ライフサイエンスコーパス: depressive

1 CI, 0.04% to 0.32%]; interaction P = .01) or depressive (0.99% [95% CI, -0.09% to 2.07%] vs -0.08% [9

2 influence of repeated BHB administration on depressive and anxiety behaviors in a rodent model of ch

3 sociation between PM2.5 and current level of depressive and anxiety symptoms using a nationally repre

4 PM2.5 was associated with depressive and anxiety symptoms, with associations the s

5 fspring stressful life events, and offspring depressive and anxious symptoms.

6 me stress, current negative life events, and depressive and posttraumatic-stress-disorder symptom sco

7 administration of BHB attenuated CUS-induced depressive- and anxiety-related behaviors.

8 t BMP signaling in the hippocampus regulates depressive behavior, and that decreasing BMP signaling m

9 on proliferation in the dentate gyrus and on depressive behavior.

10 Less than one-third of patients with major depressive disorder (MDD) achieve remission with their f

11 Converging evidence suggests that major depressive disorder (MDD) affects multiple large-scale b

12 Thirty-three outpatients with major depressive disorder (MDD) and 20 matched controls comple

13 Major depressive disorder (MDD) and alcohol dependence (AD) ar

14 The association between major depressive disorder (MDD) and obesity may stem from shar

15 Major depressive disorder (MDD) and other mood disorders remai

16 Major depressive disorder (MDD) and schizophrenia (SZ) are con

17 The neuro-anatomical substrates of major depressive disorder (MDD) are still not well understood,

18 ciated with an increased likelihood of major depressive disorder (MDD) as well as suicidal thoughts a

19 We used polygenic risk scores for major depressive disorder (MDD) calculated from the results of

20 esponse to antidepressant treatment in major depressive disorder (MDD) cannot be predicted currently,

21 vestigated intrinsic brain networks in major depressive disorder (MDD) during a depressive episode an

22 The clinical diagnosis and symptoms of major depressive disorder (MDD) have been closely associated w

23 red grey and white matter structure in Major Depressive Disorder (MDD) have been inconsistent.

24 Patients with major depressive disorder (MDD) have clinically relevant, sign

25 nosine monophosphate (cAMP) cascade in major depressive disorder (MDD) have noted that the cAMP casca

26 Major depressive disorder (MDD) in the elderly is a risk facto

27 igated NAc structural abnormalities in major depressive disorder (MDD) in two cohorts.

28 Major depressive disorder (MDD) is a debilitating condition th

29 Major depressive disorder (MDD) is a debilitating mental illne

30 Major depressive disorder (MDD) is a leading cause of disease

31 Major depressive disorder (MDD) is a prevalent psychiatric con

32 Major depressive disorder (MDD) is associated with deficits in

33 , evidence for leptin dysregulation in major depressive disorder (MDD) is conflicting.

34 Major depressive disorder (MDD) is the second largest cause of

35 criteria for mood disorders including major depressive disorder (MDD) largely ignore biological fact

36 Limited successes of gene finding for major depressive disorder (MDD) may be partly due to phenotypi

37 ct of daily stressors and a history of major depressive disorder (MDD) on inflammatory responses to h

38 cts who met DSM-IV criteria for either major depressive disorder (MDD) or bipolar disorder I/II and w

39 A channel blocker) in the treatment of major depressive disorder (MDD) over 12 weeks.

40 ns of brain functional connectivity in major depressive disorder (MDD) patients with suicidal ideatio

41 Fewer than 50% of all patients with major depressive disorder (MDD) treated with currently availab

42 ressant medication in outpatients with major depressive disorder (MDD) was examined in a 3-site, 8-we

43 50 patients with FEP, 50 patients with major depressive disorder (MDD), 50 patients with post-traumat

44 inflammation is often associated with major depressive disorder (MDD), and immunological biomarkers

45 neuropsychiatric disorders, including major depressive disorder (MDD), bipolar disorder, anxiety dis

46 ividuals with a principal diagnosis of major depressive disorder (MDD), bipolar disorder, or schizoaf

47 ings in stress disorders, particularly major depressive disorder (MDD), highlighting insights from po

48 ate, well-demonstrated heritability of major depressive disorder (MDD), there has been limited succes

49 alteration in patients diagnosed with major depressive disorder (MDD).

50 A reduction in NAc of individuals with major depressive disorder (MDD).

51 ADs) are the most common treatment for major depressive disorder (MDD).

52 -related disorders such as anxiety and major depressive disorder (MDD).

53 idence supports a role for dopamine in major depressive disorder (MDD).

54 ral network functional connectivity in major depressive disorder (MDD).

55 yet to be reported in individuals with major depressive disorder (MDD).

56 een observed frequently in adults with major depressive disorder (MDD); however, results have been in

57 = 0.82, standard error (s.e.) = 0.03), major depressive disorder (MDD; r g = 0.69, s.e. = 0.07) and s

58 with either bipolar disorder (N=34) or major depressive disorder (N=69).

59 strength predicted increased risk for future depressive disorder (odds ratio=1.54, 95% CI=1.09-2.18),

60 w-up and the proportion meeting criteria for depressive disorder (PHQ-9 score >/=10) at 4- and 12-mon

61 ), bipolar disorder (BD) and recurrent major depressive disorder (rMDD) are common psychiatric illnes

62 Remitted patients with major depressive disorder (rMDD) often report more fluctuation

63 rs predictive of treatment outcomes in major depressive disorder among treatment-naive adults.

64 ts age 60 or older with DSM-IV-defined major depressive disorder and a score of at least 15 on the Mo

65 throughout the body and is involved in major depressive disorder and antidepressant response.

66 suicide victims who had suffered from major depressive disorder and control subjects who had died fr

67 ample comprising 596 participants with major depressive disorder and healthy controls.

68 bility, neuroticism, bipolar disorder, major depressive disorder and schizophrenia (standardised beta

69 eatments for adolescents with unipolar major depressive disorder are associated with diagnostic remis

70 of reward-related iFC, predicted onset of a depressive disorder at 3-year follow-up.

71 cation for treatment-naive adults with major depressive disorder by defining a neuroimaging biomarker

72 Predicting treatment response for major depressive disorder can provide a tremendous benefit for

73 Patients with major depressive disorder completed two rtfMRI-nf sessions (18

74 Major depressive disorder is associated with raised peripheral

75 Major depressive disorder is characterized by reduced reward-r

76 (D3) were measured in 51 patients with major depressive disorder or bipolar disorder.

77 ciation studies that focused on either major depressive disorder or depressive symptoms with mostly n

78 Not all patients with major depressive disorder respond to adequate pharmacological

79 l of 154 medication-free patients with major depressive disorder seeking treatment at two university

80 ychiatric controls (CON, N=29), DSM-IV major depressive disorder suicides (MDD-S, N=21) and MDD non-s

81 g a predominantly male population with major depressive disorder unresponsive to antidepressant treat

82 Forty-nine individuals diagnosed with major depressive disorder were enrolled with intent to treat i

83 1-17 years) with a diagnosis of DSM IV major depressive disorder were randomly assigned (1:1:1), via

84 METHOD: Adult outpatients with major depressive disorder were randomly assigned to open or pl

85 In participants with major depressive disorder who are trained to upregulate their

86 ircuitry and behavior in patients with major depressive disorder will also be presented.

87 maging Genetics through Meta-Analysis) Major Depressive Disorder Working Group on cortical structural

88 ull clinical response in patients with major depressive disorder, an illness associated with dysregul

89 e X syndrome, Rett syndrome, epilepsy, major depressive disorder, and autism spectrum disorder.

90 ubjects with SZ, bipolar disorder, and major depressive disorder, and the messenger RNA was subjected

91 morphometric studies of patients with major depressive disorder, both antidepressant responders and

92 3 class I was increased in bipolar and major depressive disorder, consistent with observations in sch

93 25 adults from five diagnostic groups (major depressive disorder, N=32; bipolar disorder, N=50; schiz

94 eractivity disorder, bipolar disorder, major depressive disorder, neuroticism, schizophrenia and verb

95 cluding obsessive-compulsive disorder, major depressive disorder, posttraumatic stress disorder, and

96 ffer novel strategies for treatment of major depressive disorder.

97 ant suicidal ideation in patients with major depressive disorder.

98 luating anti-inflammatory therapies in major depressive disorder.

99 potential target for the treatment of major depressive disorder.

100 ror stress-associated diseases such as major depressive disorder.

101 idepressant responses in patients with major depressive disorder.

102 onopharmacological strategies to treat major depressive disorder.

103 to risk of inflammatory disorders and major depressive disorder.

104 , schizophrenia, bipolar disorder, and major depressive disorder.

105 induced behavioral disorders including major depressive disorder.

106 in subjects with bipolar disorder and major depressive disorder.

107 esting-state fMRI data from a study of major depressive disorder.

108 t evidence of overlap with bipolar and major depressive disorder.

109 CI: 1.01, 1.22; P = 0.027) and no history of depressive disorder.

110 error, 0.06); P = 0.911), and no history of depressive disorder.

111 iate in bipolar disorder, and least in major depressive disorder.

112 tinuum between depressive symptoms and major depressive disorder.

113 tivity specifically predicts future risk for depressive disorder.

114 ased glutamate levels in patients with major depressive disorder.

115 logic Treatment of Adult Patients with Major Depressive Disorder." The evidence review done for the g

116 l period is a time of high risk for onset of depressive disorders and is associated with substantial

117 ), even after excluding participants who had depressive disorders at baseline (odds ratio=1.52, 95% C

118 social interaction behaviors reminiscent of depressive disorders observed in human patients with dis

119 Lifetime subtypes of depressive disorders were determined using a structured

120 rget symptoms" (e.g., depressive symptoms in depressive disorders).

121 ial personality disorder, anxiety disorders, depressive disorders, and a history of violence.

122 key strategy to reduce the treatment gap for depressive disorders, the leading mental health disorder

123 nt of postpartum women experience anxiety or depressive disorders, which can have detrimental effects

124 reat the most commonly occurring anxiety and depressive disorders.

125 ny mental disorder, and 0.12 (0.05-0.20) for depressive disorders.

126 sion (OR = 1.92; 95%CI = 1.64-2.26), a brief depressive episode (OR = 2.14; 95%CI = 1.88-2.43) or dep

127 ve episode (OR = 2.14; 95%CI = 1.88-2.43) or depressive episode (OR = 2.43; 95%CI = 2.21-2.67).

128 d 795 patients who were experiencing a major depressive episode (unipolar or bipolar depression) of a

129 ed in 44 unmedicated patients during a major depressive episode and 35 healthy controls.

130 in major depressive disorder (MDD) during a depressive episode and following treatment with ketamine

131 and who were currently experiencing a major depressive episode received a single ketamine infusion (

132 Of 30 participants with major depressive episode selected for inclusion, 26 participan

133 Secondarily, the presence of a major depressive episode was assessed using the Structured Cli

134 in the ACC during a moderate to severe major depressive episode.

135 ificantly increased the odds of Wave 2 major depressive episodes (adjusted odds ratio (AOR): 1.7; 95%

136 least 2 years' duration or had three or more depressive episodes (including the current episode), and

137 were diagnosed as having unipolar or bipolar depressive episodes defined as moderate or severe by DSM

138 anced than simply one of recurring manic and depressive episodes.

139 s at the cellular level to sustain this anti-depressive function for prolonged periods remains unclea

140 ry effect on a major medical complication of depressive illness.

141 new categories of dementia praecox and manic-depressive insanity were too broad and too heterogeneous

142 rexpression of PKMzeta in mPFC prevented the depressive-like and anxiety-like behaviors induced by CU

143 h which VTA Cav1.3 mediates cocaine-related, depressive-like and social phenotypes, suggesting that C

144 ter, learned fear (via fear conditioning) or depressive-like behavior (via tail suspension and forced

145 The dynorphin (Dyn) system promotes depressive-like behavior and plays a key role in the ave

146 ior, learning and memory, socialization, and depressive-like behavior at sub-acute and chronic time p

147 wn to be prophylactic against stress-induced depressive-like behavior in mice.

148 okine production can exist in the absence of depressive-like behavior or cognitive deficits.

149 Cav1.3 channels mediate cocaine-related and depressive-like behavior through a common nucleus accumb

150 cocaine psychomotor activity while inducing depressive-like behavior, an effect not observed in S831

151 ment had no effect on either anxiety-like or depressive-like behavior, and it did not affect control

152 d TgF344-AD rats from cognitive deficits and depressive-like behavior.

153 ic mouse model of inherent susceptibility to depressive-like behavior.

154 tic deficits and development of anxiety- and depressive-like behavior.

155 g a PKMzeta dominant-negative mutant induced depressive-like behaviors after subthreshold unpredictab

156 E expression that increases vulnerability to depressive-like behaviors long after chronic stress expo

157 CUS promoted anxiety- and depressive-like behaviors that were associated with incr

158 st, or a local silencing of MKP-1 attenuates depressive-like behaviors, pointing to an important role

159 ric-related behaviors, such as addictive and depressive-like behaviors.

160 systemic dose of corticosterone blocked the depressive-like phenotype elicited by stress in female m

161 ion of TrkB in the mouse PFC ameliorated the depressive-like phenotype of TG2-overexpressed mice.

162 duced levels of TrkB in the PFC as well as a depressive-like phenotype.

163 Moreover, depressive-like phenotypes of GABAA receptor mutant mice

164 into the NAc shell reversed the cocaine and depressive-like phenotypes.

165 ial defeat sessions resulted in induction of depressive-like states measured in social interaction an

166 Mice that develop depressive-like symptoms after chronic social defeat str

167 igated as a means of improving cognitive and depressive outcomes in well-designed studies incorporati

168 In contrast, depressive patients showed an increased BTP related to t

169 Here we aim to predict post-ECT depressive rating changes and remission status using pre

170 ty, decreased anxiety-like behavior, reduced depressive-related behavior, hyperhedonia, hyperphagia,

171 Two common checklists used to measure depressive severity can produce statistically reliable c

172 ay be an underlying basis for stress-induced depressive states.

173 e used to identify clusters of symptoms in a depressive symptom checklist.

174 SE intervention is efficacious in preventing depressive symptom episodes and performs optimally among

175 The SNP association was also replicated in a depressive symptom sample that shares some individuals w

176 roup and showed significant correlation with depressive symptom severity in the OCD group.

177 ms from the self-reported Quick Inventory of Depressive Symptomatology (QIDS-SR) scale and 14 items f

178 person (B=0.4; P=0.497) associations between depressive symptomatology and mtDNAcn.

179 treatment phase (16-item Quick Inventory of Depressive Symptomatology-Clinician Rated [QIDS-C16] sco

180 d self-report scales (the Quick Inventory of Depressive Symptomatology-Self Report [QIDS-SR] or the B

181 To identify genes associated with depressive symptomology, we performed a gene-based assoc

182 Those with chronic/recurring depressive symptoms (>/=2 of 3 occasions) in the early s

183 , history of falling or gait impairment, and depressive symptoms (2-item Patient Health Questionnaire

184 d a significant earlier reduction (24.9%) in depressive symptoms (95% CI, 13.9 to 35.9; t337 = 4.46;

185 rence to treatment was associated with lower depressive symptoms (beta = -0.19; P = .001) and greater

186 roticism (beta = 1.01; 95% CI, 0.50-1.52) or depressive symptoms (beta = 0.87; 95% CI, 0.32-1.42) and

187 rect effect, 1.27; 95% CI, 0.33 to 2.86) and depressive symptoms (indirect effect, -0.39; 95% CI, -0.

188 Adolescents self-reported depressive symptoms (Mood and Feelings Questionnaire [MF

189 (OR 1.95, 95% CI 1.63-2.36, p < 0.001), and depressive symptoms (OR 1.30, 95% CI 1.12-1.52, p < 0.00

190 ion, which was significantly associated with depressive symptoms (P-value=5.2 x 10(-08), beta=7.2).

191 City Cardiomyopathy Questionnaire (P=0.009), depressive symptoms (P=0.027), and the 6-minute walk tes

192 ion (Short Physical Performance Battery) and depressive symptoms (Patient Health Questionnaire).

193 ional Assessment of Cancer Therapy-General), depressive symptoms (Patient Health Questionnaire-9), an

194 DL disability (PR, 3.22; 95% CI, 1.72-6.06), depressive symptoms (PR, 11.31; 95% CI, 4.02-31.82), les

195 relations were found between neuroticism and depressive symptoms (r g = 0.82, standard error (s.e.) =

196 ence score was significantly associated with depressive symptoms (regression coefficient a = -0.21; P

197 association between maternal and adolescent depressive symptoms (Wald test p=0.435 in the GUI cohort

198 Depressive symptoms (years 15, 20, 25) were assessed wit

199 ng nonwhite individuals, lifetime stress and depressive symptoms accounted for most of the effect (WQ

200 ssion showed that higher lifetime stress and depressive symptoms accounted for most of the effect on

201 S was unrelated to behavior, self-esteem and depressive symptoms adjusted for infant characteristics

202 n, and household income), and psychological (depressive symptoms and cognitive capacity) risk factors

203 tal Anxiety and Depression Scale anxiety and depressive symptoms and Global Mood Scale negative and p

204 ed greatest mortality for women who reported depressive symptoms and had not initiated ART.

205 ence did not mediate the association between depressive symptoms and HRQOL.

206 to positive memories significantly decreased depressive symptoms and increased the percent of specifi

207 Our results support a continuum between depressive symptoms and major depressive disorder.

208 y contribute to the emergence of anxiety and depressive symptoms and may play a critical role in the

209 found no evidence for an association between depressive symptoms and mtDNAcn.

210 The phenotypic associations between atypical depressive symptoms and obesity-related traits may arise

211 a collaborative care intervention can reduce depressive symptoms and prevent more severe depression i

212 Depressive symptoms and stronger social connectedness we

213 es over 28 years, these results suggest that depressive symptoms are a prodromal feature of dementia

214 Inventory score at 11 years (n = 6937) and depressive symptoms assessed from self-reported Patient

215 eward-related VS activity may buffer against depressive symptoms associated with poor sleep.

216 were seen in objective physical function or depressive symptoms at 12 months in any of the intervent

217 in a statistically significant difference in depressive symptoms at 4-month follow-up, of uncertain c

218 formance but did not affect the frequency of depressive symptoms at least in the short range.

219 ence suggests that NMDAR antagonists relieve depressive symptoms by forming new synapses resulting in

220 tertiary Lyme center, to investigate whether depressive symptoms can be used in clinical practice to

221 This suggests that depressive symptoms cannot be used to discriminate for L

222 r to dementia diagnosis to determine whether depressive symptoms carry risk for dementia.

223 that in those with dementia, differences in depressive symptoms compared with those without dementia

224 imaging neurofeedback (rtfMRI-nf) training, depressive symptoms diminish.

225 ell-being polygenic scores experienced fewer depressive symptoms during follow-up.

226 g polygenic score buffered against increased depressive symptoms following a spouse's death.

227 her polygenic scores were less vulnerable to depressive symptoms following the death of their spouse

228 Individuals with depressive symptoms had elevated risk of mortality on th

229 Those reporting depressive symptoms in 1985 (mean follow-up, 27 years) d

230 However, those with depressive symptoms in 2003 (mean follow-up, 11 years) h

231 to longitudinally assess the extent to which depressive symptoms in adolescents change after contact

232 primary outcome was "target symptoms" (e.g., depressive symptoms in depressive disorders).

233 ION: Our results show an association between depressive symptoms in fathers and depressive symptoms i

234 re is little evidence to guide management of depressive symptoms in older people.

235 e whether treatment with sertraline improves depressive symptoms in patients with CKD and MDD.

236 The odds ratio for moderate/severe depressive symptoms in patients with LB and positive ser

237 ilar effect and significant association with depressive symptoms in samples from the independent popu

238 erages and added sugars has been linked with depressive symptoms in several populations.

239 study objective was to assess prevalence of depressive symptoms in subgroups of patients referred to

240 ed 0.9% of sex- and age-adjusted variance of depressive symptoms in the discovery study, which is tra

241 Depressive symptoms in the early phase of the study corr

242 nonymous variation in the gene NKPD1 affects depressive symptoms in the general population.

243 96Ser variant of LIPG in the pathogenesis of depressive symptoms in the general population.

244 n between depressive symptoms in fathers and depressive symptoms in their adolescent offspring.

245 association between paternal and adolescent depressive symptoms in two large population-based cohort

246 Separate depressive symptoms may be encoded by differential chang

247 beginning antidepressant therapy to improve depressive symptoms more quickly, mitigate concomitant a

248 To characterize the trajectory of depressive symptoms over 28 years prior to dementia diag

249 on coefficient a = -0.21; P < .001), and the depressive symptoms score (c = 0.637; P < .001) was sign

250 ignificantly more effective than controls on depressive symptoms severity (beta = -0.21; Hedges g = 0

251 s in the past year had a greater decrease in depressive symptoms than those without contact (adjusted

252 mary study group, (3) reported depression or depressive symptoms using a validated instrument, and (4

253 The hazard ratio for depressive symptoms was 3.38 (95% confidence interval (C

254 ntensity of symptoms, the Quick Inventory of Depressive Symptoms was administered bimonthly, and rate

255 s, a 1 SD (three-point) increase in paternal depressive symptoms was associated with an increase of 0

256 Prevalence of moderate/severe depressive symptoms was calculated.

257 Prevalence of moderate/severe depressive symptoms was lowest in patients with no clini

258 A significant reduction in depressive symptoms was observed following ketamine admi

259 The prevalence of depressive symptoms was similar in patients with LB comp

260 Depressive symptoms were observed in 19.1% before treatm

261 Decreased depressive symptoms were observed in all 19 patients at

262 itiated ART, the hazard ratio for women with depressive symptoms who had initiated ART was 3.60 (95%

263 Using a reference category of women without depressive symptoms who had initiated ART, the hazard ra

264 d between- and within-person associations of depressive symptoms with LTL and mtDNAcn in a large comm

265 cused on either major depressive disorder or depressive symptoms with mostly negative findings.

266 of ketamine were repeatedly shown to improve depressive symptoms within 24 h after infusion and this

267 ty of alcohol abuse, craving, and anxiety or depressive symptoms) were significant after correction f

268 rer on all measures of intelligence, anxiety/depressive symptoms, and executive function (differences

269 usting for relevant baseline health factors, depressive symptoms, and health behaviors (fully adjuste

270 he psychological variables perceived stress, depressive symptoms, and neuroticism; using formal genet

271 (SES); PM2.5 was positively associated with depressive symptoms, and significantly for 30-day moving

272 also increasingly reported anxiety symptoms, depressive symptoms, and use of laxatives throughout stu

273 nd investigate its role in stress levels and depressive symptoms, as well as in HRQOL and disease act

274 emographic, health/medical risk factors, and depressive symptoms, being socially integrated was signi

275 le adjustment for age, socioeconomic status, depressive symptoms, health-related behaviours, and chro

276 on mortality, as well as a harmful effect of depressive symptoms, in a cohort of HIV-infected women.

277 A/Cr, over and above the effects of fatigue, depressive symptoms, physical activity, and psychomotor

278 In analyses stratified according to baseline depressive symptoms, PSE exerted a preventive effect amo

279 mptoms (including mood and sexual function), depressive symptoms, sleep impairment and poorer PD-rela

280 ls (CIs) were calculated for moderate/severe depressive symptoms.

281 pression and especially inflammation-related depressive symptoms.

282 ess to distress to disorder, for classifying depressive symptoms.

283 was used as a cutoff to indicate significant depressive symptoms.

284 and for psychosocial functioning, including depressive symptoms.

285 creased amygdala CBF correlated with reduced depressive symptoms.

286 ncreased prevalence of suicidal ideation and depressive symptoms.

287 sion, and 32 patients (20.8%) had borderline depressive symptoms.

288 or depression and the later manifestation of depressive symptoms.

289 o for 12 weeks did not significantly improve depressive symptoms.

290 Self-guided iCBT is effective in treating depressive symptoms.

291 , and baseline reading ability, anxiety, and depressive symptoms.

292 6Ser (P-value=7.1 x 10(-03), beta=2.55) with depressive symptoms.

293 and physical activity, while controlling for depressive symptoms.

294 ression Inventory II was completed to assess depressive symptoms.

295 ccounted for intervention effects on QOL and depressive symptoms.

296 connectivity was positively correlated with depressive symptoms.

297 een loneliness, neuroticism, and a scale of 'depressive symptoms.' We also identified weaker evidence

298 r and dropout rates; positive, negative, and depressive symptoms; quality of life; functioning; and m

299 Along with our analysis of depressive trajectories over 28 years, these results sug

300 Analysis of retrospective depressive trajectories over 28 years, using mixed model