ライフサイエンスコーパス: depressive

1 We evaluated the association of depressive and anxiety symptoms (Hopkins symptom check l

2 quality) were associated with lower risk of depressive and anxiety symptoms, aggressive behavior sym

3 eability, and mood improving potential of 32 depressive and control (depicting general neutral or pos

4 tivity in vHIP-NAc afferents during tests of depressive- and anxiety-like behavior in male and female

5 ediated weight changes and protected against depressive- and anxiety-like behavior.

6 al TLR2-system was suggested in aetiology of depressive, anxious and anorexiolytic symptoms in OSA.

7 iscrete effects of oxytocin-MCH signaling on depressive behavior and demonstrate that parenting and m

8 n the brain regulating p11, L-type VGCC, and depressive behavior has not been known.

9 ors from MCH neurons increases and decreases depressive behavior in sexually naive and late postpartu

10 p11 in these cells induced vulnerability to depressive behavior, whereas upregulation of Kv3.1 in de

11 ecular connection involved in the control of depressive behavior.

12 onal substrates that mediate SIRT1 action on depressive behaviors remain largely unknown.

13 Thus, anxio-depressive behaviours did not develop in all strains aft

14 Isoproterenol stimulation reversed the depressive contractile and Ca(2+)-kinetic parameters.

15 iable rescue treatment option in patients in depressive crisis states.

16 al design, 36 patients with first onset of a depressive disorder (Diagnostic and Statistical Manual o

17 Seventy eight adolescents with major depressive disorder (MDD) (age mean [SD] = 14.9 +/- 1.5,

18 We compare participants diagnosed with Major Depressive Disorder (MDD) (n = 64) to healthy controls (

19 Major depressive disorder (MDD) and Alzheimer's disease (AD) r

20 (LC omega-3 PUFA) have been linked to major depressive disorder (MDD) and preterm birth (PTB), and p

21 enia (SCZ), bipolar disorder (BD), and major depressive disorder (MDD) are heritable psychiatric diso

22 pressed in the brain, in subjects with major depressive disorder (MDD) as compared with age- and sex-

23 V) and HCMV has never been examined in major depressive disorder (MDD) despite the presence of inflam

24 nome-wide association analyses between major depressive disorder (MDD) genetic risk score (GRS) and 9

25 Major depressive disorder (MDD) has an enormous impact on glob

26 ontotemporal cortices of patients with major depressive disorder (MDD) has been demonstrated using fu

27 Major depressive disorder (MDD) is a leading cause of disabili

28 More severe anhedonia in major depressive disorder (MDD) is a negative predictor of ant

29 Major depressive disorder (MDD) is a serious mental illness, c

30 Major depressive disorder (MDD) is a serious, heterogeneous di

31 Although major depressive disorder (MDD) is associated with altered fun

32 Major depressive disorder (MDD) is associated with altered glo

33 Major depressive disorder (MDD) is associated with an increase

34 ct treatment response in patients with major depressive disorder (MDD) is challenging, in part becaus

35 r knowledge of the biological basis of major depressive disorder (MDD) is derived from studies of chr

36 t-traumatic stress disorder (PTSD) and major depressive disorder (MDD) on the basis of robust and dis

37 ata of 130 individuals (65 melancholic major depressive disorder (MDD) patients, 65 healthy controls)

38 itors (SSRIs) are standard of care for major depressive disorder (MDD) pharmacotherapy, but only appr

39 udy participants were 27 subjects with major depressive disorder (MDD), 29 subjects with bipolar diso

40 ssant partial- and non-responders with major depressive disorder (MDD), a systematic search of Pubmed

41 ondition (ASC), bipolar disorder (BD), major depressive disorder (MDD), and schizophrenia (SCZ; n = 2

42 s identified genetic correlations with Major Depressive Disorder (MDD), Bipolar Disorder (BD), Schizo

43 a-GWASs of self-reported and recurrent major depressive disorder (MDD), bipolar disorder and schizoph

44 n neuropsychiatric diseases, including major depressive disorder (MDD), has been postulated.

45 in psychiatric diseases, particularly major depressive disorder (MDD), remains largely unknown.

46 S-ketamine (esketamine) nasal spray in major depressive disorder (MDD), we performed a genome-wide as

47 Using RNA-Seq data from a study of major depressive disorder (MDD), we show that NPDR with covari

48 ic plasticity is often associated with major depressive disorder (MDD).

49 pha) treatment for Hepatitis-C develop major depressive disorder (MDD).

50 ntidepressant effects in patients with major depressive disorder (MDD).

51 onse has been a clinical challenge for major depressive disorder (MDD).

52 renia (SZ), bipolar disorder (BD), and major depressive disorder (MDD).

53 TMS) is a commonly- used treatment for major depressive disorder (MDD).

54 leviation and quality of life (QoL) in major depressive disorder (MDD).

55 n implicated in the pathophysiology of major depressive disorder (MDD).

56 s) may be efficacious for treatment of major depressive disorder (MDD).

57 increased in a subset of patients with major depressive disorder (MDD).

58 or treatment outcomes in patients with major depressive disorder (MDD).

59 nimal phenotyping and strictly defined major depressive disorder (MDD): the former has a lower genoty

60 tor antagonist, ketamine, for treating major depressive disorder (MDD); however, its neural mechanism

61 autism spectrum disorder (N = 126), or major depressive disorder (N = 398; total N = 2937 from 12 sit

62 3 individuals with treatment-resistant major depressive disorder (TRD) and 25 healthy volunteers (HVs

63 e FDA for treating treatment-resistant major depressive disorder (TRD) in 2019, almost 50 years after

64 n models, PSs indexing 6 risk factors (major depressive disorder [MDD], attention deficit/hyperactivi

65 d to pathological circuitry, including major depressive disorder and Alzheimer disease.

66 The search terms included cytokine, depressive disorder and antidepressant and their synonym

67 the shared molecular genetic basis of major depressive disorder and bipolar disorder and to highligh

68 c associations, and genetic studies of major depressive disorder and bipolar disorder can be combined

69 Analyzing subtypes of major depressive disorder and bipolar disorder provides eviden

70 Mood disorders (including major depressive disorder and bipolar disorder) affect 10% to

71 enetic association with schizophrenia, major depressive disorder and bipolar disorder.

72 Synergistic effects of depressive disorder and NR3C1 hypermethylation on long-t

73 nd bipolar disorder, and an additional major depressive disorder cohort from UK Biobank (total: 185,2

74 Major depressive disorder is a common mental health condition

75 Major depressive disorder is a common psychiatric disorder ass

76 Major depressive disorder is a leading cause of disability and

77 Major depressive disorder is a remarkably common and often sev

78 Major depressive disorder is associated with aberrant resting-

79 ics, the biological characteristics of major depressive disorder may be close to those of HCS.

80 a diagnosis of major depressive disorder or depressive disorder not otherwise specified and no prior

81 ntrols and from patients with remitted major depressive disorder on antidepressants.

82 67,807 individuals with a diagnosis of major depressive disorder or depressive disorder not otherwise

83 markers in human NAc from nonmedicated major depressive disorder patients.

84 lso observed in human fibroblasts from major depressive disorder patients.

85 ession, and many prominent theories of major depressive disorder propose a role for abnormal cortico-

86 arched for all case-control studies on major depressive disorder that reported microarray or RNA sequ

87 at Pdcd4 might be a new potential target for depressive disorder therapy.

88 high risk for transition from a diagnosis of depressive disorder to one of bipolar disorder.

89 A total of 116 participants with major depressive disorder treated with sertraline in stage 1 s

90 Genes abnormally expressed in major depressive disorder were enriched for innate immune-rela

91 ge 2 sample comprised 87 patients with major depressive disorder who switched medication and 38 healt

92 Major depressive disorder with psychotic features (psychotic d

93 om the Psychiatric Genomics Consortium Major Depressive Disorder Working Group and the UK Biobank.

94 with schizophrenia, bipolar disorder, major depressive disorder, and obsessive-compulsive disorder.

95 m spectrum disorder, bipolar disorder, major depressive disorder, and schizophrenia.

96 m spectrum disorder, bipolar disorder, major depressive disorder, and schizophrenia.

97 ion, FMRP targets were associated with major depressive disorder, and we present novel evidence of as

98 Brain structural abnormalities in major depressive disorder, bipolar disorder, schizophrenia, an

99 icrobiota dysbiosis has been linked to major depressive disorder, but the mechanisms whereby the micr

100 tic risk for behavioral disinhibition, major depressive disorder, depressive symptoms, autism spectru

101 s that CRY1Delta11 was associated with major depressive disorder, insomnia, and anxiety.

102 ere made from 2007 to 2012, including DSM-IV depressive disorder, NR3C1 methylation, and various demo

103 ible novel treatment for diseases like major depressive disorder, obesity, chronic pain, and certain

104 ant enrichments of the heritability of major depressive disorder, obsessive-compulsive disorder and s

105 insically linked to the development of major depressive disorder, originate in part from the dysregul

106 Lithium has been used to treat major depressive disorder, yet the neural circuit mechanisms u

107 s is a primary objective when treating major depressive disorder-a disease that afflicts ~20% of the

108 able response for a drug treatment for major depressive disorder.

109 ively representing 2,928 patients with major depressive disorder.

110 otherapy practice, CBT, in adults with major depressive disorder.

111 n between the Netrin-1/DCC pathway and major depressive disorder.

112 r for ACS in combination with a diagnosis of depressive disorder.

113 S to real RNA-Seq data from a study of major depressive disorder.

114 ngly with recurrent and single-episode major depressive disorder.

115 to BDNF expression is associated with major depressive disorder.

116 s in women not formally diagnosed with major depressive disorder.

117 s an effective add-on intervention for major depressive disorder.

118 re a particularly disabling feature of major depressive disorder.

119 l cortex (mPFC) has been implicated in major depressive disorder.

120 cores for behavioral disinhibition and major depressive disorder.

121 t stress, modeling multiple aspects of major depressive disorder.

122 sing real RNA-seq data from a study of major depressive disorder.The cnCV method has similar training

123 samples of SSRI-treated patients with major depressive disorder: the MARS (n = 253, P = 0.0169) and

124 ed genetic variants of SIRT1 linked to major depressive disorders.

125 ed MS effects, while hM3Dq prevented the pro-depressive effects and short-term memory impairment of M

126 rate of any mood episode (RR-any, primary), depressive episode (RR-dep) and manic/hypomanic/mixed ep

127 712 youth with a lifetime history of a major depressive episode and 712 typically developing (TD) you

128 N = 31) appetite and weight in their current depressive episode and healthy control participants (N =

129 ee individuals with MDD currently in a major depressive episode were enrolled in an open-label study

130 Twenty patients suffering a major depressive episode were randomized to pretreatment with

131 f a syndromal, hypomanic episode and a major depressive episode.

132 or the occurrence, severity, and duration of depressive episodes.

133 s accumulated from case-control studies that depressive illness is associated with blunted reward act

134 , and noradrenaline-dependent and persistent depressive-like and anhedonic behaviors in females.

135 Moreover, 1-methyl tryptophan reduced depressive-like behavior (P <= 0.001) compared to contro

136 circDYM expression significantly attenuated depressive-like behavior and inhibited microglial activa

137 ow that prophylactics against stress-induced depressive-like behavior can be developed in a sex-speci

138 white matter injury and improved anxiety and depressive-like behavior following TBI.SIGNIFICANCE STAT

139 e, and (2R,6R)-HNK preventing stress-induced depressive-like behavior in both sexes.

140 on of (R,S)-ketamine prevents stress-induced depressive-like behavior in male mice, perhaps by alteri

141 7,333 was ineffective against stress-induced depressive-like behavior in the forced swim test (FST),

142 ahippocampal Reelin infusions on measures of depressive-like behavior, cognition, and hippocampal neu

143 xhibited antidepressant properties, reducing depressive-like behavior, intestinal SAA1 and SAA2 produ

144 that is a powerful modulator of anxiety- and depressive-like behavior.

145 nmental factors that potentiate anxiety- and depressive-like behavior.

146 ed learned fear and decreased stress-induced depressive-like behavior.

147 leting GluN2D in the BNST leads to increased depressive-like behaviors and increased excitatory drive

148 Th17 cells were required to promote depressive-like behaviors by AI-2, as AI-2 administratio

149 Chronic stress and depressive-like behaviors in basic neuroscience research

150 nistration did not promote susceptibility to depressive-like behaviors or SAA1 and SAA2 production in

151 s were significantly correlated with various depressive-like behaviors, thus reinforcing MGB axis per

152 ing DA neurons, and also rescued CMS-induced depressive-like behaviors.

153 to be used as a novel biomarker of sickness/depressive-like behaviors.

154 ection was also associated with anxiety- and depressive-like behaviors.

155 rum N-glycans were altered in mice displayed depressive-like behaviors.

156 e microbiome and quorum-sensing molecules on depressive-like behaviors.

157 single peripheral LPS challenge that led to depressive-like behaviour in the forced swim test.

158 affective changes reflective of anxiety- and depressive-like behaviour were only observed for F344/DU

159 al glutaminergic signalling may underpin the depressive-like behaviours that result from both inflamm

160 d with higher neuronal density and decreased depressive-like behaviours.

161 In addition, the depressive-like macaques were characterized by changes i

162 t both microbial and metabolic signatures of depressive-like macaques were significantly different fr

163 al blood of patients with MDD and in the two depressive-like mouse models: the chronic unpredictable

164 cted with lipopolysaccharide (LPS) display a depressive-like phenotype twenty-four hours after endoto

165 to LAN on three consecutive nights increased depressive-like responses compared to mice housed in dar

166 M) model lowers pain thresholds and produces depressive-like symptoms.

167 the Tinnitus Questionnaire (TQ), severity of depressive mood states examined using the Beck Depressio

168 y outcome assessments to subjects with major depressive or psychotic disorders who had at least moder

169 t strains possessing stress hyper-reactive-, depressive- or anxiety-like phenotypes may possess more

170 genetic reduction of activated RhoA prevents depressive outcomes to stress by preventing loss of D1-M

171 omes included any neuropsychiatric, anxiety, depressive, personality, or substance use disorders.

172 hat the psychiatric problems, especially the depressive problems, were significantly associated with

173 s is related to whether or not the child has depressive problems.

174 on has been previously reported to have anti-depressive properties.

175 Depressive rumination is considered a prominent risk fac

176 eatment options have been developed to treat depressive rumination of which mindfulness based program

177 ated with larger brainstem volumes and lower depressive scores, and that brainstem volume mediates th

178 excitability and anhedonia-a key feature in depressive states.

179 e stratified into high (N = 1921) versus low-depressive strata based on baseline ratings.

180 Patients in the high depressive stratum showed modest but significant effects

181 Structural connectivity was linked to depressive symptom change under STN-DBS.

182 group (609 depression or clinically relevant depressive symptom events; 12.9/1000 person-years) and t

183 group (625 depression or clinically relevant depressive symptom events; 13.3/1000 person-years) (haza

184 4 years, 59% females) endorsing at least one depressive symptom on the EURO-D scale for depression (N

185 lites may mediate an inflammation-associated depressive symptom profile via CNS KP metabolites that c

186 t produced a clinically meaningful change in depressive symptom severity, this did not differ from sh

187 Primary outcome was change in depressive symptom severity, while secondary outcomes we

188 igh plasma CRP (>3 mg/L) and correlated with depressive symptom severity.

189 exposure or other covariates, the antepartum depressive symptom trajectory was associated with reduce

190 e of spirituality on the association between depressive symptomatology and QOL in stroke survivor-car

191 derated the association between care partner depressive symptomatology and survivor psychological QOL

192 Depressive symptomatology may be associated with dementi

193 d future studies should consider subtypes of depressive symptomatology when examining its relationshi

194 lth status, less social support, and greater depressive symptomology were associated with higher risk

195 vel >8%), obesity (body mass index >30), and depressive symptoms (2-item Patient Health Questionnaire

196 No associations were seen with postpartum depressive symptoms (7% of women) or with any of the per

197 recall, delayed recall, verbal fluency) and depressive symptoms (EURO-D scale) were conducted at 2-y

198 Conversely, anti-TNF significantly improved depressive symptoms (Hospital Anxiety and Depression Rat

199 ndividuals presenting clinically significant depressive symptoms (indicating >=15 on the PHQ-9) and 5

200 2.6 years) showed significant improvement in depressive symptoms (k = 7, Hedges' g = 0.44, 95% confid

201 Core depressive symptoms (low mood, anhedonia) were measured

202 ghttime sleep was negatively associated with depressive symptoms (OR=0.88, 95% CI: 0.84 to 0.92), whi

203 me nap displayed a positive association with depressive symptoms (OR=0.88, 95% CI: 0.84 to 0.92).

204 re analysis was from the genetic loading for depressive symptoms (p = 0.001, standardized coefficient

205 vated neurodevelopmental, externalizing, and depressive symptoms (R(2) = 0.26-1.69%), but not with an

206 y attenuated the average treatment effect on depressive symptoms (SMD = 0.20, 95% CI: 0.06-0.35), but

207 howed modest but significant effects on core depressive symptoms (SMD = 0.29, 95% CI [0.12-0.45]) and

208 he risk of depression or clinically relevant depressive symptoms (total of incident and recurrent cas

209 ment in positive (weight = 0.62) and anxious/depressive symptoms (weight = 0.49).

210 d assessed anxiety [Beck Anxiety Inventory], depressive symptoms [Beck Depression Inventory-II], and

211 ere significantly associated with persistent depressive symptoms across the study period.

212 are mildly effective interventions to reduce depressive symptoms among adolescents.

213 thors examined the prevalence of burnout and depressive symptoms among North American psychiatrists,

214 ighborhood disorder and social cohesion with depressive symptoms among persons aged 50 years or more

215 e nap was associated with lower incidence of depressive symptoms among the elderly after adjusting al

216 dinal association between sleep duration and depressive symptoms among the elderly in China.

217 89-0.97) was also negatively associated with depressive symptoms among the elderly.

218 Stool samples from 10 people with current depressive symptoms and 10 matched healthy control subje

219 abolites and inflammatory markers along with depressive symptoms and antidepressant treatment respons

220 icant improvements in a composite measure of depressive symptoms and cardiometabolic indices at 24 mo

221 derated the association between care partner depressive symptoms and care partner physical (B=0.05, P

222 ates relationships between prenatal maternal depressive symptoms and child behavior.

223 ted the relationship between third trimester depressive symptoms and child externalizing behavior in

224 Depressive symptoms and cognition were assessed prior to

225 x mediated the relationship between maternal depressive symptoms and externalizing behavior in boys,

226 95% CI: 0.2, 4.5) of the association between depressive symptoms and HIV incidence.

227 A measures were associated with decreases in depressive symptoms and improvements in mental and physi

228 icipants had information about self-reported depressive symptoms and no CVD history at baseline.

229 on; (2) Relative to the combined Z values of depressive symptoms and processing speed, sleep quality

230 It is uncertain whether depressive symptoms are independently associated with su

231 rlying the association of hyperglycemia with depressive symptoms are unknown.

232 of substances (alcohol and khat) and women's depressive symptoms as measured by the Patient Health Qu

233 fusivity and analyzed with maternal prenatal depressive symptoms as well as child behavior.

234 Incident depression was defined as minimal depressive symptoms at baseline and clinically significa

235 hyroidism versus euthyroidism, adjusting for depressive symptoms at baseline, age, sex, education, an

236 Depressive symptoms before and after STN-DBS surgery wer

237 Identify distinct trajectories of change in depressive symptoms by mid-treatment during psychotherap

238 ding status, mothers experiencing antepartum depressive symptoms delivered offspring who exhibited lo

239 with data on thyroid status at baseline and depressive symptoms during follow-up.

240 clinical thyroid dysfunction at baseline and depressive symptoms during follow-up.

241 Participants with increasing depressive symptoms had the fastest decline, while those

242 Children of mothers with worse depressive symptoms had weaker white matter connectivity

243 scence was associated with a higher level of depressive symptoms in adulthood during all follow-up pe

244 oeconomic disadvantage and increased risk of depressive symptoms in adulthood is well established.

245 We characterized the network structure of depressive symptoms in late-life and used indices of "st

246 analysis focused on the network structure of depressive symptoms in late-life because of their distin

247 ST led to clinically meaningful reduction in depressive symptoms in patients with MDD and produced mi

248 hronic hyperglycemia, cortical thinning, and depressive symptoms in T1D.

249 joint training-set map predicted changes in depressive symptoms in the independent test-set.

250 at antidepressants were also efficacious for depressive symptoms in those without diagnosis of MDD.

251 onal migrants showed above average levels of depressive symptoms on a 12-item standardized short-form

252 c inflammation may influence trajectories of depressive symptoms over time, perhaps differentially by

253 Finally, depressive symptoms reduce happiness more in volatile th

254 Distinct clusters of depressive symptoms responded better to different TMS ta

255 8, 95% CI [0.26-0.70]) had larger effects on depressive symptoms than other drug classes.

256 onflict using the Decisional Conflict Scale, depressive symptoms using the Patient Health Questionnai

257 Worsening of depressive symptoms was associated with left prefrontal

258 Therefore, the relation of sleep on depressive symptoms was dependent on grandparent caregiv

259 Risk of depression or clinically relevant depressive symptoms was not significantly different betw

260 Depressive symptoms were assessed from wave 1 (2002-03)

261 Emotional processing and depressive symptoms were assessed using emotional tasks

262 Depressive symptoms were more prominent in the standard

263 The trajectories of depressive symptoms were obtained using latent growth mi

264 Greater patient depressive symptoms were related to greater patient deci

265 y whether poor sleep quality results in more depressive symptoms when older individuals are also cari

266 ystems in somatic versus cognitive-affective depressive symptoms which remains largely unexplored.

267 ositively associated with incident "elevated depressive symptoms" (EDS: CES-D(total) >= 16) among AA

268 es of psychological distress (anxiety and/or depressive symptoms) and normalized characteristic path

269 emotional well-being (enjoyment of life and depressive symptoms), and social function (organizationa

270 mated the magnitude of change in disability, depressive symptoms, and HRQL with hierarchical segmente

271 Disability, depressive symptoms, and impaired health-related quality

272 individual differences in pain sensitivity, depressive symptoms, and reward processing.

273 egiving status was significant in predicting depressive symptoms, and the interactions examining glob

274 Validated items on burnout, depressive symptoms, and well being were included in the

275 al disinhibition, major depressive disorder, depressive symptoms, autism spectrum disorder, psychosis

276 chronic pain), emotional wellbeing (e.g. few depressive symptoms, good sleep), greater physical activ

277 Covariates included age, sex, education, depressive symptoms, nonmilitary trauma, alcohol use, an

278 ore regression and polygenic risk scores for depressive symptoms, schizophrenia, neuroticism, and sub

279 Mediating variables include depressive symptoms, sleep quality and processing speed.

280 <0.01); (3) Processing speed was affected by depressive symptoms, sleep quality, and in turn, yieldin

281 cognitive function was partially mediated by depressive symptoms, sleep quality, and processing speed

282 Measures of depressive symptoms, sleep quality, processing speed, an

283 sleep difficulties were associated with more depressive symptoms.

284 sleep, nighttime sleep and daytime nap, and depressive symptoms.

285 brainstem volume mediates the seasonality of depressive symptoms.

286 focused on transient rather than persistent depressive symptoms.

287 ant confounders, including prenatal maternal depressive symptoms.

288 us edema, poorer physical function, and more depressive symptoms.

289 modestly worse health regarding obesity and depressive symptoms.

290 young children exposed to maternal prenatal depressive symptoms.

291 between subclinical thyroid dysfunction and depressive symptoms.

292 mechanistic role in inflammation-associated depressive symptoms.

293 othyroidism to reduce the risk of developing depressive symptoms.

294 ntal areas were associated with worsening of depressive symptoms.

295 s surveyed reported experiencing burnout and depressive symptoms.

296 n, and are associated with the trajectory of depressive symptoms.

297 thyroidism in particular, is associated with depressive symptoms.

298 structural connectivity explaining change in depressive symptoms.

299 ose in life, optimism, resilient coping, and depressive symptoms.

300 should be avoided to maximize improvement of depressive symptoms.