ライフサイエンスコーパス: methylphenidate

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

2 binding and D2/3 receptor binding following methylphenidate.

3 ve been correlated with orally administrated methylphenidate.

4 hanced by treatment with the psychostimulant methylphenidate.

5 l reversal with a single therapeutic dose of methylphenidate.

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

7 ep deprivation; both after placebo and after methylphenidate.

8 inistration of a single oral dose (60 mg) of methylphenidate.

9 ciated with a greater risk of psychosis than methylphenidate.

10 thened with higher synthesis capacity and by methylphenidate.

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

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

13 ), modafinil (50 [40%] of 125 patients), and methylphenidate (51 [40%] of 129 patients).

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

15 , we examined the effects of ADHD status and methylphenidate, a common ADHD medication, on explore/ex

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

17 Here, we used methylphenidate, a DA reuptake inhibitor, and [(11)C]-(+

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

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

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

21 Methylphenidate, a psychostimulant drug used to treat AD

22 uted tomography (SPECT) predicts response to methylphenidate, a stimulant with dopaminergic effects.

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 ing and D2/3 receptor binding following oral methylphenidate administration.

31 men.ConclusionFour months of treatment with methylphenidate affects specific tracts in brain white m

32 The cognitive effects of methylphenidate after traumatic brain injury were only s

33 Methylphenidate also improved cognition, functional stat

34 sequence; 34 (24%) patients to the placebo, methylphenidate, amantadine, and modafinil sequence; 35

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

36 = 2.5) enrolling 242 participants receiving methylphenidate and 181 participants receiving placebo w

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

38 Conversely, methylphenidate and amphetamine are both used clinically

39 Thus, methylphenidate and amphetamine at therapeutic blood/pla

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

41 The prescription use of the stimulants methylphenidate and amphetamine for the treatment of att

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

43 Both methylphenidate and amphetamine modulate extracellular c

44 The catecholamine agonists methylphenidate and atomoxetine effectively treat attent

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

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

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

48 CONCLUSIONS Treatment with methylphenidate and atomoxetine produces symptomatic imp

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

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

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

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 s change in choice reaction time produced by methylphenidate and its relationship to stratification o

56 gnitive symptoms include CNS stimulants (eg, methylphenidate and modafinil), medications used in pati

57 ointed to an association between the dose of methylphenidate and overall improvement in ADHD severity

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

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

60 triatal dopamine synthesis capacity, whereas methylphenidate and sulpiride, a selective D2 receptor a

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

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

63 4.815, p = 0.053) between subjects receiving methylphenidate and those taking placebos.

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

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

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

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

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

69 (25%) patients to the modafinil, amantadine, methylphenidate, and placebo sequence; and 37 (26%) pati

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

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

72 Stimulants such as methylphenidate are increasingly used for cognitive enha

73 Modafinil and methylphenidate are medications that inhibit the neurona

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

75 The cognitive enhancing effects of methylphenidate are well established, but the mechanisms

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

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

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

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

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

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

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

83 o find eligible individuals who had received methylphenidate between Jan 1, 2007 and June 30, 2012.

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

85 Methylphenidate blocks the dopamine transporter, which i

86 Methylphenidate boosted choices of cognitive effort over

87 We recently demonstrated that methylphenidate boosts cognitive motivation by enhancing

88 These findings demonstrate that methylphenidate boosts the perceived benefits versus cos

89 We found that methylphenidate boosts willingness to expend cognitive e

90 modafinil shares mechanisms with cocaine and methylphenidate but has a unique pharmacological profile

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

92 This effect was potentiated by methylphenidate, but not by modafinil pretreatments, ind

93 We show that methylphenidate, but not modafinil, maintained intraveno

94 s, indicating dopamine-dependent actions for methylphenidate, but not modafinil.

95 hey were not observed in adults treated with methylphenidate.(C) RSNA, 2019Online supplemental materi

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

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

98 ng showed improvement in response times with methylphenidate compared to placebo [median change = -16

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

100 pants' ability to adapt learning rate: Under methylphenidate, compared with placebo, participants exh

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

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

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

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

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

106 s than controls in all three study days, and methylphenidate did not affect these outcomes.

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

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

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

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

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

112 We tested methylphenidate effects relative to placebo in functiona

113 The catecholamine transporter blocker methylphenidate enhanced participants' ability to adapt

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

115 s) who had been treated in regular care with methylphenidate for more than 2 years were randomly assi

116 iscriminate use of amantadine, modafinil, or methylphenidate for the treatment of fatigue in multiple

117 0 person-years): 106 episodes (0.10%) in the methylphenidate group and 237 episodes (0.21%) in the am

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

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

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

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

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

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

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

125 Methylphenidate has been used to mediate cocaine addicti

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

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

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

129 Methylphenidate hydrochloride, an indirect dopamine agon

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

131 Methylphenidate improved apathy in a group of community-

132 Behaviourally, methylphenidate improved sustained attention in a baseli

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

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

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

136 cal studies that investigated the effects of methylphenidate in children with ADHD and ID.

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

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 In controls, methylphenidate increased dopamine in dorsal (effect siz

141 Methylphenidate increases synaptic dopamine by blocking

142 Furthermore, administrated methylphenidate increases the drug metabolism activity a

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

144 We show that methylphenidate induced significant DA increases in stri

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

146 ng simultaneous PET/MR imaging, we show that methylphenidate-induced changes in endogenous dopamine l

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

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

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

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

151 Methylphenidate-induced dopamine increases were greater

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

153 idea, the SERT blocker fluoxetine abolished methylphenidate-induced locomotor activity in DAT Val559

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

155 The methylphenidate-induced normalization of synaptic circui

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

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

158 ncidence of psychotic events 12 weeks before methylphenidate initiation and during a 12-week period o

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

160 The median age at methylphenidate initiation was 17 years, and a history o

161 g the 12-week period one calendar year after methylphenidate initiation.

162 12-week periods immediately before and after methylphenidate initiation.

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

164 between baseline values and values following methylphenidate injection.

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

166 Infusion of methylphenidate into the anterior cingulate cortex, infr

167 Methylphenidate is a first-line treatment for ADHD, howe

168 Methylphenidate is associated with improvement in ADHD s

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

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

171 Methylphenidate is thought to exert its effects on cogni

172 Methylphenidate is used extensively to treat attention d

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

174 The meta-analysis showed that methylphenidate led to a significant improvement in ADHD

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

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

177 considered the complementary hypothesis that methylphenidate might also act by changing the weight on

178 ghted by the finding that the stimulant drug methylphenidate mitigated the hyperactivity.

179 Methylphenidate, modafinil, and amantadine are commonly

180 acebo sequence; and 37 (26%) patients to the methylphenidate, modafinil, placebo, and amantadine sequ

181 Patients on methylphenidate monotherapy displayed an increased rate

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

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

184 (24 controls and 24 marijuana abusers) with methylphenidate (MP), a drug that elevates extracellular

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

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

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

188 Methylphenidate (MPH) is a first line treatment for ADHD

189 Methylphenidate (MPH) is a stimulant that increases extr

190 Methylphenidate (MPH) is an effective treatment for ADHD

191 Methylphenidate (MPH) is commonly diverted for recreatio

192 Methylphenidate (MPH) is commonly prescribed for childre

193 Methylphenidate (MPH) is used clinically to treat attent

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

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

196 Methylphenidate (MPH), a commonly used dopaminergic agen

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

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

199 Psychostimulants, including methylphenidate (MPH), improve cognitive processes depen

200 increased by many therapeutic drugs, such as methylphenidate (MPH), which also alters behavioral and

201 Here, we focus on methylphenidate (MPH), which binds to the dopamine trans

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

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

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

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

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

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

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

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

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

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

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

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

214 d a diagnosis of ADHD and who started taking methylphenidate or amphetamine between January 1, 2004,

215 Treatment with methylphenidate or atomoxetine based on prescription dat

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

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

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

219 Patients received either methylphenidate or placebo for 1 year.

220 leted the bandit task at baseline, and after methylphenidate or placebo in counter-balanced order.

221 Patients received 0.3 mg/kg of methylphenidate or placebo twice a day in 2-week blocks.

222 7 weeks (36 or 54 mg/day of extended-release methylphenidate) or gradual withdrawal over 3 weeks, to

223 Psychotropic Medication on Brain Development-Methylphenidate, or ePOD-MPH) among ADHD referral center

224 4) with modafinil, and 38.6 (36.2-41.0) with methylphenidate (p=0.20 for the overall medication effec

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

226 They were tested on methylphenidate, placebo, as well as the selective D2-re

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

228 on inhibitor, antagonized modafinil, but not methylphenidate potentiation of cocaine self-administrat

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

230 Both modafinil and methylphenidate pretreatments potentiated cocaine self-a

231 te's effects on cognition, and suggests that methylphenidate reduces the cost of mental labor by incr

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

233 The authors investigated whether methylphenidate remains beneficial after 2 years of use.

234 Continued treatment with methylphenidate remains effective after long-term use.

235 Our study suggests that methylphenidate retains its efficacy in children with AD

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

237 is the target of therapeutic drugs, such as methylphenidate (Ritalin), which blocks the dopamine tra

238 Methylphenidate's effect varied across individuals with

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

240 tudy strengthens the motivational account of methylphenidate's effects on cognition, and suggests tha

241 rence about dopamine receptor selectivity of methylphenidate's effects.

242 s to the amantadine, placebo, modafinil, and methylphenidate sequence; 34 (24%) patients to the place

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

244 e widely held view in clinical practice that methylphenidate should be avoided, or its use restricted

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

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

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

248 Methylphenidate significantly increased dopamine levels

249 Methylphenidate significantly reduced activation of diff

250 ication of the dopamine transporter blocker, methylphenidate, significantly increased dopamine levels

251 In contrast, methylphenidate strengthened several corticolimbic and c

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

253 There is a clinical concern that prescribing methylphenidate, the most common pharmacological treatme

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

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

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

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

258 d reassure clinicians considering initiating methylphenidate treatment for ADHD in adolescents and yo

259 The benefits of long-term use of methylphenidate treatment in children and adolescents wi

260 Twelve months of methylphenidate treatment increased striatal dopamine tr

261 Sixteen weeks of methylphenidate treatment increased the cerebral blood f

262 rns, we found no evidence that initiation of methylphenidate treatment increases the risk of psychoti

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

264 ts increases immediately after initiation of methylphenidate treatment or, in the longer term, 1 year

265 ts in the 12-week period after initiation of methylphenidate treatment relative to that in the 12-wee

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

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

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

269 (3647 children) linking the effectiveness of methylphenidate treatment with DNA variants.

270 these registers to identify those receiving methylphenidate treatment, and who were aged 12-30 years

271 s of psychotic events after the initation of methylphenidate treatment, relative to the events before

272 ed to baseline levels during continuation of methylphenidate treatment.

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

274 esponsiveness of the behavioral phenotype to methylphenidate treatment.

275 -0.56) in favor of the group that continued methylphenidate treatment.

276 ermine whether there is a continued need for methylphenidate treatment.

277 Given that amphetamine and methylphenidate, unlike cocaine, lack high-affinity inte

278 aily), modafinil (up to 100 mg twice daily), methylphenidate (up to 10 mg twice daily), or placebo, e

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

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

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

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

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

286 Methylphenidate was associated with an increased risk of

287 Therefore, methylphenidate was infused into prefrontal and orbitofr

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

289 Methylphenidate was superior to placebo in all five meta

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

291 -years of follow up; 110,923 patients taking methylphenidate were matched with 110,923 patients takin

292 Amantadine, modafinil, and methylphenidate were not superior to placebo in improvin

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

294 report that, in contrast to amphetamine and methylphenidate, which induce significant locomotor acti

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

296 ensity scores to match patients who received methylphenidate with patients who received amphetamine i

297 d one calendar year before the initiation of methylphenidate with the incidence of these events durin

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

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

300 ual patients may, however, be withdrawn from methylphenidate without deterioration.