapeutic response to methylphenidate, further corroborating the relevance of

113 re was more prominent in the citalopram plus methylphenidate group compared with the other two groups

114 er burden, CGI scores, and depression in the methylphenidate group compared with the placebo group.

115 After adjusting for baseline, the methylphenidate group had significantly greater improvem

116 e rate of improvement in the citalopram plus methylphenidate group was significantly higher than that

117 k and a network with greater strength in the methylphenidate group, and between the low-attention net

118 While only methylphenidate had a drug-specific effect of improving

119 ssion, whereas others, including cocaine and methylphenidate, had no effect.

120 Methylphenidate has been used to mediate cocaine addicti

121 er (ADHD); however, the action mechanisms of methylphenidate have not been fully elucidated.

122 , the risk of mania was lower after starting methylphenidate (hazard ratio=0.6, 95% CI=0.4-0.9).

123 Juvenile male rhesus monkeys treated with methylphenidate hydrochloride (MPH) to evaluate genetic

124 Although numerous children receive methylphenidate hydrochloride for the treatment of atten

125 omatic improvement with use of the stimulant methylphenidate hydrochloride vs the nonstimulant atomox

126 Methylphenidate hydrochloride, an indirect dopamine agon

127 Stimulants, such as methylphenidate hydrochloride, are the most common treat

128 Methylphenidate improved apathy in a group of community-

129 Behaviourally, methylphenidate improved sustained attention in a baseli

130 Methylphenidate improves motor response inhibition, typi

131 dolescents with ADHD under either placebo or methylphenidate in a randomized controlled trial while p

132 e authors sought to determine whether use of methylphenidate in adults is associated with elevated ra

133 cted role in the therapeutic effects of oral methylphenidate in attention deficit/hyperactivity disor

134 Similar effects of cocaine were produced by methylphenidate in both wild-type and DAT-CI mice.

135 mine and brain glucose metabolism induced by methylphenidate in controls and alcoholics.

136 eceptor signaling in the arousing effects of methylphenidate in humans.

137 Furthermore, local administration of methylphenidate in the lateral amygdala enhanced cue-rew

138 atomoxetine and reductions in activation for methylphenidate in the right inferior frontal gyrus, lef

139 however, the neural systems-level effects of methylphenidate in this population have not yet been des

140 For failed inhibitions, methylphenidate increased activation within performance-

141 In controls, methylphenidate increased dopamine in dorsal (effect siz

142 Chronic methylphenidate increased the density of dendritic spine

143 Methylphenidate increases synaptic dopamine by blocking

144 Furthermore, administrated methylphenidate increases the drug metabolism activity a

145 vity following injection of d-amphetamine or methylphenidate, indicating that CK1 activity has a prof

146 alysis techniques to unveil that cocaine and methylphenidate induced a marked depression of the synap

147 We show that methylphenidate induced significant DA increases in stri

148 e was no relationship between [(18)F]FMT and methylphenidate-induced [(11)C]raclopride displacement.

149 arkedly attenuated dopaminergic effects, the methylphenidate-induced changes in ventral striatum were

150 The effect of smoking status on methylphenidate-induced DA release tended to be lower in

151 Methylphenidate-induced decreases in SSRT were positivel

152 pamine D2/D3 (D2R) receptor availability and methylphenidate-induced dopamine (DA) release, we retros

153 Methylphenidate-induced dopamine changes were evaluated

154 For both groups, methylphenidate-induced dopamine increases were associat

155 Methylphenidate-induced dopamine increases were greater

156 e participants, we also measured intravenous methylphenidate-induced dopamine release to measure dopa

157 for dopamine receptor subtypes in mediating methylphenidate-induced enhancements of neural transmiss

158 Interestingly, the methylphenidate-induced increase in the density of relat

159 ater in controls than in alcoholics, whereas methylphenidate-induced metabolic decreases were greater

160 The methylphenidate-induced normalization of synaptic circui

161 opamine D2/D3 receptor availability and with methylphenidate-induced striatal dopamine increases in h

162 Methylphenidate infusion into the dorsomedial PFC, but n

163 with a noradrenergic mechanism of action of methylphenidate, infusion of the noradrenaline reuptake

164 ly increased hazard ratio of mania following methylphenidate initiation in bipolar patients not takin

165 ate (p = 0.1) or putamen (p = 0.8) following methylphenidate injection.

166 between baseline values and values following methylphenidate injection.

167 Here we show that non-contingent cocaine or methylphenidate injections (UCS retrieval) 1 h before th

168 Infusion of methylphenidate into the anterior cingulate cortex, infr

169 Methylphenidate is associated with improvement in ADHD s

170 The PET DAT marker (11)C-methylphenidate is commonly used to quantify DAT functio

171 Higher in vivo concentration of methylphenidate is observed with increasing feeding dose

172 Methylphenidate is the psychostimulant medication most c

173 Methylphenidate is thought to exert its effects on cogni

174 ion, most commonly the catecholamine agonist methylphenidate, is the most effective treatment for att

175 performed at a relatively high mass of (11)C-methylphenidate (low SA), the additional nonspecific bin

176 availability during long-term treatment with methylphenidate may decrease treatment efficacy and exac

177 pram (mean=32 mg) and from 5 mg to 40 mg for methylphenidate (mean=16 mg).

178 However, the dopamine increases induced by methylphenidate (measured as decreases in D2/D3 receptor

179 Patients on methylphenidate monotherapy displayed an increased rate

180 e of the study was to compare the effects of methylphenidate (MP) with those of placebo (PL) on CRF a

181 baseline (placebo) and after challenge with methylphenidate (MP), a dopamine-enhancing drug, in 24 a

182 (24 controls and 24 marijuana abusers) with methylphenidate (MP), a drug that elevates extracellular

183 It is known that methylphenidate (MPD) (also known as Ritalin), a drug us

184 Psychostimulants like amphetamine and methylphenidate (MPD) are used to treat attention defici

185 Since methylphenidate (MPD) is widely used to treat attention

186 current studies examined the degree to which methylphenidate (MPH) (Ritalin) acts within distinct fro

187 placebo and after challenge with 60 mg oral methylphenidate (MPH) (to measure DA release) to assess

188 se changes by examining the effects of 40 mg methylphenidate (MPH) administration.

189 Methylphenidate (MPH) ameliorates attention problems exp

190 There is a rise in the concurrent use of methylphenidate (MPH) and fluoxetine (FLX) in pediatric

191 Although it is well established that methylphenidate (MPH) enhances sustained attention, the

192 Methylphenidate (MPH) has long been used to treat attent

193 Methylphenidate (MPH) is a stimulant that increases extr

194 Methylphenidate (MPH) is an effective treatment for ADHD

195 Methylphenidate (MPH) is commonly diverted for recreatio

196 Methylphenidate (MPH) is commonly prescribed for childre

197 Methylphenidate (MPH) is used clinically to treat attent

198 Methylphenidate (MPH) normalizes cortical function, enha

199 ithout pharmacological enhancement (ie, with methylphenidate (MPH) or placebo), for treating persiste

200 Pharmacotherapy with methylphenidate (MPH) seems to be the first-line treatme

201 Here, we determined the effects of chronic methylphenidate (MPH) treatment on brain dopamine (DA) s

202 Methylphenidate (MPH), a commonly used dopaminergic agen

203 hy (PET), the effects of orally administered methylphenidate (MPH), a first-line treatment for attent

204 Low doses of psychostimulants, including methylphenidate (MPH), are highly effective in the treat

205 The effects of methylphenidate (MPH), atomoxetine (ATMX), and/or physic

206 ATO) and the mixed DA/NE re-uptake inhibitor methylphenidate (MPH), both with proven clinical efficac

207 in these mice is reversed by treatment with methylphenidate (MPH), suggesting a defect in brain cate

208 We also show that methylphenidate (MPH), which competitively inhibits DA u

209 ly treated with stimulant medication such as methylphenidate (MPH); however, approximately 25% of pat

210 Rats received direct infusions of methylphenidate (MPH; 6.25, 25.0, or 100mug), amphetamin

211 Recent work in rodents demonstrates that methylphenidate (MPH; Ritalin) elicits a narrow inverted

212 ore and after 6 to 8 weeks of treatment with methylphenidate (n = 18) or atomoxetine (n = 18) using a

213 N=222), 18-54 mg/day of osmotically released methylphenidate (N=220), or placebo (N=74) for 6 weeks.

214 ram plus placebo (N=48), and citalopram plus methylphenidate (N=47).

215 ood flow response to an acute challenge with methylphenidate, noninvasively assessed using pharmacolo

216 thors' objective was to study the effects of methylphenidate on apathy in Alzheimer's disease.

217 estigate the effects of orally administrated methylphenidate on lipids in the brain of Drosophila mel

218 he current study, we assessed the effects of methylphenidate on neural networks of inhibitory control

219 aging successfully visualizes the effects of methylphenidate on the chemical structure of the fly bra

220 ge-dependent and possibly lasting effects of methylphenidate on the human dopaminergic system.

221 In general, the effect of methylphenidate on the increase of shorter spines (class

222 rovides information concerning the effect of methylphenidate on the nervous system.

223 Treatment with either methylphenidate or a matched placebo for 16 weeks.

224 Treatment with methylphenidate or atomoxetine based on prescription dat

225 study we have examined the effects of daily methylphenidate or atomoxetine treatment across 7 days o

226 We compared the effects of chronic methylphenidate or cocaine (15 mg/kg, 14 days for both)

227 cocaine-like interoceptive effects of either methylphenidate or d-amphetamine, these results suggest

228 clinically effective psychostimulant (e.g., methylphenidate or dextroamphetamine/amphetamine combina

229 d double-blinded placebo-controlled trial of methylphenidate or galantamine to treat emotional and co

230 Patients received either methylphenidate or placebo for 1 year.

231 Methylphenidate OROS also produced higher activation in

232 Methylphenidate OROS increased daMCC activation during t

233 inergic deficits assessed with (11)C-d-threo-methylphenidate PET were not detected.

234 reatment response in three treatment groups: methylphenidate plus placebo (N=48), citalopram plus pla

235 -release oral methylphenidate, a long-acting methylphenidate preparation, in patients with attention

236 Among 25 629 patients with methylphenidate prescriptions, 154 had their first recor

237 study hypothesis that the chosen long-acting methylphenidate product would decrease cancer-related fa

238 formance differences were normalized only by methylphenidate, relative to both atomoxetine and placeb

239 ed with a previously implicated biomarker of methylphenidate response (systolic blood pressure).

240 Methylphenidate restored inhibitory ability to control l

241 Although methylphenidate (Ritalin) has been used therapeutically

242 mined their strength in healthy adults given methylphenidate (Ritalin), a common ADHD treatment, comp

243 Methylphenidate's effect varied across individuals with

244 size 0.89; P<0.001), but in cocaine abusers methylphenidate's effects did not differ from placebo an

245 ersus rested sleep, with the assumption that methylphenidate's effects would be greater if, indeed, d

246 Further, methylphenidate's interaction with the DAT is unique and

247 mine did not alter MAD scores in any strain, methylphenidate selectively increased MAD scores in WKY

248 acterize the neural systems-level effects of methylphenidate; severity of cocaine addiction was asses

249 As predicted, individuals on methylphenidate showed connectivity signatures of better

250 As predicted, individuals given methylphenidate showed patterns of connectivity associat

251 The fMRI analysis showed that methylphenidate significantly enhanced activation in bil

252 A challenge dose of 0.5 mg/kg intravenous methylphenidate significantly increased dopamine in stri

253 Methylphenidate significantly increased dopamine levels

254 Methylphenidate significantly reduced activation of diff

255 an unadulterated orange-flavored solution, a methylphenidate solution, or a dl-amphetamine mixture.

256 In contrast, methylphenidate strengthened several corticolimbic and c

257 cits differed in degree of correctability by methylphenidate, suggesting that they may be mediated by

258 ine, but not following either amphetamine or methylphenidate, suggests that delay discounting in SHR

259 signed in a double-blinded manner to receive methylphenidate (target dose, 54 mg/d) or placebo for 4

260 ontal and temporal cortices with intravenous methylphenidate that were also associated with decreases

261 The authors evaluated the potential of methylphenidate to improve antidepressant response to ci

262 e before and after stimulant administration (methylphenidate) to measure striatal D(2/3) receptor bin

263 ined elevated immediately after the start of methylphenidate treatment and returned to baseline level

264 do not support a causal association between methylphenidate treatment and suicide attempts.

265 Early age at initiation of methylphenidate treatment in children with ADHD does not

266 Twelve months of methylphenidate treatment increased striatal dopamine tr

267 Sixteen weeks of methylphenidate treatment increased the cerebral blood f

268 ata and demonstrate age-dependent effects of methylphenidate treatment on human extracellular dopamin

269 alent increases in endogenous dopamine after methylphenidate treatment to that observed in healthy co

270 overall incidence of suicide attempts during methylphenidate treatment was 9.27 per 10 000 patient-ye

271 In this small pilot study, methylphenidate treatment was associated with clinically

272 (3647 children) linking the effectiveness of methylphenidate treatment with DNA variants.

273 esponsiveness of the behavioral phenotype to methylphenidate treatment.

274 inattention and hyperactivity with long-term methylphenidate treatment.

275 n the period immediately before the start of methylphenidate treatment.

276 ed to baseline levels during continuation of methylphenidate treatment.

277 of treatment-emergent mania associated with methylphenidate, used in monotherapy or with a concomita

278 ar arrhythmia was 2.17 (95% CI=1.63-2.83) in methylphenidate users and 0.98 (95% CI=0.89-1.08) in non

279 A total of 43,999 new methylphenidate users were identified and matched to 175

280 All new methylphenidate users with at least 180 days of prior en

281 n improvement in usual fatigue was 19.7 with methylphenidate v 2.1 with placebo; P = .02).

282 blind, randomized, placebo-controlled trial (methylphenidate versus placebo) was conducted in communi

283 RESULTS Treatment with methylphenidate vs atomoxetine was associated with compa

284 reased alertness and reduced sleepiness when methylphenidate was administered after sleep deprivation

285 rs, we also compared dopamine increases when methylphenidate was administered concomitantly with a co

286 Although initiation of methylphenidate was associated with a 1.8-fold increase

287 paradoxical inhibitory effect of cocaine and methylphenidate was associated with a decrease in synaps

288 Methylphenidate was associated with an increased risk of

289 Therefore, methylphenidate was infused into prefrontal and orbitofr

290 was detected during the 90-day period before methylphenidate was initiated, with an incidence rate ra

291 Methylphenidate was superior to placebo in all five meta

292 Descriptive analyses showed that methylphenidate was superior to placebo in patients assi

293 After 6 weeks, patients treated with methylphenidate were switched to atomoxetine under doubl

294 Stimulant medications, such as methylphenidate, which are effective treatments for atte

295 Finally, methylphenidate, which blocks dopamine uptake like cocai

296 The effect of drugs such as methylphenidate, which can be used to augment rehabilita

297 spite their attenuated dopamine responses to methylphenidate, which suggests an impaired modulation o

298 g Scale total score) to osmotically released methylphenidate with response to atomoxetine and placebo

299 In particular, the effects of methylphenidate within striatal and cortical pathways co

300 ncreased the cerebral blood flow response to methylphenidate within the thalamus (mean difference, 6.