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1 ompleted both assessments (18 placebo and 16 pramipexole).
2 4 and D2 receptor subtypes in the effects of pramipexole.
3 with pregabalin as compared with placebo and pramipexole.
4 ly lower with pregabalin than with 0.5 mg of pramipexole.
5 cessary, placebo recipients were assigned to pramipexole.
6 of inefficacy or an adverse event related to pramipexole.
7 ne patient who became hypomanic while taking pramipexole.
8 educed by treatment with the antioxidant S(-)pramipexole.
9 ntribute to the anti-parkinsonian effects of pramipexole.
10 ompound to compare the results obtained with pramipexole.
11 le, and two in the group receiving 0.5 mg of pramipexole.
12 ificant difference between early and delayed pramipexole (-0.4 points, 95% CI -2.2 to 1.4, p=0.65).
13   Patients were randomly assigned to receive pramipexole, 0.5 mg 3 times per day with levodopa placeb
14 e, to receive double-blind either placebo or pramipexole (1.5 mg a day) and followed them up for 15 m
15                          More patients given pramipexole (10 [83%] of 12) than patients given placebo
16 th 300 mg of pregabalin, 178 with 0.25 mg of pramipexole, 180 with 0.5 mg of pramipexole, and 179 wit
17 scale scores was greater for patients taking pramipexole (48%) than for those taking placebo (21%).
18                        In the present study, pramipexole, a D3-preferring DA agonist effective in tre
19               The neuroprotective effects of pramipexole, a dopamine agonist, were investigated in 3-
20                           We postulated that pramipexole acts in both of these models to reduce the e
21      Forty-two percent of patients receiving pramipexole and 14% of those receiving placebo achieved
22   Overall, 180 (81%) of patients given early pramipexole and 179 (84%) patients given delayed pramipe
23 ients, 261 were randomly assigned to receive pramipexole and 274 to receive placebo.
24                               Treatment with pramipexole and bromocriptine partially, but significant
25 nsistent with the neurochemical effect, both pramipexole and bromocriptine prevented 3-AP-induced los
26                                         Both pramipexole and bromocriptine significantly attenuated 3
27 lity of life data show no difference between pramipexole and levodopa after 4 years.
28                                              Pramipexole and levodopa are effective medications to tr
29 fective in RLS, including dopamine agonists (pramipexole and ropinirole) and alpha2 delta ligands (ga
30            Eight (67%) of 12 patients taking pramipexole and two (20%) of 10 taking placebo had an im
31 h 0.25 mg of pramipexole, 180 with 0.5 mg of pramipexole, and 179 with placebo.
32 pamine agonists, particularly ropinirole and pramipexole, and management of motor and behavioral comp
33 lin, three in the group receiving 0.25 mg of pramipexole, and two in the group receiving 0.5 mg of pr
34               Dopaminergic agonists, such as pramipexole, appear to have neuroprotective and neurores
35 eks, the VAS pain score decreased 36% in the pramipexole arm and 9% in the placebo arm (treatment dif
36 th pregabalin at a dose of 300 mg per day or pramipexole at a dose of 0.25 mg or 0.5 mg per day or 12
37 ignificantly lower with pregabalin than with pramipexole at a dose of 0.5 mg (2.1% vs. 7.7%, P=0.001)
38                                              Pramipexole at the 1 mg/kg, p.o., dose level was able to
39 valence model revealed that after 8 weeks on pramipexole, BPD patients attended more readily to feedb
40 d in healthy subjects after a single dose of pramipexole, but its potential to induce abnormalities i
41              Patients initially treated with pramipexole demonstrated a reduction in loss of striatal
42 p=0.64); however, at week 8, BPD patients on pramipexole demonstrated a significantly greater tendenc
43  2.1) for early and -14.6% (2.0) for delayed pramipexole (difference -0.5 percentage points, 95% CI -
44                        Amisulpride (400 mg), pramipexole dihydrochloride (0.5 mg), or placebo were ad
45                                 In contrast, pramipexole dosing (1 mg/kg, p.o., 1 h after the last me
46 d with the placebo group, patients receiving pramipexole experienced gradual and more significant imp
47               We also found that the agonist pramipexole failed to stimulate activation of Akt in PC1
48  nausea), and 22 (10%) patients in the early pramipexole group and 17 (8%) in the delayed pramipexole
49                     62 patients in the early pramipexole group and 61 patients in the delayed pramipe
50 om baseline was significantly reduced in the pramipexole group compared with the levodopa group: 7.1%
51 pramipexole group and 17 (8%) in the delayed pramipexole group had serious events, two of which (hall
52 ipexole group and 61 patients in the delayed pramipexole group were included in the neuroimaging subs
53                         Those patients given pramipexole had significantly reduced loss of striatal u
54 e results do not support the hypothesis that pramipexole has disease-modifying effects.
55 minergic neuronal loss, the dopamine agonist pramipexole has exhibited neuroprotective properties.
56 algesia and/or were disabled, treatment with pramipexole improved scores on assessments of pain, fati
57                    Although more potent than pramipexole in inhibiting SNPC cells, PNU-91356A, a D2-p
58 l neuroprotectant selegiline and patients on pramipexole in the SPECT study appear to have been clini
59 ne the safety and antidepressant efficacy of pramipexole in treatment-resistant bipolar depression.
60 lective dopamine (DA) D2/D3 receptor agonist pramipexole in two models of nigrostriatal (NS) degenera
61 ned to identify whether early versus delayed pramipexole initiation has clinical and neuroimaging ben
62 synaptic alterations, chronic treatment with pramipexole is associated not only with a reduced risk o
63  We recently reported that the D2/D3 agonist pramipexole may have pro-cognitive effects in euthymic p
64 symptoms of dementia and antidepressants and pramipexole may improve depression.
65 us studies suggest that the dopamine agonist pramipexole may possess antidepressant properties.
66     In vitro and animal studies suggest that pramipexole may protect and that levodopa may either pro
67 ssigned to receive placebo or flexibly dosed pramipexole (mean maximum dose=1.7 mg/day, SD=1.3) added
68                                          The Pramipexole On Underlying Disease (PROUD) study was desi
69 ents pre- and post 8 weeks of treatment with pramipexole or placebo by using the Iowa Gambling Task (
70 1 (pramipexole:placebo) to receive 4.5 mg of pramipexole or placebo orally every evening.
71     Treatment with dopamine agonists such as pramipexole or ropinirole allows levodopa to be delayed,
72 of rates of augmentation with pregabalin and pramipexole over a period of 40 or 52 weeks of treatment
73                  Secondary outcomes favoring pramipexole over placebo included the total FIQ score (t
74 opa/levodopa, 25/100 mg 3 times per day with pramipexole placebo (n = 40).
75 ients with fibromyalgia were randomized 2:1 (pramipexole:placebo) to receive 4.5 mg of pramipexole or
76 sencephalic (VM) cultures in the presence of pramipexole (PPX) and other drugs with dopamine (DA) D3
77 vative LIGA20, the dopamine receptor agonist pramipexole (PPX) and the caspase inhibitor Z-VAD-FMK bu
78                         The dopamine agonist pramipexole (PPX) can increase impulsiveness, and PPX th
79            This study examined the effect of pramipexole (PPX), a selective dopamine (DA) D(3)/D(2) a
80                At clinically relevant doses, pramipexole produced statistically robust decreases in r
81 ipexole and 179 (84%) patients given delayed pramipexole reported adverse events (most frequently nau
82 ere significant targets for locally perfused pramipexole, ropinirole, and gabapentin, which significa
83 that other mechanisms may also contribute to pramipexole's dopaminergic neuroprotection.
84      The dose-response curve and duration of pramipexole's effects suggest that these rCBF responses
85                           In a second model, pramipexole's effects were examined on methamphetamine-i
86        Based on a preliminary examination of pramipexole's oxidation potential, it appears that the c
87       By clinical and neuroimaging measures, pramipexole showed little evidence differentiating 15-mo
88                                              Pramipexole suppressed PLMS without affecting electroenc
89 ments in CGI severity were also greater with pramipexole than placebo.
90 ater, and the D3-preferring dopamine agonist pramipexole to identify D3-mediated regional cerebral bl
91                                              Pramipexole treatment also significantly attenuated the
92 ine, some outcomes showed a better trend for pramipexole treatment than for placebo, but failed to re
93 documented in Parkinson's disease (PD) after pramipexole treatment.
94                                              Pramipexole was a safe and effective antidepressant amon
95  series of compounds structurally related to pramipexole were designed, synthesized, and evaluated as
96 e most common adverse events associated with pramipexole were transient anxiety and weight loss.
97  group received a single oral dose of 0.25mg pramipexole, whereas a second group received a single or

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