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1 rt-term benefits of stimulant medication and atomoxetine.
2 herapy), but this connection was restored by atomoxetine.
3 sign, following either placebo or 40-mg oral atomoxetine.
4 thesis of an important pharmaceutical agent, atomoxetine.
5 y used ADHD therapeutics methylphenidate and atomoxetine.
6 id not use methylphenidate, amphetamines, or atomoxetine.
7 to-striatal effective connectivity following atomoxetine.
8 motically released methylphenidate than with atomoxetine.
9 sed methylphenidate was superior to that for atomoxetine.
10 henidate, 30 (43%) subsequently responded to atomoxetine.
11 ns of the aryloxypropanamine template (e.g., atomoxetine, 2) led to a novel series of 1-(3-amino-2-hy
12  years) with ADHD were randomized to receive atomoxetine (20-50 mg BID, N = 220) or placebo (N = 225)
13 g twice daily (BID) or the active comparator atomoxetine (40 mg BID) vs placebo for 28 days.
14                  The response rates for both atomoxetine (45%) and methylphenidate (56%) were markedl
15 CALL2, which could be rescued by tomoxetine (atomoxetine), a clinical medication for ADHD.
16                                  Response to atomoxetine, a nonstimulant norepinephrine-specific reup
17 compulsivity or under chronic treatment with atomoxetine, a noradrenergic reuptake inhibitor used to
18           To this end, we administered 40 mg atomoxetine, a selective noradrenaline re-uptake inhibit
19                  We test this approach using atomoxetine, a selective noradrenaline reuptake inhibito
20  to receive 6 weeks of treatment with either atomoxetine (administered once daily) or placebo.
21  authors assessed the efficacy of once-daily atomoxetine administration in the treatment of children
22 naptic catecholamine levels by administering atomoxetine, an NE transporter blocker, and examined the
23 there was no overall behavioral benefit from atomoxetine, analyses of individual differences revealed
24 using the norepinephrine transporter blocker atomoxetine and demonstrate consistent, causal effects o
25 ed only by methylphenidate, relative to both atomoxetine and placebo.
26 ly released methylphenidate with response to atomoxetine and placebo.
27 ated to gains in task-related activation for atomoxetine and reductions in activation for methylpheni
28  design of the influence of methylphenidate, atomoxetine, and citalopram on error awareness in 27 hea
29 ethylphenidate and amphetamine formulations, atomoxetine, and extended-release guanfacine to improve
30 esign after single doses of methylphenidate, atomoxetine, and placebo in functional magnetic resonanc
31 such as methylphenidate, dexamphetamine, and atomoxetine, and psychosocial interventions, to those se
32 mulant methylphenidate and the non-stimulant atomoxetine are used in the pharmacotherapy of attention
33 iptions for methylphenidate, amphetamine, or atomoxetine at baseline.
34        The effects of methylphenidate (MPH), atomoxetine (ATMX), and/or physical exercise (EX) on ori
35 ects of the selective NE re-uptake inhibitor atomoxetine (ATO) and the mixed DA/NE re-uptake inhibito
36                                              Atomoxetine (ATO), a selective noradrenaline reuptake in
37 amphetamine (AMPH; 0.25, 1.0, or 4.0mug), or atomoxetine (ATO; 1.0, 4.0, or 16.0mug) into either medi
38 ethylphenidate (MPH), a psychostimulant, and atomoxetine (ATX), a selective norepinephrine reuptake i
39            Treatment with methylphenidate or atomoxetine based on prescription data.
40 rom the pre-supplementary motor cortex; (ii) atomoxetine can enhance downstream modulation of frontal
41           Here we tested the hypotheses that atomoxetine can restore functional brain networks for re
42 reduced stop-signal reaction time) following atomoxetine correlated with structural connectivity as m
43 e selective noradrenaline reuptake inhibitor atomoxetine could improve response inhibition, gambling
44                                      Rather, atomoxetine decreased V(max) and DAT cell surface expres
45                                              Atomoxetine did not alter DAT kinetic parameters or loca
46 ve previously shown that methylphenidate and atomoxetine, drugs widely used for the treatment of atte
47 e catecholamine agonists methylphenidate and atomoxetine effectively treat attention-deficit/hyperact
48                                              Atomoxetine enhanced stop-related RIFG activation in pro
49 inically effective drugs methylphenidate and atomoxetine enhanced stopping abilities.
50 pharmaceutical agents, including duloxetine, atomoxetine, fluoxetine and tolterodine.
51                Both the 4 mg BID ABT-894 and atomoxetine groups demonstrated significant improvement
52 %) of the 69 patients who did not respond to atomoxetine had previously responded to osmotically rele
53 dual differences in behavioural responses to atomoxetine highlight the need for patient stratificatio
54 improvements in symptoms with stimulants and atomoxetine; however, data on long-term benefits and ris
55 lphenidate hydrochloride vs the nonstimulant atomoxetine hydrochloride.
56                                              Atomoxetine improved stopping accuracy on the Stop Signa
57 s in future investigations on the effects of atomoxetine in Parkinson's disease and support the hypot
58                                              Atomoxetine increased connectivity from the right IFG to
59               These results suggest that (i) atomoxetine increases sensitivity of the inferior fronta
60                             In addition, the atomoxetine-induced change in connectivity from right IF
61 sion of the noradrenaline reuptake inhibitor atomoxetine into these same regions also reduced social
62                 Once-daily administration of atomoxetine is an effective treatment for children and a
63 ity in compulsive disorders and suggest that atomoxetine may be a useful treatment for patients suffe
64 ctivation and frontostriatal connectivity by atomoxetine may improve response inhibition in Parkinson
65      The results support the hypothesis that atomoxetine may restore prefrontal networks related to e
66 f treatment with methylphenidate (n = 18) or atomoxetine (n = 18) using a parallel-groups design.
67 assigned to receive 0.8-1.8 mg/kg per day of atomoxetine (N=222), 18-54 mg/day of osmotically release
68 atments that augment noradrenergic activity (atomoxetine; norepinephrine reuptake inhibitor) during e
69  compared the effects of methylphenidate and atomoxetine on brain function in ADHD, and none during t
70 e selective noradrenaline reuptake inhibitor atomoxetine on response inhibition in a stop-signal para
71 he inhibitory effects of methylphenidate and atomoxetine on social play are mediated through a distri
72    A single dose of methylphenidate, but not atomoxetine or citalopram, significantly improved the ab
73                      Patients received 40 mg atomoxetine or placebo, orally.
74           Twenty-one patients received 40 mg atomoxetine or placebo.
75 NCLUSIONS Treatment with methylphenidate and atomoxetine produces symptomatic improvement via both co
76       This study investigates the effects of atomoxetine ((R)-N-methyl-gamma-(2-methylphenoxy)-benzen
77                                       First, atomoxetine reduced the strength of inter-regional corre
78  received prescribed stimulant medication or atomoxetine relative to the risk during months in which
79  placebo were reduced by methylphenidate and atomoxetine, respectively, but neither survived rigorous
80 nts who received methylphenidate followed by atomoxetine responded better to one or the other, sugges
81 1) was similar to those observed in previous atomoxetine studies that used twice-daily dosing.
82 re for Evidence-Based Medicine criteria) and atomoxetine than for the extended-release alpha2-adrener
83 he individual differences in the response to atomoxetine: the reduction in stop-signal reaction time
84 the way to new stratified clinical trials of atomoxetine to treat impulsivity in selected patients wi
85                               Outcomes among atomoxetine-treated patients were superior to those of t
86 ined the effects of daily methylphenidate or atomoxetine treatment across 7 days on circadian clock g
87                                              Atomoxetine treatment both decreased impulsivity and pre
88                                        Prior atomoxetine treatment did not augment cocaine self-admin
89 HR OFC, indicating that inhibition of NET by atomoxetine treatment during adolescence indirectly redu
90 reated with methylphenidate were switched to atomoxetine under double-blind conditions.
91                                        Thus, atomoxetine, unlike methylphenidate, does not enhance vu
92 as observed in young adults with ADHD in the atomoxetine versus placebo group as measured by changes
93 tly greater mean reductions were seen in the atomoxetine versus placebo group for the BRIEF-A Global
94    RESULTS Treatment with methylphenidate vs atomoxetine was associated with comparable improvements
95 evealed that enhanced response inhibition by atomoxetine was associated with increased RIFG activatio

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