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1 ulfate, pill placebo, and combined CBGT plus phenelzine.
2 ne (DMI), or the monoamine oxidase inhibitor phenelzine.
3 ebo-treated patients originally treated with phenelzine.
4 s of anxiety would respond preferentially to phenelzine.
5 ents with symmetry obsessions did respond to phenelzine.
6 nfirmed to be inhibited by the marketed drug phenelzine.
7 , and the monoamine oxidase inhibitor (MAOI) phenelzine (10 mg/kg) increased BDNF protein levels in t
8  23% for patients maintained on a regimen of phenelzine, 41% for those maintained on a regimen of imi
9 ly greater after cognitive therapy (58%) and phenelzine (58%) than after pill placebo (28%).
10 s were randomly assigned to receive placebo, phenelzine (60 mg/day), or fluoxetine (80 mg/day).
11  of the gated-synchrony system in yeast with phenelzine, an antidepressant drug used in the treatment
12                                     Combined phenelzine and CBGT treatment is superior to either trea
13                                              Phenelzine and cognitive therapy also reduced symptoms s
14 rence rates after the switch to placebo from phenelzine and imipramine could be due to the two drugs'
15               We therefore hypothesized that phenelzine and imipramine would also affect brainstem GR
16 g effects of the monoamine oxidase inhibitor phenelzine and the tricyclic antidepressant imipramine o
17  report contrasting effects of chronic MAOI (phenelzine) and TCA (imipramine) treatment on neural cor
18 , 16 of 34 (47.1%) (CBGT), 19 of 35 (54.3%) (phenelzine), and 23 of 32 (71.9%) (combined treatment) (
19 n paroxetine, lithium augmentation more than phenelzine, and selegiline more than placebo.
20 otonin in rats treated with vehicle, DMI, or phenelzine but had no effect on the clearance of seroton
21                                 We show that phenelzine can block histone H3K4Me demethylation in cel
22           Imipramine typically increased and phenelzine decreased GR expression in other feedback-rel
23     The scores between cognitive therapy and phenelzine did not differ significantly.
24  addition, patients switched to placebo from phenelzine experienced a recurrence of depressive sympto
25  blood pressure rise in rats pretreated with phenelzine followed by tyramine, and in accord with the
26 nificantly more than those in the placebo or phenelzine group.
27 limited to feedback-related regions, whereas phenelzine had additional effects to decrease accumbens
28 f hepatotoxicity are iproniazid, nefazodone, phenelzine, imipramine, amitriptyline, duloxetine, bupro
29 y provides no evidence to support the use of phenelzine in OCD except possibly for those patients wit
30               GR expression was decreased by phenelzine in the locus coeruleus and decreased by imipr
31                                              Phenelzine increased locus coeruleus TH and imipramine i
32 noamine oxidase with daily administration of phenelzine increased nicotine intake by approximately 50
33            The neuroprotection observed with phenelzine is in agreement with previous studies of alde
34 depression are at high risk of recurrence if phenelzine is withdrawn 6 months after initial improveme
35 tidepressants, such as imipramine, rolipram, phenelzine, ketamine, and its metabolite 2R,6R-hydroxyno
36 Rv7/MAO-A signaling with the antidepressants phenelzine or clorgyline can restore Enz sensitivity to
37                         Targeting MAO-A with phenelzine or clorgyline, the FDA-approved drugs for ant
38 I-treated rats but not in those treated with phenelzine or DMI.
39      We re-explored MAO antidepressant agent phenelzine (phenethylhydrazine), previously reported to
40  monoamine oxidase inhibitors, we found that phenelzine provided robust neuroprotection in the gerbil
41        We also found that in addition to HZ, phenelzine (PZ), a structurally distinct acrolein scaven
42 vival analysis showed a marked advantage for phenelzine relative to placebo.
43 eatment with the monoamine oxidase inhibitor phenelzine sulfate for social phobia.
44 e therapy or clinical management plus either phenelzine sulfate or placebo.
45   Cognitive behavioral group therapy (CBGT), phenelzine sulfate, pill placebo, and combined CBGT plus
46 hronic inhibition of monoamine oxidase using phenelzine sulfate.
47                                 Furthermore, phenelzine that mimics the PCLAF-DREAM transcriptional s
48                              After 12 weeks, phenelzine therapy and CBGT led to superior response rat
49                         After 12 weeks, both phenelzine therapy and CBGT were associated with marked
50  therapy was more evident after 6 weeks, and phenelzine therapy was also superior to CBGT after 12 we
51                         However, response to phenelzine therapy was more evident after 6 weeks, and p
52                                     Although phenelzine therapy was superior to CBGT on some measures
53 ents from 2 sites received 12 weeks of CBGT, phenelzine therapy, pill placebo administration, or educ
54 we investigated if the hydrazine function of phenelzine was capable of sequestering reactive aldehyde
55 e, we found that aldehyde sequestration with phenelzine was neuroprotective.
56 ed the discontinuation trial on a regimen of phenelzine were more chronically depressed than the imip
57 tion and who had improved with imipramine or phenelzine were stabilized for 6 months and then randoml