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1 erent medication intake that often occurs in antidepressant therapy.
2 h MDD and an inadequate response to standard antidepressant therapy.
3 (1A) autoreceptor desensitization under SSRI antidepressant therapy.
4 his single cell type plays a pivotal role in antidepressant therapy.
5 epression and identified regions affected by antidepressant therapy.
6 epressant medication change or were starting antidepressant therapy.
7 thors also examined naturalistically applied antidepressant therapy.
8 l intervention and which should continue the antidepressant therapy.
9 e model of group Problem Management Plus and antidepressant therapy.
10 plete remission after conventional monoamine antidepressant therapy.
11 cture makes an interesting target for future antidepressant therapies.
12 cological target for developing rapid-acting antidepressant therapies.
13 tial basis for developing novel rapid-acting antidepressant therapies.
14 t an approach to the development of improved antidepressant therapies.
15 fy the mechanisms that underlie rapid-acting antidepressant therapies.
16  rates and times superior to other available antidepressant therapies.
17 nobutyric acid (GABA) that are normalized by antidepressant therapies.
18                     After discontinuation of antidepressant therapy, 92 patients with clinically defi
19 ectivity with the DN as a brain mechanism of antidepressant therapy action.
20 ients with MDD and an inadequate response to antidepressant therapy (ADT) in FORWARD-4 and FORWARD-5:
21 d glutamate neurotransmission) adjunctive to antidepressant therapy (ADT) in patients with major depr
22 DD), who did not respond adequately to prior antidepressant therapy (ADT).
23 ional impairment that standard-of-care (SOC) antidepressant therapies (ADTs) can take weeks to treat.
24 ing tapering of antidepressant medication vs antidepressant therapy alone (hazard ratio [HR], 0.86; 9
25 cronymic) is regulated in the hippocampus by antidepressant therapies and animal models of depression
26 ptors and adenylyl cyclase may underlie both antidepressant therapy and depressive illnesses.
27                                      Current antidepressant therapies are effective in only some pati
28 y modest and differences in efficacy between antidepressant therapies are small.
29 S) therapy, a fast-acting and very effective antidepressant therapy, are poorly understood.
30 with a recent depression diagnosis who began antidepressant therapy but had not used antidepressants
31          Earlier studies have indicated that antidepressant therapy confers a modest reduction in dep
32 sociations for manic/hypomanic states during antidepressant therapy, current mixed mood symptoms, and
33  of 114 untreated depressed patients started antidepressant therapy during hospitalization (nine with
34      A majority of the patients discontinued antidepressant therapy during the first 30 days (42.4%).
35 uring hospitalization, only 11% received any antidepressant therapy during the median 11-month follow
36                                    Optimized antidepressant therapy followed by a pain self-managemen
37 ment recommend 4 to 9 months of continuation antidepressant therapy following remission of acute symp
38                                Research into antidepressant therapies for TRD has evolved from explor
39 on treatment guidelines recommend continuing antidepressant therapy for at least 4 to 9 months, many
40 those remaining on their initial regimens of antidepressant therapy for at least 6 months were more l
41 ed to fully assess the benefits and risks of antidepressant therapy for bipolar disorder.
42         Only 27.6% of the patients continued antidepressant therapy for more than 90 days.
43  receiving a mood stabilizer plus adjunctive antidepressant therapy had a durable recovery, as did 51
44 until safety and efficacy are determined for antidepressant therapy in patients who recently have had
45  the effects of maintaining or discontinuing antidepressant therapy in this setting.
46 hat these patients have reduced responses to antidepressant therapy, including selective serotonin re
47  287,543 adults aged 18 years and older with antidepressant therapy initiated, we observed outcome ra
48                           Mood disorders and antidepressant therapy involve alterations of monoaminer
49                     Early discontinuation of antidepressant therapy is widespread in the community tr
50 nse, and the delayed onset of the effects of antidepressant therapies, leave many patients inadequate
51 ned in a 1:1 ratio to maintain their current antidepressant therapy (maintenance group) or to taper a
52            The limited efficacy of available antidepressant therapies may be due to how they affect t
53 ly contribute to depressive disorders, while antidepressant therapies may enhance GABAergic synaptic
54                                     However, antidepressant therapy may be beneficial for patients wh
55 nt large randomized trials suggest tricyclic antidepressant therapy may be effective in functional dy
56 , which is implicated in stress, reward, and antidepressant therapy, may play a role.
57                               Termination of antidepressant therapy often has negative consequences.
58 -controlled trial to evaluate the effects of antidepressant therapy on symptoms, gastric emptying (GE
59 tment with a mood stabilizer plus adjunctive antidepressant therapy or a mood stabilizer plus a match
60 ent for erectile dysfunction associated with antidepressant therapy or subsyndromal depression.
61 was designed to determine whether adjunctive antidepressant therapy reduces symptoms of bipolar depre
62 amethasone, growth factors, nitric oxide and antidepressant therapies regulate the expression of p11.
63 n who are euthymic in the context of ongoing antidepressant therapy should be aware of the associatio
64 ervention consisted of 12 weeks of optimized antidepressant therapy (step 1) followed by 6 sessions o
65                                Donepezil and antidepressant therapy temporarily improved global cogni
66 bition ratio represents a novel strategy for antidepressant therapies that reproduces behavioral and
67 ractices who felt well enough to discontinue antidepressant therapy, those who were assigned to stop
68 o patients with depression who are beginning antidepressant therapy to improve depressive symptoms mo
69 ammatory therapies as adjunctive to standard antidepressant therapy to improve treatment efficacy, pa
70                                 Intensity of antidepressant therapy was predicted by severity of depr
71 om their primary care physician thought that antidepressant therapy was warranted and who completed a
72            The two well-established chemical antidepressant therapies were also ineffective, indicati
73 ll as well as before and after initiation of antidepressant therapy were compared for patients who re
74        Characteristics of patients receiving antidepressant therapy were examined to identify factors
75  failure with citalopram and still requiring antidepressant therapy were identified in the STAR*D (Se
76  mood stabilizer with or without concomitant antidepressant therapy were randomly assigned to receive
77                                              Antidepressant therapy with 15 to 45 mg/d of mirtazapine