ライフサイエンスコーパス: SSRI

1 SSRI exposure was confirmed in a subset of participants

2 SSRI treatment decreased plasma serotonin concentrations

3 SSRI treatment increased activation in both the left dor

4 SSRI treatment significantly increased rolipram binding

5 SSRI withdrawal syndrome occurs often and can be severe,

6 SSRI-induced motor deficits can be reversed by systemic

7 SSRIs induce SNr hyperactivity and SNc hypoactivity that

8 SSRIs may exert their effects by remediating emotion reg

9 SSRIs selectively inhibited hippocampal long-term depres

10 1R antagonism is sufficient to prevent acute SSRI-induced enhancements in aversive learning.

11 cells is enhanced by chronic, but not acute, SSRI administration.

12 unmedicated MDD patients and increased after SSRI treatment.

13 do not show any improvement during or after SSRI treatment.

14 -2.60]; 13 trials and 831 patients), and all SSRIs (class effect -3.49 [95% credible interval -5.12 t

15 Although SSRI use during pregnancy was also associated with such

16 Although SSRIs are considered the first-choice antidepressant for

17 tients enrolled in the Mayo Clinic PGRN-AMPS SSRI trial.

18 n of the p11/AnxA2/SMARCA3 heterohexamer, an SSRI-inducible protein complex.

19 SSRI treatment alone, the combined use of an SSRI and a statin was associated with a significantly lo

20 Initiation of an SSRI with higher versus lower QT-prolonging potential wa

21 When administered with an SSRI, 5-HTP SR enhanced 5-HT-sensitive behaviors and neu

22 ram PET scan 8 weeks after treatment with an SSRI.

23 am PET scan ~8 weeks after treatment with an SSRI.

24 n-rated anxiety symptoms pre-to-post CBT and SSRI treatment among youth with current anxiety.

25 n-rated anxiety symptoms pre-to-post CBT and SSRI treatment.

26 faces predicted greater response to CBT and SSRI treatment.

27 sociated with plasma 5-HT concentrations and SSRI clinical response remained unclear.

28 al overweight before or during pregnancy and SSRI use during pregnancy, retained their high level of

29 nical observations showing that n-3 PUFA and SSRI have antidepressant affects, which may be additive.

30 ns from three extreme SSRI-remitters (R) and SSRI-nonremitters (NR).

31 t stem cells (iPSCs) from SSRI-remitters and SSRI-nonremitters.

32 Infants in the SSRI and SSRI plus benzodiazepine groups had lower motor scores a

33 ral drug classes, including cannabinoids and SSRIs, are ineffective.

34 idence supports the effectiveness of CBT and SSRIs for reducing childhood anxiety symptoms.

35 Cognitive behavioral therapy, exercise, and SSRIs may reduce symptoms of poststroke depression, but

36 Limited doses of aspirin, NSAIDs, and SSRIs might not increase the risk, although higher doses

37 Is), SSRIs with concomitant benzodiazepines (SSRI plus benzodiazepine), and no maternal depression or

38 en the OCD and HC groups, as well as between SSRI responders and nonresponders.

39 lly significant positive association between SSRI dose and efficacy.

40 tions for understanding associations between SSRIs and child development.

41 during emotion perception is reduced by both SSRI and CBT treatments, and predicts anxiety and depres

42 Results showed that both SSRI and CBT treatments similarly attenuated insula and

43 cents aged 12-17 years since 2005, driven by SSRI prescriptions, but a decrease in children aged 5-11

44 vioral despair model, which was prevented by SSRI treatment.

45 termine the modulation of Ca(2+) channels by SSRIs.

46 The inhibition of long-term depression by SSRIs was mediated by a direct block of voltage-activate

47 g data of serotonin transporter occupancy by SSRIs and found that hyperbolically reducing doses of SS

48 ggest that reduction of threat reactivity by SSRIs may be mediated by their actions in the amygdala.S

49 pumps, 5-HTP IR with injections, and chronic SSRI with dietary fluoxetine.

50 activated prior to the onset of the chronic SSRI response.

51 ons mimics the motor deficits due to chronic SSRI treatment, whereas local SNr 5-HT2C receptor antago

52 inephrine reuptake inhibitors (collectively: SSRIs), SSRIs with concomitant benzodiazepines (SSRI plu

53 Current SSRI use was associated with an increased risk for ICH (

54 ncing affect or reward sensitivity directly, SSRIs might amplify an interaction between the two, givi

55 The neural basis of this early SSRI effect is not known.

56 disruptive contaminants in the environment, SSRIs affect reproduction in aquatic organisms.

57 We provide strong evidence that exogenous SSRI fluoxetine selectively increases serotonin-immunore

58 and serotonergic neurons from three extreme SSRI-remitters (R) and SSRI-nonremitters (NR).

59 For SSRIs (99 treatment groups), the dose-efficacy curve sho

60 h antidepressant treatment, particularly for SSRIs, and may be a potential substrate of the clinical

61 eta-analysis model with flexible splines for SSRIs, venlafaxine, and mirtazapine.

62 induced pluripotent stem cells (iPSCs) from SSRI-remitters and SSRI-nonremitters.

63 Yet, many patients withdraw from SSRI therapy due to sexual side effects (e.g., infertili

64 Furthermore, SSRIs protected both wild-type and SERT knockout mice fr

65 follow-up of 22.8 months, 79285 [66.3%] had SSRI or SNRI exposure.

66 We identified SSRIs as a new potentially chemoprotective medication.

67 % in TCA users, 31.3% in SNRI users, 6.3% in SSRI users, 5.2% in Atypical antidepressant users, and 3

68 rger FC of the RN-left MTG was also found in SSRI nonresponders compared to responders, which was a s

69 nstream of SSRI treatment may play a role in SSRI resistance in MDD.

70 otonin concentrations and may have a role in SSRI treatment outcomes.

71 The authors identified 872,216 incident SSRI users, of whom 113,108 (13.0%) used a statin concom

72 wide cohort study that included all incident SSRI users in Denmark between 1997 and 2012, the authors

73 y to selective serotonin reuptake inhibitor (SSRI) antidepressants, all other non-SSRI antidepressant

74 the selective serotonin reuptake inhibitor (SSRI) antidepressants, has been thought to be effective

75 the selective serotonin reuptake inhibitor (SSRI) citalopram decreases amyloid-beta generation and p

76 the selective serotonin reuptake inhibitor (SSRI) citalopram downregulates the expression of the hum

77 the selective serotonin reuptake inhibitor (SSRI) citalopram or placebo.

78 the selective serotonin reuptake inhibitor (SSRI) citalopram synergistically reduced operant respond

79 amine (5-HT) (serotonin) reuptake inhibitor (SSRI) fluoxetine (Flx) is ineffective as a prophylactic,

80 The selective serotonin reuptake inhibitor (SSRI) fluoxetine (FLX), the active ingredient of the ant

81 on a selective serotonin reuptake inhibitor (SSRI) initially experience increased anxiety, which can

82 the selective serotonin reuptake inhibitor (SSRI) sertraline or cognitive behavior therapy (CBT), pa

83 d to selective serotonin reuptake inhibitor (SSRI) therapy.

84 and selective serotonin reuptake inhibitor (SSRI) treatment outcome in two independent samples of pa

85 rnal selective serotonin reuptake inhibitor (SSRI) use during pregnancy (OR 1.84, 1.60-2.11).

86 of a selective serotonin reuptake inhibitor (SSRI), citalopram.

87 of a selective serotonin reuptake inhibitor (SSRI), fluoxetine, increases D1 receptor expression in m

88 m, a selective serotonin reuptake inhibitor (SSRI), on brain activation during face processing.

89 th a selective serotonin reuptake inhibitor (SSRI).

90 th a selective serotonin reuptake inhibitor (SSRI).

91 th a selective serotonin reuptake inhibitor (SSRI).

92 of a selective serotonin reuptake inhibitor (SSRI, citalopram) are studied over longer timescales, le

93 nts-selective serotonin reuptake inhibitors (SSRIs) and cognitive-behavioral therapy (CBT).

94 by selective serotonin reuptake inhibitors (SSRIs) and the tricyclic class of antidepressant (TCA) a

95 Selective serotonin reuptake inhibitors (SSRIs) are a first-line treatment for PTSD, but treatmen

96 Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed for depression, but sexua

97 Selective Serotonin Reuptake Inhibitors (SSRIs) are commonly used drugs for the treatment of psyc

98 Selective serotonin reuptake inhibitors (SSRIs) are first-line pharmacological agents for treatin

99 Selective serotonin reuptake inhibitors (SSRIs) are standard of care for major depressive disorde

100 ich selective serotonin reuptake inhibitors (SSRIs) are the first line of treatment.

101 Selective serotonin reuptake inhibitors (SSRIs) are the most commonly used class of antidepressan

102 Selective serotonin reuptake inhibitors (SSRIs) are the most prescribed antidepressants.

103 Selective serotonin reuptake inhibitors (SSRIs) are the most widely prescribed drugs for mood dis

104 Selective serotonin reuptake inhibitors (SSRIs) are widely used antidepressants.

105 otonin (5-HT) selective reuptake inhibitors (SSRIs) are widely used in the treatment of depression an

106 ith selective serotonin reuptake inhibitors (SSRIs) confirmed the causal relationship between amygdal

107 Selective serotonin reuptake inhibitors (SSRIs) constitute a first-line antidepressant interventi

108 hat selective serotonin reuptake inhibitors (SSRIs) do not reduce cannabis use or improve treatment r

109 to selective serotonin reuptake inhibitors (SSRIs) during pregnancy influences susceptibility to the

110 of selective serotonin reuptake inhibitors (SSRIs) has been associated with an increased cataract ri

111 of selective serotonin-reuptake inhibitors (SSRIs) has been associated with an increased risk of bon

112 T), selective serotonin reuptake inhibitors (SSRIs) improve mood in adults but have paradoxical long-

113 by selective serotonin reuptake inhibitors (SSRIs) in hippocampal brain slices from wild-type rats a

114 to selective serotonin reuptake inhibitors (SSRIs) in major depressive disorder follows a flat respo

115 ith selective serotonin reuptake inhibitors (SSRIs) leads to novelty-induced exploration deficits in

116 Selective serotonin reuptake inhibitors (SSRIs) may increase the risk for spontaneous intracrania

117 bo, selective serotonin reuptake inhibitors (SSRIs) significantly reduced primary anxiety symptoms an

118 Selective Serotonin Reuptake Inhibitors (SSRIs) such as fluoxetine are widely prescribed to pregn

119 the selective serotonin reuptake inhibitors (SSRIs), citalopram and escitalopram prolong the QT inter

120 rom selective serotonin reuptake inhibitors (SSRIs), including larger serotonin (5-HT) release and di

121 ing selective serotonin reuptake inhibitors (SSRIs), initiate their drug actions by rapid elevation o

122 of selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SN

123 oth selective serotonin reuptake inhibitors (SSRIs), sertraline and escitalopram.

124 of selective serotonin reuptake inhibitors (SSRIs), without the usual adverse events associated with

125 or selective serotonin reuptake inhibitors (SSRIs).

126 to selective serotonin reuptake inhibitors (SSRIs).

127 ing selective serotonin reuptake inhibitors (SSRIs).

128 otonin (5-HT) selective reuptake inhibitors (SSRIs).

129 to selective serotonin reuptake inhibitors (SSRIs).

130 and selective serotonin reuptake inhibitors (SSRIs).

131 our selective serotonin reuptake inhibitors (SSRIs: citalopram, paroxetine, fluoxetine and sertraline

132 ive selective serotonin reuptake inhibitors (SSRIs; citalopram, escitalopram, fluoxetine, paroxetine,

133 ith selective serotonin reuptake inhibitors (SSRIs; e.g., Prozac).

134 ine (serotonin-specific reuptake inhibitors [SSRI]), or venlafaxine-extended release (serotonin and n

135 es (selective serotonin reuptake inhibitors [SSRI], serotonin-norepinephrine reuptake inhibitors [SNR

136 se (selective serotonin reuptake inhibitors [SSRIs] or serotonin-norepinephrine reuptake inhibitors [

137 es (selective serotonin reuptake inhibitors [SSRIs], tricyclic and related antidepressants [TCAs], se

138 am (selective serotonin reuptake inhibitors, SSRIs) treatment increased adenylyl cyclase (AC) and BDN

139 (47.1%) hemodialysis patients who initiated SSRIs with higher QT-prolonging potential and 34,722 (52

140 g potential and 34,722 (52.9%) who initiated SSRIs with lower QT-prolonging potential.

141 death among hemodialysis patients initiating SSRIs with a higher potential for prolonging the QT inte

142 pram) versus the risk among those initiating SSRIs with lower QT-prolonging potential (fluoxetine, fl

143 se nearly half of patients show insufficient SSRI responses, serotonergic dysfunction in heterogeneou

144 ine the outcomes of in utero and lactational SSRI exposure on C57BL6 pup bone microarchitecture.

145 Using week-long SSRI treatment in healthy volunteer participants, we sho

146 In monocyte-derived macrophages, SSRI treatment decreased expression of CD4 (p < .0001) a

147 In the water flea Daphnia magna, SSRIs increase offspring production in a food ration-dep

148 s from analyses of SSRI antidepressants, non-SSRI antidepressants, and nonantidepressant psychotropic

149 ibitor (SSRI) antidepressants, all other non-SSRI antidepressants, or other nonantidepressant psychot

150 disorders, and those treated with other non-SSRI QT-prolonging medications.

151 within individuals who received CBT but not SSRIs.

152 Drugs, notably SSRIs, that elevate brain extracellular 5-HT (5-HTExt) a

153 genic responses to chronic administration of SSRI.

154 Results from analyses of SSRI antidepressants, non-SSRI antidepressants, and nona

155 dose among youths with more than 150 days of SSRI or SNRI use (RR, 2.39; 95% CI, 1.04-5.52 for >15.0

156 ) but not among youths with 1 to 150 days of SSRI or SNRI use.

157 naptic forebrain hyperactivity downstream of SSRI treatment may play a role in SSRI resistance in MDD

158 categories in order to assess the effect of SSRI dosing on the efficacy and tolerability of SSRIs fo

159 findings indicate that the initial effect of SSRI treatment is to alter processing of aversive stimul

160 approach to improve therapeutic efficacy of SSRI antidepressants.

161 The authors evaluated the impact of SSRI treatment on CSF biomarkers and progression from mi

162 While the mechanism of SSRI action is still unknown, SSRIs are thought to exert

163 Exposure of interest was the number of SSRI prescriptions and prescriptions for other antidepre

164 s and statins with people who had periods of SSRI treatment alone.

165 alized to a more heterogeneous population of SSRI users.

166 severity before treatment and predictive of SSRI response.

167 onders, which was a significant predictor of SSRI response after 16 weeks.

168 Our findings support the prescription of SSRI antidepressants in a wider group of participants th

169 on in two independent prospective samples of SSRI-treated patients with major depressive disorder: th

170 Current long-term use of SSRI (>/=20 prescriptions) was not associated with an in

171 The use of SSRI less than or equal to median had a decreased risk o

172 In these data, use of SSRI was not associated with an increased risk of catara

173 is study identifies a dual mode of action of SSRIs on bone remodeling and suggests a therapeutic stra

174 The slightly increased benefits of SSRIs at higher doses are somewhat offset by decreased t

175 Higher doses of SSRIs appear slightly more effective in major depressive

176 found that hyperbolically reducing doses of SSRIs reduces their effect on serotonin transporter inhi

177 Higher doses of SSRIs were associated with an increased likelihood of dr

178 Doses of SSRIs were converted to fluoxetine equivalents.

179 for both reduction of motor side effects of SSRIs and augmentation of therapeutic antidepressant and

180 We tested the behavioral effects of SSRIs in the chronic behavioral despair model of depress

181 roles for 5-HT2C receptors in the effects of SSRIs on motor function and affective behavior, highligh

182 d further elucidate the long-term effects of SSRIs on various social-emotional tasks in IED.

183 ics the antidepressant behavioral effects of SSRIs, suggesting that these cells may represent a novel

184 h SERT-dependent and -independent effects of SSRIs, we developed a knock-in mouse model whereby high-

185 the antidepressant and anxiolytic effects of SSRIs.

186 -controlled trials examining the efficacy of SSRIs for treating adults with major depressive disorder

187 The heterogeneous QT-prolonging potential of SSRIs may differentially affect cardiac outcomes in the

188 However, the relative cardiac safety of SSRIs in the hemodialysis population is unknown.

189 method could have relevance for tapering of SSRIs.

190 I dosing on the efficacy and tolerability of SSRIs for major depressive disorder.

191 nd unpublished randomized clinical trials of SSRIs or SNRIs in youths with DD, AD, OCD, or PTSD were

192 The use of SSRIs and more generally of antidepressants with strong

193 SSRI treatment alone, the concomitant use of SSRIs and statins was not associated with significant in

194 people who had periods of concomitant use of SSRIs and statins with people who had periods of SSRI tr

195 Current use of SSRIs compared with TCAs and strong compared with weak s

196 the risk for ICH associated with the use of SSRIs compared with tricyclic antidepressants (TCAs) amo

197 reater during current use than former use of SSRIs or SNRIs (absolute risk, 1.29 per 10000 person-mon

198 rt of youths insured by Medicaid, the use of SSRIs or SNRIs-the most commonly used antidepressant sub

199 ymptoms of poststroke depression, but use of SSRIs to prevent depression or improve motor function wa

200 pproximately half of these patients remit on SSRI therapy.

201 uctural MRI scans and received either CBT or SSRI treatment.

202 days, after which either vehicle control or SSRI (10(-6) mol/L) was added for 2 hours.

203 Notably, a history of statin or SSRI usage reduced the risk of EAC or HGD by 49% or 61%,

204 ith 5-HT2A receptor (5-HT2AR) antagonists or SSRIs revealed that functional 5-HT2ARs, not SERTs, are

205 and 12 weeks later, following either CBT or SSRIs in the patient sample.

206 ent decisions regarding engagement in CBT or SSRIs, especially among individuals with an enhanced ERN

207 We modeled oral SSRI treatment via fluoxetine in the water, in a regimen

208 Overall, SSRIs (62.6%) were the most commonly prescribed first an

209 In PBMCs, SSRI treatment decreased expression of CD4 (p = .009), C

210 feeding women, yet the effects of peripartum SSRI exposure on neonatal bone are not known.

211 date has examined the effects of peripartum SSRIs on long bone growth or mass.

212 Compared with placebo, SSRIs and SNRIs are more beneficial than placebo in chil

213 rmed in a subset of participants with plasma SSRI levels.

214 In adult populations, SSRI use is associated with compromised bone health, and

215 ed exploration in adulthood due to postnatal SSRI exposure.

216 d stratified subgroup analysis by predefined SSRI dose categories in order to assess the effect of SS

217 fluoxetine (Flx), one of the most-prescribed SSRIs, acts on bone remodeling through two distinct mech

218 nce for the actions of two widely prescribed SSRIs, fluoxetine and citalopram, in tests sensitive to

219 ting women due to a low side effect profile, SSRI exposure may compromise fetal and neonatal bone dev

220 Offspring of mothers who purchased SSRIs at least twice during pregnancy had a significant

221 atric disorders with a history of purchasing SSRIs during pregnancy; 9537 were in the unmedicated gro

222 ic disorders without a history of purchasing SSRIs during pregnancy; and 31207 were in the unexposed

223 hiatric diagnosis or a history of purchasing SSRIs.

224 a significant percentage of patients remain SSRI-resistant and it is unclear whether and how alterat

225 ic activation of SNc DAergic neurons reverse SSRI-induced motor deficits.

226 er explored mutually exclusive use of single SSRI substances.

227 e reuptake inhibitors (collectively: SSRIs), SSRIs with concomitant benzodiazepines (SSRI plus benzod

228 ents with a history of depression, long-term SSRI treatment (>4 years) was significantly associated w

229 Long-term SSRI treatment may delay progression from MCI to Alzheim

230 5 years of age in association with long-term SSRI use needs to be investigated in further studies.

231 tly increased risk of cataract for long-term SSRI users (adjusted OR, 1.24; 95% CI, 1.15-1.34) compar

232 roximately 3 years, compared with short-term SSRI treatment, treatment with other antidepressants, or

233 The TPJ findings suggest that SSRI administration may reduce aggressive tendencies tow

234 These findings suggest that SSRI treatment, independent of depression status, downre

235 We conclude that SSRIs show promise as potential therapeutic compounds fo

236 These findings indicate that SSRIs may inhibit neuroendocrine dopamine release throug

237 Here we show in mice that SSRIs impair motor function by acting on 5-HT2C receptor

238 Here, we show that SSRIs can inhibit hypothalamic dopamine neurons that nor

239 Analysis showed that SSRIs and SNRIs were significantly more beneficial compa

240 The findings also suggest that SSRIs have the capacity to alter individual differences

241 Side effect profiles suggest that SSRIs reduce dopaminergic (DAergic) activity, but specif

242 We therefore suggest that SSRIs should be tapered hyperbolically and slowly to dos

243 y and effectively elevate 5-HTExt beyond the SSRI effect and represent a novel treatment for TRD.

244 e suggests that elevating 5-HTExt beyond the SSRI effect enhances antidepressant efficacy, but previo

245 ized with SSRI to elevate 5-HTExt beyond the SSRI effect.

246 uring sustained 5-HTExt elevation beyond the SSRI effect.

247 yptophan (5-HTP) elevates 5-HTExt beyond the SSRI effect.

248 Infants in the SSRI and SSRI plus benzodiazepine groups had lower motor

249 Infants in the SSRI plus benzodiazepine group had the least favorable s

250 risk of these disorders in offspring in the SSRI-exposed and unmedicated groups compared with offspr

251 were no differences between offspring in the SSRI-exposed group and in the unmedicated group.

252 speech/language disorders was 0.0087 in the SSRI-exposed group vs 0.0061 in the unmedicated group (h

253 ere 3 groups of offspring: 15596 were in the SSRI-exposed group, ie, had mothers diagnosed as having

254 The suppressive effects of the SSRI on receptor expression did not differ as a function

255 of interleukin-2 with vehicle control or the SSRI (10(-6) mol/L) for 2 hours.

256 ltered in OCD patients and could predict the SSRI response.

257 vortioxetine by comparing its effect to the SSRI citalopram on the binding of [(11)C]AZ10419369 to t

258 rgic neurotransmission may contribute to the SSRI resistance observed in approximately 30% of major d

259 is replicated by early-life exposure to the SSRI, fluoxetine (from P2 to P14), that also causes anxi

260 t-wide blunting of the DRN output, while the SSRI fluoxetine noticeably enhances DRN functional conne

261 Treatment with the SSRI at a physiologic dose decreased CD4, CCR5, and CXCR

262 A combination of 11 with the SSRI sertraline increased the anorectic effect.

263 ogenic effects of chronic treatment with the SSRI, fluoxetine, are abolished by mossy cell-specific k

264 im, veterans with PTSD were treated with the SSRI, paroxetine.

265 The SSRIs produced a relatively large effect size for ADs (g

266 ason indicated optimal acceptability for the SSRIs in the lower licensed range between 20 mg and 40 m

267 We further demonstrate that the SSRIs, fluoxetine and sertraline, directly suppress TIDA

268 neuron glutamate co-transmission mimics this SSRI-induced hypolocomotion, while optogenetic activatio

269 Thus, SSRIs impair serotonin-regulation of reproductive invest

270 nd the resulting circuitry may contribute to SSRI resistance in MDD patients.

271 ations in serotonergic neurons contribute to SSRI resistance in these patients.

272 nical observation of early adverse events to SSRI treatment in some patients with anxiety disorders.

273 ed to assess cataract risk after exposure to SSRI or to other antidepressant drugs in a large electro

274 ciated with metabolites that were related to SSRI response.

275 signals of threat predict better response to SSRI and CBT treatment in anxious youth and that neuroim

276 and as an adjunctive augmentation therapy to SSRI therapy.

277 limiting food conditions, females exposed to SSRIs produce more but smaller offspring, which is a mal

278 Conclusions and Relevance: Exposure to SSRIs during pregnancy was associated with an increased

279 is reduced in animals exposed postnatally to SSRIs.

280 post-treatment among patients randomized to SSRIs, but remained stable among patients randomized to

281 were associated with better response to two SSRIs (paroxetine and fluoxetine).

282 Such effects may partly underlie SSRIs' impact in treating psychological illnesses.

283 e mechanism of SSRI action is still unknown, SSRIs are thought to exert therapeutic effects by elevat

284 ute and chronic actions of two commonly used SSRIs in these tests, and reinforce the utility of the S

285 gs, ultimately there may be a role for using SSRI treatment adjunctively in HIV and acquired immunode

286 Furthermore, for youths currently using SSRIs or SNRIs, the risk of type 2 diabetes increased wi

287 bone health, and infants exposed to in utero SSRIs have a smaller head circumference and are shorter,

288 Clomipramine was not better than were SSRIs (-1.23 [-3.41 to 0.94]).

289 Objective: To examine whether SSRI exposure during pregnancy is associated with speech

290 tions, which were themselves associated with SSRI response for MDD patients enrolled in the Mayo Clin

291 hose SNPs were significantly associated with SSRI treatment outcomes in four independent MDD trials.

292 Compared with SSRI treatment alone, the combined use of an SSRI and a

293 Compared with SSRI treatment alone, the concomitant use of SSRIs and s

294 with greater reduction in PTSD symptoms with SSRI treatment, irrespective of pre-treatment severity.

295 es of mice, adjunct 5-HTP SR synergized with SSRI to elevate 5-HTExt beyond the SSRI effect.

296 se events are significantly more common with SSRIs and SNRIs than placebo.

297 resulted in robust advantages compared with SSRIs alone.

298 mall or too short to assess suicidality with SSRIs or SNRIs.

299 mong them, 54 OCD patients were treated with SSRIs for 16 weeks, resulting in 26 responders and 28 no

300 uralistic cohort, concomitant treatment with SSRIs and statins resulted in robust advantages compared