ライフサイエンスコーパス: antidepressant

1 e on the clinical effects of bupropion as an antidepressant.

2 ncing a clinical resurgence as a fast-acting antidepressant.

3 which are the targets of novel rapid-acting antidepressants.

4 nts do not respond adequately to traditional antidepressants.

5 reduced the probability of being prescribed antidepressants.

6 omarker that is related to the mechanisms of antidepressants.

7 oach to improve therapeutic efficacy of SSRI antidepressants.

8 ein associated with depression and action of antidepressants.

9 s ephedrine and methamphetamine, and certain antidepressants.

10 mediating the delayed behavioral response to antidepressants.

11 s with remitted major depressive disorder on antidepressants.

12 ological and behavioral responses to chronic antidepressants.

13 velopment of cell-type specific, fast-acting antidepressants.

14 -converting enzyme (ACE) inhibitors (17.9%), antidepressants (17.8%), and lipid-lowering medications

15 Ketamine exerts rapid antidepressant action in depressed and treatment-resista

16 The scale and mechanism of antidepressant action of BoNT is unclear and maybe hypot

17 m as potential biomarkers for depression and antidepressant action, these were examined in LCLs.

18 ke phenotype, suggesting it was important to antidepressant action.

19 uggest a role for astrocytes in both MDD and antidepressant action.

20 AR) antagonist, produces rapid and sustained antidepressant actions in depressed patients, addressing

21 e dentate gyrus act as a pivotal mediator of antidepressant actions in mice.

22 Understanding the neurobiology of antidepressant actions may lead to development of improv

23 pyramidal neurons in mPFC mediate the rapid antidepressant actions of ketamine and rapastinel.

24 in Sst interneurons blocked or occluded the antidepressant actions of ketamine and revealed sex-spec

25 The results demonstrated that the antidepressant actions of ketamine were blocked by GluN2

26 1-pyramidal cell signaling that underlie the antidepressant actions of NMDAR-positive modulation vs.

27 e mPFC of male mice is sufficient to produce antidepressant actions, and conversely if activation of

28 Marked antidepressant activity and dose-dependent receptor occu

29 t 4E-BP1 and 4E-BP2 are key effectors of the antidepressant activity of ketamine and (2R,6R)-HNK, and

30 our data show that 4E-BPs are central to the antidepressant activity of ketamine.

31 The antidepressant activity of the drugs is mediated by 4E-B

32 Antidepressant activity was tested using the forced-swim

33 rvations showing that n-3 PUFA and SSRI have antidepressant affects, which may be additive.

34 ived areas were more likely to be prescribed antidepressants after adjusting for region.

35 Almost all antidepressant agents suppress REM sleep and a time-and-

36 t 5-HT2C receptor antagonism potentiates the antidepressant and anxiolytic effects of SSRIs.

37 cts of SSRIs and augmentation of therapeutic antidepressant and anxiolytic effects.

38 and anxiety disorder health care visits and antidepressant and anxiolytic prescriptions in 2015 as a

39 ood and anxiety disorder health care visits, antidepressant and anxiolytic prescriptions, and hospita

40 mimetic compound, ketamine, is a fast-acting antidepressant and induces synapse formation.

41 Both antidepressant and locomotion responses to TCP were enha

42 tudy, and warrant further exploration of the antidepressant and pro-cognitive effects of NSI-189.

43 aluated ketamine metabolites as mediators of antidepressant and psychotomimetic effects and their rel

44 ith the advent of ketamine as a rapid-acting antidepressant and the development and refinement of too

45 s included cytokine, depressive disorder and antidepressant and their synonyms.

46 n-3 PUFAs) have been reported to act as both antidepressants and anti-inflammatories, but the mechani

47 as likely to have received prescriptions for antidepressants and anxiolytics, and more than six times

48 by which TRPC4 mediates itch to serotonergic antidepressants and demonstrated the antipruritic effect

49 have suggested an association between taking antidepressants and dental implant failure.

50 an and serve as targets for drugs, including antidepressants and psychostimulants.

51 has led to new insights into the biology of antidepressants and the FDA approval of its s-isomer, Es

52 onse-inhibition task can predict response to antidepressants and whether its changes over time are co

53 hrine reuptake inhibitors [SNRIs], and other antidepressants), and for individual drugs.

54 e with bipolar disorders, and has antimanic, antidepressant, and anti-suicide effects.

55 ither before or after discontinuation of the antidepressant, and followed up for six months to assess

56 e that may be relevant to the antipsychotic, antidepressant, and side effect profiles of the drug.

57 e data to estimate US prescription fills for antidepressants, anxiolytics, antipsychotics, opioids, a

58 Antidepressants are widely prescribed for bipolar disord

59 Antidepressants are widely prescribed, but their efficac

60 challenges of developing novel rapid-acting antidepressants based solely on the receptor or regional

61 fferentiation, and may mimic effects of some antidepressants by increasing production of neurotrophic

62 ceiving alternative or no treatment and some antidepressants can be prescribed for other indications.

63 ased connectivity in a previously identified antidepressant CFP.

64 in each year were calculated overall, for 4 antidepressant classes (selective serotonin reuptake inh

65 to investigate the association of different antidepressant classes with dental implant failure.

66 0 for randomized controlled trials examining antidepressants compared to placebo.

67 However, the optimal antidepressant dose remains unknown.

68 cepted for its involvement in resilience and antidepressant drug action, is a common genetic locus of

69 te mechanism of action, and may inform novel antidepressant drug mechanisms that could yield superior

70 ralones, including a precursor to Zoloft, an antidepressant drug.

71 peutic strategies exist for depression, most antidepressant drugs require several weeks before reachi

72 SERT activity is modulated by antidepressants, e.g., S-citalopram and imipramine, to a

73 find that AP-1 function is required for the antidepressant effect in vivo.

74 bility in the forced swim test, mimicking an antidepressant effect.

75 nsmitter systems are necessary to achieve an antidepressant effect.

76 produced, can have an anti-inflammatory and antidepressant effect.

77 Ketamine produces immediate antidepressant effects and has inspired research into ne

78 lator (PAM), and antagonist, can exert rapid antidepressant effects as shown in several animal and hu

79 Novel immune-therapeutics can produce antidepressant effects in depressed patients with primar

80 hetic ketamine evokes rapid and long-lasting antidepressant effects in human patients.

81 onist, which produces rapid and long-lasting antidepressant effects in patients with major depressive

82 t (2S,6S;2R,6R)-hydroxynorketamine (HNK) had antidepressant effects in rodents, and that (2R,6R)-HNK

83 in the mPFC produced dose and time-dependent antidepressant effects in the forced swim and novelty su

84 agonist(2,3), provide rapid and long-lasting antidepressant effects in these patients(4-6), but the m

85 The antidepressant effects of ketamine and (2R,6R)-HNK in ro

86 Rapamycin pretreatment did not alter the antidepressant effects of ketamine at the 24-h timepoint

87 p = 0.04), suggesting a prolongation of the antidepressant effects of ketamine by rapamycin.

88 The discovery of the rapid-acting antidepressant effects of ketamine has 1) led to a parad

89 e rapamycin pretreatment failed to block the antidepressant effects of ketamine, but it prolonged ket

90 systemic vs. local blockade of mTORC1 in the antidepressant effects of ketamine, provides preliminary

91 Although antidepressant effects of mesenchymal stem cells (MSCs)

92 e, we showed that encapsulation enhanced the antidepressant effects of MSCs by attenuating depressive

93 discovery of the strikingly rapid and robust antidepressant effects of r/s-ketamine for the treatment

94 - but not Gad1-expressing neurons blocks the antidepressant effects of rapastinel.

95 In addition, the antidepressant effects of rapid-acting drugs are thought

96 interneurons blocks the rapid and sustained antidepressant effects of scopolamine, a nonselective ac

97 , and leaden paralysis) and may moderate the antidepressant effects of standard or novel (e.g., anti-

98 sociative side effects are necessary for its antidepressant effects remains unclear.

99 ectional modulation of NMDARs causes similar antidepressant effects remains unknown.

100 igation method (-32.4%) did not yield better antidepressant effects than the standard method (-40.6%)

101 nistration, ketamine exerts rapid and robust antidepressant effects that are thought to be mediated b

102 Ketamine has been proposed to exert its antidepressant effects through its metabolite (2R,6R)-hy

103 Ketamine, shown to have rapid antidepressant effects, fails to reverse elevated arousa

104 cts of ketamine, but it prolonged ketamine's antidepressant effects.

105 acute psychotomimetic symptoms and sustained antidepressant effects.

106 sts a manner in which n-3 PUFA could augment antidepressant effects.

107 -ketamine (ketamine) exerts rapid and robust antidepressant effects.

108 Ketamine has shown promising antidepressant efficacy for adolescent treatment-resista

109 ates PFC excitatory transmission and confers antidepressant efficacy in preclinical models.

110 study, our objective was to investigate the antidepressant efficacy of piTBS monotherapy.

111 o elucidate the genetic underpinnings of the antidepressant efficacy of S-ketamine (esketamine) nasal

112 Mounting evidence supports the rapid antidepressant efficacy of the N-methyl-D-aspartate rece

113 e to neuronal activity, to contribute to the antidepressant efficacy of the serotonin/norepinephrine

114 eural mechanism by which ketamine exerts its antidepressant efficacy, via rapid blunting of aberrant

115 c, wound healing, anti-HIV, anti-anxiety and antidepressant, etc.

116 rmamentarium for major depression, including antidepressants, evidence-based psychotherapies, nonphar

117 analysis of the association between prenatal antidepressant exposure and autism risk, the authors exa

118 ns supported an association between prenatal antidepressant exposure and autism.

119 ional studies of the association of prenatal antidepressant exposure with autism.

120 downregulated in MDD patients, regardless of antidepressant exposure.

121 Antidepressant fluoxetine disrupts the interaction betwe

122 sensor is presented for the determination of antidepressant fluvoxamine in urine and blood plasma sam

123 .6%) were the most commonly prescribed first antidepressant, followed by TCAs (35.7%).

124 serotonin reuptake inhibitors as first-line antidepressants for adults with major depressive disorde

125 Moreover, we found that antidepressants had a heterogeneous effect on the identi

126 mer of ketamine, in conjunction with an oral antidepressant, has been approved by the FDA for treatin

127 To identify how commonly used tricyclic antidepressants impact the molecular composition in thes

128 lator (PAM), is currently being tested as an antidepressant in clinical trials, but the mechanism and

129 34.1% of those who were first prescribed an antidepressant in the study period.

130 The use of antidepressants in children and adolescents remains cont

131 etworks may characterize acute recovery with antidepressants in depression.

132 To assess the therapeutic benefits of antidepressants in depressive women during and after men

133 mand for fast and sensitive determination of antidepressants in human body fluids because of the pres

134 iology of major depression and the action of antidepressants, in the dentate gyrus of the hippocampus

135 In contrast to slow-acting antidepressants, in which targeting monoaminergic recept

136 Most antidepressants, including selective serotonin reuptake

137 e inhibitors (SSRIs) constitute a first-line antidepressant intervention, though the precise cognitiv

138 estigated the metabolic impact in the NAc of antidepressant LAC treatment in chronically-stressed mic

139 The antidepressant lead-in employing single-blind placebo an

140 The success rate of open-label antidepressant lead-ins without placebo or using double-

141 dulator, L-655,708, reproduces the sustained antidepressant-like (AD-like) effect of R,S-ketamine in

142 tamine (HNK) retains the rapid and sustained antidepressant-like actions of ketamine, but is spared i

143 as been shown to play a critical role in the antidepressant-like actions of ketamine.

144 Together, these results demonstrate antidepressant-like actions of the NMDAR PAM AGN-241751

145 role of GluN2B-containing NMDAR in mediating antidepressant-like behavioral effects of AGN-241751.

146 terneuron-selective Ahnak KO mice display an antidepressant-like behavioral phenotype.

147 n and, in vivo, it preferentially exerted an antidepressant-like effect in the Porsolt forced swimmin

148 We demonstrate that AGN-241751 exerts antidepressant-like effects and reverses behavioral defi

149 GPR56 peptide agonists have antidepressant-like effects and upregulated AKT/GSK3/EIF

150 mechanism and NMDAR subunit(s) mediating its antidepressant-like effects are unknown.

151 ypes 2 (mGlu(2)) and 3 (mGlu(3)) exert rapid antidepressant-like effects by enhancing prefrontal cort

152 While (2R,6R)-HNK is thought to exert its antidepressant-like effects by potentiating alpha-amino-

153 ist 8-OH-DPAT induces rapid and long-lasting antidepressant-like effects in the forced swim, novelty-

154 Finally, we found that the antidepressant-like effects induced by high-dose lithium

155 sion, our results demonstrate anxiolytic and antidepressant-like effects of GHRH analogs that could i

156 n addition, the results demonstrate that the antidepressant-like effects of intra-mPFC infusion of 8-

157 the serotonergic system is important for the antidepressant-like effects of ketamine, a non-competiti

158 reveal a metabolic signature in the NAc for antidepressant-like effects of LAC in vulnerable mice ch

159 y in LepRb-expressing neurons, abolishes the antidepressant-like effects of leptin.

160 ng that both mGlu(2) and mGlu(3) NAMs induce antidepressant-like effects through related but divergen

161 eptor in the mPFC exerts rapid and sustained antidepressant-like effects via activation of AMPA recep

162 into the dorsal hippocampus has fast-acting antidepressant-like effects, and that some of these effe

163 nnabinoid signaling produces anxiolytic- and antidepressant-like effects, but the neural circuits inv

164 th MIA-690 and MR-409 induced anxiolytic and antidepressant-like effects, increased norepinephrine an

165 in turn is indispensable for leptin-induced antidepressant-like effects.

166 l- and heroin-seeking behaviour, and produce antidepressant-like effects.

167 DA receptor (NMDAR) activity can exert rapid antidepressant-like effects.

168 otonin receptor 7 gene (HTR7) resulted in an antidepressant-like phenotype, suggesting it was importa

169 ion-related phenotype (along with a ketamine antidepressant-like response).

170 hem are modulated by existing drugs, such as antidepressants, lithium and omega-3 fatty acids.

171 Ketamine's antidepressant mechanism is predominantly mediated by th

172 eed to better understand the neural basis of antidepressant medication (ADM) response with respect to

173 rain regions predict differential outcome to antidepressant medication (sertraline) compared with pla

174 eatment for PTSD and failed to respond to an antidepressant medication for MDD.

175 % chance of receiving either an experimental antidepressant medication or placebo.

176 ession samples, wherein it reflected general antidepressant medication responsivity and related diffe

177 ctivity moderated response to sertraline, an antidepressant medication that targets these neurotransm

178 ristics (recurrent status, remission status, antidepressant medication use, age of onset, or symptom

179 nt daily dose, and dopamine agonist (DA) and antidepressant medication use.

180 67,807 individuals who received at least one antidepressant medication, 925 (1.36%) subsequently rece

181 Vortioxetine, an antidepressant medication, has putative procognitive and

182 ial role in mediating the effects of chronic antidepressant medication.

183 active candidates for the development of new antidepressant medications.

184 order, who received at least one of the nine antidepressant medications.

185 s, this suggest that the limited efficacy of antidepressants might be compensated by combining therap

186 n module, taking antiretroviral therapy, and antidepressant-naive.

187 Prescription of antidepressants occurred in 47.0% of visits for bipolar

188 ailure included smoking (OR = 5.221), use of antidepressants (OR = 4.285), posterior maxilla location

189 treatment receive benzodiazepines, tricyclic antidepressants, or a drug that is not Food and Drug Adm

190 thin the hippocampus may differ according to antidepressant outcome, and that larger amounts of hippo

191 clinical trials for adjunctive therapies for antidepressant partial- and non-responders with major de

192 geting the Enz/ARv7/MAO-A signaling with the antidepressants phenelzine or clorgyline can restore Enz

193 treet tree density and species richness with antidepressant prescribing for 9751 inhabitants of Leipz

194 is provides evidence of a continuing rise of antidepressant prescribing in adolescents aged 12-17 yea

195 e examined trends over time and variation in antidepressant prescribing in children and young people

196 Moreover, antidepressant prescription in bipolar disorder is assoc

197 the prevalence and misidentifying the first antidepressant prescription.

198 disorder diagnosis within 3 months of index antidepressant prescription.

199 ed additive models, we found a lower rate of antidepressant prescriptions for people living within 10

200 Incidence and prevalence rates of antidepressant prescriptions in each year were calculate

201 Antidepressant prescriptions persisted despite a lack of

202 ur empirical strategy compares the number of antidepressant prescriptions written by providers practi

203 es at any distance, were not associated with antidepressant prescriptions.

204 o compare to active placebo the rapid acting antidepressant properties of a broad range of subanesthe

205 he volume change of the DG is related to the antidepressant properties of ECT, and may reflect neurog

206 Oleic acid, an AI-2 inhibitor, exhibited antidepressant properties, reducing depressive-like beha

207 Until the discovery of the rapid acting antidepressant (RAAD) effects of ketamine, treatments we

208 refrontal cortex pyramidal cells, leading to antidepressant-relevant actions.

209 rs as well as in the effects of rapid-acting antidepressants remains to be determined.

210 , fatigue, and sexual function in women with antidepressant-resistant major depression.

211 sterone cream in 101 women, ages 21-70, with antidepressant-resistant major depression.

212 effects of r/s-ketamine for the treatment of antidepressant-resistant symptoms of depression has led

213 a sequential molecular network to track the antidepressant response and provide a new avenue that co

214 between (2S,6S;2R,6R)-HNK concentration and antidepressant response at 3 and 7 days post-infusion.

215 ne concentration positively predicted distal antidepressant response at Day 11 post-infusion, and an

216 re the relationship between dissociation and antidepressant response at the molecular, biomarker, and

217 Predicting antidepressant response has been a clinical challenge fo

218 Establishing Moderators and Biosignatures of Antidepressant Response in Clinical Care (EMBARC) study

219 Establishing Moderators and Biosignatures of Antidepressant Response in Clinical Care (EMBARC, n = 29

220 (2S,6S;2R,6R)-HNK concentrations and weaker antidepressant response in humans and provide further ra

221 hat role hippocampal plasticity plays in the antidepressant response to ECT.

222 ciative effects and acute and longer-lasting antidepressant response to ketamine and other N-methyl-D

223 onclusion that dissociation is necessary for antidepressant response to ketamine.

224 er of genetic variants to be associated with antidepressant response, the sample sizes are small and

225 ve disorder (MDD) is a negative predictor of antidepressant response.

226 support the role of HTR7 in association with antidepressant response.

227 indings uncover a potential role of GPR56 in antidepressant response.

228 plasticity may not be conducive to positive antidepressant response.

229 10 (p11), linking neuronal plasticity to the antidepressant response.

230 mma power changes as potential biomarkers of antidepressant response.

231 at could be used to accelerate or potentiate antidepressant responses by triggering neuroplasticity.

232 tes synaptic plasticity that underlies rapid antidepressant responses.

233 ts and hinder favorable prognosis, including antidepressant responses.

234 the most important variables for predicting antidepressant responses.

235 VICE 5: Neuromodulators, including tricyclic antidepressants, selective serotonin reuptake inhibitors

236 nhibition of GRK2 by the clinically approved antidepressant, serotonin reuptake inhibitor paroxetine

237 predicted in a manner both specific for the antidepressant sertraline (versus placebo) and generaliz

238 Both ACE inhibitors and antidepressants showed statistically higher intake frequ

239 In silico analysis predicts tricyclic antidepressants such as nortriptyline as potential thera

240 Antidepressants target the serotonin transporter (SERT)

241 ke inhibitors [SSRIs], tricyclic and related antidepressants [TCAs], serotonin and norepinephrine reu

242 olinic acid (QUIN), is a promising potential antidepressant that targets glutamate functioning via th

243 The limited efficacy of available antidepressant therapies may be due to how they affect t

244 cture makes an interesting target for future antidepressant therapies.

245 ients with MDD and an inadequate response to antidepressant therapy (ADT) in FORWARD-4 and FORWARD-5:

246 , which is implicated in stress, reward, and antidepressant therapy, may play a role.

247 st inhibition of MAOA/B, the clinically used antidepressant tranylcypromine (TCP) was employed.

248 < 0.001) rates were significantly higher in antidepressant-treated groups compared to those with con

249 ed PFC samples show elevated MMP-9 levels in antidepressant-treated MDD patients compared with contro

250 changes were reduced in postmortem NAc from antidepressant-treated subjects.

251 Antidepressant treatment ameliorated stress-induced beha

252 ripheral cytokine levels and the response to antidepressant treatment and to evaluate whether changes

253 y a neurobiological signature of response to antidepressant treatment as compared to placebo.

254 in acetylation (due to HDAC6 inhibition) and antidepressant treatment decreased the proportion of Gal

255 ibited no responses to at least one adequate antidepressant treatment for the prevailing episode were

256 MDD patients who responded to antidepressant treatment had lower baseline IL-8 levels

257 ion in the NAc of depressed patients without antidepressant treatment in line with CLDN5 loss.

258 levels were associated with the response to antidepressant treatment in patients with MDD.

259 lasticity induced by both chondroitinase and antidepressant treatment is mediated by TRKB activation

260 ee to which such measures are ameliorated by antidepressant treatment is unclear.

261 ripheral cytokine levels are associated with antidepressant treatment outcome.

262 ipheral cytokine levels were associated with antidepressant treatment outcomes in MDD.

263 Ht volume is a prognostic biomarker for antidepressant treatment outcomes in patients with MDD.

264 in depressed patients may be associated with antidepressant treatment outcomes.

265 d whether early changes in irritability with antidepressant treatment predict subsequent levels of SI

266 Treatment resistance was defined as an antidepressant treatment record level of 1 to 4 in a cur

267 tion selectively and differentially predicts antidepressant treatment response and correlates with sy

268 Predicting antidepressant treatment response has been a clinical ch

269 y markers along with depressive symptoms and antidepressant treatment response were measured in 72 un

270 avenue for identifying biological markers of antidepressant treatment response.

271 Antidepressant treatment significantly decreased levels

272 advance the neurobiological understanding of antidepressant treatment through an EEG-tailored computa

273 ps between reward processing and response to antidepressant treatment using clinical, behavioral, and

274 ated depression scales both before and after antidepressant treatment were included.

275 ify neural signatures of remission following antidepressant treatment, and to identify connectomic pr

276 ings emerged in covariate-adjusted models of antidepressant treatment, such that patients with substa

277 ntions by guiding individual-level choice of antidepressant treatment.

278 ase to produce cAMP, and this is reversed by antidepressant treatment.

279 ance of such changes to human depression and antidepressant treatment.

280 ) by chondroitinase treatment, or by chronic antidepressant treatment.

281 pocampal volumes predict remission following antidepressant treatment.

282 y patients with depression do not respond to antidepressant treatment.

283 , executive dysfunction and poor response to antidepressant treatment.

284 epressive disorder, and may be normalized by antidepressant treatment.

285 New antidepressant treatments are needed that are effective,

286 ay guide the development of more efficacious antidepressant treatments.

287 s, thereby controlling for overall trends in antidepressant use and all time-invariant differences ac

288 re to fatal school shootings increases youth antidepressant use by 21.4% in the following 2 y.

289 national investigation of fracture risk with antidepressant use by class, drug, and indication.

290 the following: elevated depressive symptoms, antidepressant use, or depression history.

291 the effects of 44 school shootings on youth antidepressant use.

292 The antidepressant venlafaxine, a selective serotonin and no

293 isk estimates after prenatal exposure to any antidepressant were decidedly different for population-b

294 Subgroup analysis indicated that antidepressants were also efficacious for depressive sym

295 Users of antidepressants were at higher risk of implant failure t

296 We could not assess whether antidepressants were dispensed or taken.

297 The 5 most commonly prescribed antidepressants were either licensed in the UK for use i

298 Desipramine is a tricyclic antidepressant with immune-modulatory activity, whose ef

299 Prescription of an antidepressant without a mood stabilizer increased subst

300 pensive and, in some cases (i.e., open-label antidepressant without placebo or with double-blind plac