ライフサイエンスコーパス: antidepressant

1 der (MDD) achieve remission with their first antidepressant.

2 th of inhibition of serotonin reuptake of an antidepressant.

3 less likely to receive a prescription for an antidepressant.

4 ver a 12-week course, in addition to ongoing antidepressant.

5 ct is not moderated by the concurrent use of antidepressants.

6 ling may be required for the effects of some antidepressants.

7 us (DG) initiate the therapeutic response to antidepressants.

8 nd another 6,068 (13%) had been treated with antidepressants.

9 he therapeutic benefits of both rapid acting antidepressants.

10 pindolol used in conjunction with classical antidepressants.

11 ior efficacy compared to placebo or existing antidepressants.

12 and biochemical end points of rapidly acting antidepressants.

13 ressive disorder (MDD) and in the actions of antidepressants.

14 new class of rapidly-acting and long-lasting antidepressants.

15 t are less likely to respond to conventional antidepressants.

16 er were enriched for both antipsychotics and antidepressants.

17 ants and in 819 children (0.5%) unexposed to antidepressants.

18 iomarker for the development of rapid acting antidepressants.

19 ion-based cohort study included new users of antidepressants 18 years or older from January 1, 1995,

20 Among a cohort of 1363990 incident users of antidepressants (36.8% male; 63.2% female; mean [SD] age

21 CI, 1.34-2.64) and tricyclic or other cyclic antidepressants (absolute risk, 0.89 per 10000 person-mo

22 , 2.15; 95% CI, 1.06-4.36), but not of other antidepressants (absolute risk, 1.15 per 10000 person-mo

23 conclude that increased cycling precedes the antidepressant action at behaviorally effective doses an

24 ochondria have a critical role for mediating antidepressant action including the rapid ketamine respo

25 ndings indicate that Narp contributes to the antidepressant action of ECT and implicate the ability o

26 n suggested to have a role in depression and antidepressant action, although it is unknown whether BD

27 r antagonist ketamine GLYX-13 produces rapid antidepressant actions in depressed patients and in prec

28 However, the mechanisms underlying the antidepressant actions of GLYX-13 have not been characte

29 Here we investigate the antidepressant actions of inhibitors of monoacylglycerol

30 release within the mPFC is necessary for the antidepressant actions of scopolamine.

31 r characterize the mechanisms underlying the antidepressant actions of this agent.

32 rch suggests that B. caapi preparations show antidepressant activity, a therapeutic effect that has b

33 icacy of novel agents or identify doses with antidepressant activity.

34 Antidepressants (ADs) are the most common treatment for

35 order (MDD) treated with currently available antidepressants (ADs) show full remission.

36 elective serotonin reuptake inhibitor (SSRI) antidepressants, all other non-SSRI antidepressants, or

37 Here, we investigated the potential antidepressant and anti-inflammatory effects of BHB on r

38 c prebiotic FOS+GOS treatment exhibited both antidepressant and anxiolytic effects.

39 ate-severe AD patients had increased risk of antidepressant and anxiolytic medication use, while pati

40 enzodiazepine use in those with simultaneous antidepressant and benzodiazepine new use, and identify

41 ulator of neurotransmission and a target for antidepressants and addictive drugs.

42 Treatment with antidepressants and alosetron (a 5HT3 antagonist) has sh

43 mined the links between prenatal exposure to antidepressants and autism spectrum disorders (ASDs) in

44 s common and can be effectively treated with antidepressants and electroconvulsive therapy.

45 action of NMDAR antagonists as rapid-acting antidepressants and how they engage a neuron's or neural

46 s diagnosed in 37 children (0.9%) exposed to antidepressants and in 819 children (0.5%) unexposed to

47 n the antidepressant effects of conventional antidepressants and ketamine were also investigated.

48 solve key discrepancies between rapid-acting antidepressants and local homeostatic mechanisms.

49 predicting which patients will improve with antidepressants and which type of antidepressant may be

50 Postpartum AD was defined as use of antidepressants and/or hospital contact for PPD within 6

51 nhibitors [SNRIs], tricyclic or other cyclic antidepressants, and other antidepressants) was assessed

52 ehaviors, including impulsivity, response to antidepressants, and response to psychostimulants, point

53 rmeant PPARgamma-selective agonist, elicited antidepressant- and anxiolytic-like behavioral effects i

54 lfonamide) exhibited a broad antipsychotic-, antidepressant-, and anxiolytic-like activity, not elici

55 BACKGROUND & AIMS: Central neuromodulators (antidepressants, antipsychotics, and other central nervo

56 of dementia (BPSD) are nowadays addressed by antidepressant, anxiolytic, and antipsychotic drugs, oft

57 glitazone-induced adiponectin expression and antidepressant/anxiolytic-like effects.

58 s, alone and in combination, antipsychotics, antidepressants, anxiolytics, and hypnotics.

59 opioids and concomitant co-administration of antidepressants, anxiolytics, and psychological therapie

60 n meta-analyses of studies that suggest that antidepressants are minimally effective, not effective,

61 Antidepressants are one of the most commonly prescribed

62 nd pharmacological inhibition of GLO1 in two antidepressant assay models: the tail suspension test (T

63 e among adults with depression initiating an antidepressant, assess antidepressant treatment length b

64 treated for depression; however, those given antidepressants before breast cancer had a significantly

65 ssion and reduction of functional Ih produce antidepressant behavior.

66 amycin into the medial PFC (mPFC) blocks the antidepressant behavioral actions of GLYX-13, indicating

67 -dependent Ca(2+) channels (VDCCs) block the antidepressant behavioral actions of GLYX-13.

68 inally, inhibition of CCK neurons mimics the antidepressant behavioral effects of SSRIs, suggesting t

69 Switch to a different antidepressant, bupropion (switch group, n = 511); augme

70 d mediates the long duration of kappa opioid antidepressants by an uncharacterized, arrestin-independ

71 Antidepressants can be gradually tapered over a period o

72 The major pollutants observed were the antidepressants (citalopram, paroxetine, sertraline, ven

73 pregnancy rather than antenatal exposure to antidepressants could have a major role in the risk for

74 nonpsychotic MDD, unresponsive to at least 1 antidepressant course meeting minimal standards for trea

75 ker of successful treatment and a target for antidepressants' development.

76 r evaluation of isoflurane as a rapid-acting antidepressant devoid of the psychotomimetic effects and

77 ester antidepressant use and first-trimester antidepressant dispensations.

78 the egg, mimicking maternal transfer of this antidepressant, disrupts developmental programming using

79 Novel approaches to understanding of antidepressant drug action include a focus on early chan

80 urely neurotransmitter-based explanation for antidepressant drug action is challenged by the delayed

81 signaling cascades may be novel targets for antidepressant drug development.

82 ology of depression, which can aid in future antidepressant drug discovery efforts.

83 site of common transcriptional regulation by antidepressant drugs and in both reversing susceptibilit

84 ract risk after exposure to SSRI or to other antidepressant drugs in a large electronic primary care

85 mice mimicked the effects of anxiolytic and antidepressant drugs in a number of behavioral tests, wi

86 on-deficit/hyperactivity disorder drugs, and antidepressant drugs) and for 9 of the 19 AMCs that impl

87 ention-deficit/hyperactivity disorder drugs, antidepressant drugs, and antipsychotic drugs) comparing

88 (SSRIs) are the most commonly used class of antidepressant drugs, but the cellular and molecular mec

89 RI prescriptions and prescriptions for other antidepressant drugs.

90 ar target for the development of fast-acting antidepressant drugs.

91 n be reversed by treatment with conventional antidepressants drugs, as well as by subanesthetic doses

92 sociation between ASDs and fetal exposure to antidepressants during pregnancy for each trimester of p

93 ed in offspring born to mothers treated with antidepressants during pregnancy.

94 Here we provide new support for the antidepressant effect of an anesthetic drug, ketamine, b

95 symptoms within 24 h after infusion and this antidepressant effect was attributed to increased alpha-

96 e an association between ketamine's clinical antidepressant effects and circadian timekeeping.

97 ressant fluoxetine produces rapid or delayed antidepressant effects in acute stress- or chronic corti

98 se, and thus, MAGL inhibitors, which produce antidepressant effects in chronic corticosterone-exposed

99 lcholine receptor antagonist, produces rapid antidepressant effects in patients with depression.

100 loride's ability to produce rapid and robust antidepressant effects in patients with mood and anxiety

101 ll as six treatments that possess fast-onset antidepressant effects in the clinic: electroconvulsive

102 his is consistent with previous reports that antidepressant effects of amisulpride in depression emer

103 sticity could be a major contribution to the antidepressant effects of ayahuasca.

104 The involvement of PKMzeta in the antidepressant effects of conventional antidepressants a

105 The results demonstrate that the antidepressant effects of GLYX-13 are blocked by intra-m

106 ling is required for the rapid and sustained antidepressant effects of GLYX-13.

107 s study was to characterize the dose-related antidepressant effects of ketamine in patients with trea

108 The mechanisms of action of the rapid antidepressant effects of ketamine, an N-methyl-D-aspart

109 t both biochemically and behaviorally to the antidepressant effects of ketamine.

110 expression in mPFC and PKMzeta mediated the antidepressant effects of ketamine.

111 activity-dependent BDNF release in the rapid antidepressant effects of scopolamine.

112 A low-dose of MAGL inhibitors produces antidepressant effects on acute stress-exposed mice, thr

113 rtial agonist properties that produces rapid antidepressant effects, but without the psychotomimetic

114 These data suggest that, in addition to its antidepressant effects, ketamine also has a salutary eff

115 ich increase cAMP cascade activity, may have antidepressant effects.

116 but not Bdnf, in the DRN results in loss of antidepressant efficacy and increased aggression-related

117 antidepressant trials distort the picture of antidepressant efficacy for teen depression.

118 Ketamine has rapid antidepressant efficacy, but it is unknown if ketamine i

119 iponectin significantly predicted ketamine's antidepressant efficacy, suggesting an adverse metabolic

120 Conversely, dHc TLQP-62 infusion had rapid antidepressant efficacy, which was reduced in BDNF floxe

121 electroconvulsive seizures (ECS), blocks its antidepressant efficacy.

122 een-group differences (25%-30%) that support antidepressant efficacy.

123 measures of depression-related behavior and antidepressant efficacy.

124 bility; this change appears to be related to antidepressant efficacy.

125 nomous role for BDNF in the DRN in mediating antidepressant efficacy.

126 d treatment outcomes for three commonly used antidepressants (escitalopram, sertraline, and extended-

127 ts) evidenced a positive association between antidepressant exposure and ASDs (odds ratio [OR], 1.81;

128 ses for associations between first-trimester antidepressant exposure and birth and neurodevelopmental

129 ge in Ontario, Canada, in utero serotonergic antidepressant exposure compared with no exposure was no

130 d autism spectrum disorder with serotonergic antidepressant exposure during pregnancy may have been c

131 Prenatal antidepressant exposure has been associated with adverse

132 ternal, and paternal traits, first-trimester antidepressant exposure was associated with preterm birt

133 Serotonergic antidepressant exposure was defined as 2 or more consecu

134 or potential confounders, the RR of ID after antidepressant exposure was estimated at 1.33 (95% CI, 0

135 The conventional antidepressant fluoxetine produces rapid or delayed anti

136 The antidepressants fluoxetine, desipramine and ketamine inc

137 se primary care physician newly initiated an antidepressant for depression.

138 troversy surrounds the efficacy of the newer antidepressants for children and adolescents with depres

139 elective serotonin reuptake inhibitor (SSRI) antidepressants, has been thought to be effective for tr

140 of a conventional monoamine-based tricyclic antidepressant, imipramine, and a rapidly acting, non-mo

141 ndary outcomes were the associations between antidepressants in each individual trimester or before p

142 ulation of PPCPs and the selective uptake of antidepressants in fish from the Niagara River, which co

143 Antidepressants in general (8 of 9 treatments) were more

144 Examining transcriptional regulation by antidepressants in key neural circuits implicated in dep

145 We review the effects of classical antidepressants in these models, as well as six treatmen

146 Patients taking antidepressants, including Clomipramine (CLP), have an i

147 The use of antidepressants increased (24.1%-27.5%).

148 ith benzodiazepines, simultaneous new use at antidepressant initiation and the benzodiazepine regimen

149 One-tenth of antidepressant initiators with depression simultaneously

150 onset of therapeutic efficacy of traditional antidepressants is delayed by several weeks.

151 herefore, identification of novel fast-onset antidepressants is desirable.

152 A major limitation of classical antidepressants is that 2-4 weeks of continuous treatmen

153 Venlafaxine, a widely prescribed antidepressant, is a selective serotonin and norepinephr

154 d in the mechanism of action of rapid-acting antidepressant ketamine: activation of brain-derived neu

155 e, and a rapidly acting, non-monoamine-based antidepressant, ketamine, in mice subjected to chronic s

156 standardized behavioral approach to measure antidepressant-like activity of KT and SD.

157 hannel trafficking and its relationship with antidepressant-like behavior using a viral rescue approa

158 comotion, reduced anxiety-like behavior, and antidepressant-like behavior.

159 ctionally influences channel trafficking and antidepressant-like behavior.

160 b-interacting protein (TRIP8b) also produces antidepressant-like behavioral effects and suggests that

161 tibody infusions into the mPFC prevented the antidepressant-like behavioral effects of scopolamine.

162 ed HCN-channel trafficking and increased the antidepressant-like behavioral phenotype of TRIP8b KO mi

163 that a single isoflurane anesthesia produces antidepressant-like behavioural effects in the learned h

164 ontal cortex (PFC) of mice recapitulates the antidepressant-like effect observed in cacna1c HET mice

165 ntimanic-like effects of lithium but not the antidepressant-like effects in mice.

166 t to be tested in humans but have fast-onset antidepressant-like effects in one or more of these anti

167 f Tet1 in NAc neurons of adult mice produced antidepressant-like effects in several behavioral assays

168 hat inhibiting TRIP8b function could produce antidepressant-like effects without affecting the heart.

169 These findings demonstrate that BHB exerts antidepressant-like effects, possibly by inhibiting NLRP

170 Here, we demonstrate that the antidepressant-like efficacy of three unique drugs, with

171 have been previously reported to exhibit an antidepressant-like phenotype, the molecular and circuit

172 sed following REDD1-mediated reversal of the antidepressant-like phenotype.

173 A-33 has an antidepressant-like profile as indicated by reduced immo

174 since agonists of this receptor induce rapid antidepressant-like responses in rodents.

175 ostasis that promotes both pro-resilient and antidepressant-like responses.

176 the other treatments received (ie, CBCM and antidepressants) likely produced a ceiling effect beyond

177 are important to understand in reviewing the antidepressant literature: the strengths and weaknesses

178 prove with antidepressants and which type of antidepressant may be most effective.

179 iod of several weeks, but discontinuation of antidepressants may be associated with relapse or recurr

180 Preclinical studies indicate that most antidepressants may counteract this dysregulation.

181 Although antidepressants may effectively treat depression in olde

182 100 person-years; for women with postpartum antidepressant medication after first birth, it was 35.0

183 (95% CI 31.5-68.4) and women with postpartum antidepressant medication after their first birth had a

184 f remission and treatment failure to CBT and antidepressant medication and survived application of th

185 ble-blind, placebo-controlled trial (RCT) of antidepressant medication for 10-week's duration in pati

186 nd either an evidence-based psychotherapy or antidepressant medication for nonpsychotic major depress

187 een cognitive-behavioral therapy (CBT) or an antidepressant medication for treatment-naive adults wit

188 on of cognitive behavioral therapy (CBT) and antidepressant medication improved depression symptoms,

189 fety of riluzole vs placebo as an adjunct to antidepressant medication in outpatients with major depr

190 Nonadherence to antidepressant medication is common and leads to poor ou

191 in children exposed during pregnancy to any antidepressant medication or specifically to selective s

192 Many older patients need the same doses of antidepressant medication that are used for younger adul

193 Maternal antidepressant medication use during pregnancy has previ

194 To examine the association of maternal antidepressant medication use during pregnancy with ID i

195 er a prospective or a historical trial of an antidepressant medication were randomized in a 2 : 3 : 3

196 12 weeks of randomized treatment with CBT or antidepressant medication.

197 onset chronic depression who were not taking antidepressant medication.

198 onse and can occur shortly after exposure to antidepressant medication.

199 in had a significant association with use of antidepressant medications (P = .045) but not with tear

200 Depression and use of antidepressant medications are both associated with incr

201 ders, suggest a broad and important role for antidepressant medications in pediatric internalizing co

202 with nonocular comorbidities such as use of antidepressant medications rather than with clinical sig

203 Conventional antidepressant medications, which act on monoaminergic s

204 o treatment both within and across different antidepressant medications.

205 ne trends in simultaneous benzodiazepine and antidepressant new use among adults with depression init

206 Although first-line antidepressants offer therapeutic benefit, about 35% of

207 ressant-like effects in one or more of these antidepressant onset sensitive models.

208 seven rodent models currently used to assess antidepressant onset: olfactory bulbectomy, chronic mild

209 ffects of GLO1 inhibition in three models of antidepressant onset: the chronic FST (cFST), chronic mi

210 the novel object recognition test but had no antidepressant or anxiolytic benefit.

211 d depression or anxiety or prescriptions for antidepressants or anxiolytics.

212 egan antidepressant therapy but had not used antidepressants or benzodiazepines in the prior year.

213 o be treated with neuromodulators (primarily antidepressants), or psychological interventions (psycho

214 r (SSRI) antidepressants, all other non-SSRI antidepressants, or other nonantidepressant psychotropic

215 rmone binding protein (CRHBP) gene predicted antidepressant outcomes for remission, response, and sym

216 genotype was again associated with favorable antidepressant outcomes, with comparable effect sizes.

217 to emotional stimuli in a manner similar to antidepressant pharmacotherapy.

218 ll-validated assay models exist that predict antidepressant potential, few thoroughly tested animal m

219 %) and increased further after RYGB-that is, antidepressants (PR = 1.13; 95% CI = 1.07-1.19), antipsy

220 type (WT) littermates in tail suspension, an antidepressant-predictive assay, and amphetamine hyperlo

221 ance abuse, schizophrenia, and the potential antidepressant properties of ketamine, and comparisons w

222 Among neurobiological mechanisms underlying antidepressant properties of ketamine, structural remode

223 hree unique drugs, with reported rapid onset antidepressant properties, is coupled with a rapid trans

224 lude: (1) low to modest dosages of tricyclic antidepressants provide the most convincing evidence of

225 nts receiving placebo, patients receiving an antidepressant reported significantly more treatment-eme

226 Preclinical identification of fast-onset antidepressants requires animal models that can accurate

227 sychoradiological studies have reported that antidepressant responders and nonresponders show differe

228 atients with major depressive disorder, both antidepressant responders and nonresponders, using the a

229 ociated with susceptibility, resilience, and antidepressant response and nonresponse in the prefronta

230 tamine, which mirrors the time course of the antidepressant response and reversal of the molecular de

231 Results from these studies suggest that an antidepressant response in association with ketamine occ

232 ut not FLX, induced molecular markers of the antidepressant response including brain-derived neurotro

233 In hippocampus, the antidepressant response to ketamine is associated with r

234 In addition, evidence of an antidepressant response to subanesthetic-dose ketamine h

235 is involved in major depressive disorder and antidepressant response.

236 o June 2016 to identify studies focussing on antidepressant response.

237 target and the subgenual cingulate predicts antidepressant response.

238 s has been linked to risk for depression and antidepressant response.

239 re significantly enriched in this cluster of antidepressant-response genes.

240 strengthen the role of TrkB signaling in the antidepressant responses and encourage further evaluatio

241 which on administration produces fast-acting antidepressant responses in patients with major depressi

242 DG protection leads to stress resilience and antidepressant responses via epigenetic programming of a

243 involvement of the circadian clock in rapid antidepressant responses.

244 nalogues of natural product (-)-nicotine and antidepressant sertraline by late-stage amination and az

245 The Chronic Kidney Disease Antidepressant Sertraline Trial (CAST) was a randomized,

246 ference in the efficacy of second-generation antidepressants (SGAs) versus most other treatments for

247 fore, it was hypothesized that responders to antidepressants show a) a high level of EEG-vigilance (a

248 disposition and efficacy of several opiates, antidepressants, statins, and antibiotics.

249 Many antidepressants stimulate adult hippocampal neurogenesis

250 hannel function has been proposed as a novel antidepressant strategy.

251 tient expectancy mediates placebo effects in antidepressant studies.

252 isk of incident type 2 diabetes in youths by antidepressant subclass and according to duration of use

253 use of SSRIs or SNRIs-the most commonly used antidepressant subclass-was associated with an increased

254 used to prevent bone loss in patients taking antidepressants, such as CLP.

255 Higher brain arousal level in responders to antidepressants supports the concept that dysregulation

256 nhibitors (SSRIs) and the tricyclic class of antidepressant (TCA) agents.

257 y modest and differences in efficacy between antidepressant therapies are small.

258 bition ratio represents a novel strategy for antidepressant therapies that reproduces behavioral and

259 nobutyric acid (GABA) that are normalized by antidepressant therapies.

260 with a recent depression diagnosis who began antidepressant therapy but had not used antidepressants

261 o patients with depression who are beginning antidepressant therapy to improve depressive symptoms mo

262 lated by chronic treatment with conventional antidepressants through BDNF/TrkB signaling.

263 n a minority of individuals after first-line antidepressant treatment ( approximately 35%); predictor

264 9608 youths aged 5 to 20 years who initiated antidepressant treatment (59087 female youths and 60521

265 as recorded 14 +/- 1 days following onset of antidepressant treatment (T1).

266 No meaningful difference in antidepressant treatment at 6 months was observed by sim

267 y, mitigate concomitant anxiety, and improve antidepressant treatment continuation.

268 Response to antidepressant treatment in major depressive disorder (M

269 ression initiating an antidepressant, assess antidepressant treatment length by simultaneous new use

270 e utilized the large variance in response to antidepressant treatment occurring in DBA/2J mice, enabl

271 changes in BMP signaling mediate effects of antidepressant treatment on neural progenitor cell proli

272 henotype and display an enhanced response to antidepressant treatment when tested in paradigms for mo

273 y a role in emergent suicidal ideation after antidepressant treatment), GRIK4 (which may influence tr

274 years; 507 451 women [66.3%]) who initiated antidepressant treatment, 81020 (10.6%) also initiated b

275 etic protein (BMP) signaling is modulated by antidepressant treatment, and that the changes in BMP si

276 th major depressive disorder unresponsive to antidepressant treatment, augmentation with aripiprazole

277 depression's risk, severity, and response to antidepressant treatment, through a systematic review on

278 nterference by repeated disease episodes and antidepressant treatment, we conducted the first multimo

279 e is downregulated in MDD and upregulated by antidepressant treatment.

280 ocial defeat stress, which are normalized by antidepressant treatment.

281 e are few reliable predictors of response to antidepressant treatments.

282 clude the large number of industry-sponsored antidepressant trials distort the picture of antidepress

283 d regulatory context for the large number of antidepressant trials in the late 1990s and early 2000s;

284 Antidepressant use (selective serotonin reuptake inhibit

285 Maternal self-reported first-trimester antidepressant use and first-trimester antidepressant di

286 To assess the association between antidepressant use and the risk of incident type 2 diabe

287 Psychiatric diagnoses or antidepressant use during the study period were consider

288 h the stronger association specifically with antidepressant use may reflect that this endpoint better

289 Associations were stronger when only antidepressant use was used to define cases (for ozone,

290 in Denmark who had no psychiatric diagnoses, antidepressant use, or hormonal contraceptive use before

291 risk of type 2 diabetes in association with antidepressant use.

292 e recommendations for identifying fast-onset antidepressants using rodent behavioral models and molec

293 Conventional antidepressants usually require several weeks to achieve

294 1000 person-years among children exposed to antidepressants vs 2.03 per 1000 person-years among unex

295 eduled during a 6-week period just after the antidepressant was prescribed.

296 In addition, preconception exposure to antidepressants was significantly associated with an inc

297 c or other cyclic antidepressants, and other antidepressants) was assessed using the following 4 time

298 The antidepressants were selectively taken up by various fis

299 tricyclic ring structure common to tricyclic antidepressants, which may be toxicologically relevant.

300 The use of SSRIs and more generally of antidepressants with strong inhibition of serotonin reup