ライフサイエンスコーパス: depression

1 rticipants (312 healthy and 33 with clinical depression).

2 redictable mild stress (CUMS) mouse model of depression.

3 ing in food insecure hotspot communities and depression.

4 n used to find affected glycoproteins during depression.

5 luded 1 suicide attempt, related to comorbid depression.

6 ence of shifts in symptoms of mild or severe depression.

7 d treatment of reward processing deficits in depression.

8 n on emotional attributions in patients with depression.

9 e sex are associated with increased risk for depression.

10 pollution and daily hospital admissions for depression.

11 the previous year, and comorbid anxiety and depression.

12 ve treatment for severe medication-resistant depression.

13 equilibrium, a process that is disrupted in depression.

14 an increased risk for developing anxiety and depression.

15 studies support its use in the treatment of depression.

16 to food insecurity, to reduce the burden of depression.

17 t and treat their psychological distress and depression.

18 vulnerability factor for the development of depression.

19 tecting depression and assessing severity of depression.

20 chronic social defeat stress (CSDS) model of depression.

21 ontrol processes that directly contribute to depression.

22 ing a specific agonist induced resilience to depression.

23 her risk of developing anxiety disorders and depression.

24 ciated with CHD risk was not associated with depression.

25 cal power to identify novel genetic loci for depression.

26 ls contribute to social learning deficits in depression.

27 Drug Administration for treatment-resistant depression.

28 centage predicted), cognitive impairment, or depression.

29 e, and the development of new treatments for depression.

30 between reward processing abnormalities and depression.

31 ge and drinking and the other one related to depression.

32 assessed the correlation between burnout and depression.

33 posure for their positive effects on mood in depression.

34 otics have proven to be effective in bipolar depression.

35 sed post-tetanic potentiation, and increased depression.

36 isease modifier, promoting susceptibility to depression.

37 postmortem cortical samples of patients with depression.

38 t the use of vitamin D3 in adults to prevent depression.

39 de range of potential modifiable factors for depression.

40 d emotion regulation and subsequent risk for depression.

41 ity and PROMs, but a strong correlation with depression.

42 abnormalities may be confounded by comorbid depression.

43 ein (CRP) are likely causal risk factors for depression.

44 rability to psychiatric disorders, including depression.

45 sychotic disorders who had at least moderate depression.

46 d be targets for treatment and prevention of depression.

47 uently accompanied by insomnia, anxiety, and depression.

48 f health outcomes, 7.3% were obese, 8.7% had depression, 19.5% reported smoking, 16.1% reported drug

49 sorders among FSWs in LMICs were as follows: depression 41.8% (95% CI 35.8%-48.0%), anxiety 21.0% (95

50 f-report scores for anxiety (55.2 vs. 50.0), depression (50.2 vs. 46.1), and somatization (70.3 vs. 6

51 new understanding of the pathophysiology of depression, a paradigm shift from monoamine to glutamate

52 The risk of depression according to perceived neighborhood disorder

53 stematic investigation of decision making in depression across tasks.

54 Depression affects all aspects of an individual's life b

55 redundancy, and T-wave inversion/ST-segment depression (all p < 0.0001) but not with mitral regurgit

56 ic diameter, and T-wave inversion/ST-segment depression (all p <= 0.001).

57 All methods are acceptable for women with depression, although medical comorbidities may dictate a

58 a, excessive daytime sleepiness, anxiety and depression among African gamers, (2) the association bet

59 vironment might be an important predictor of depression among older adults, systematic reviews point

60 ctors that increase the risk for burnout and depression among psychiatrists and has implications for

61 ions to reduce the high rates of burnout and depression among psychiatrists.

62 were positively associated with the risk of depression among women.

63 iagnoses was a limitation since ascertaining depression and ADHD from prescriptions omitted affected

64 Depression and anxiety were assessed with the Patient He

65 Symptoms of depression and anxiety, aggressive behavior, and attenti

66 mmon mental health disorders (CMDs), such as depression and anxiety, but we know little about nature-

67 Patient Health Questionnaire for symptoms of depression and anxiety.

68 f-administered instrument used for detecting depression and assessing severity of depression.

69 t of PTSD and psilocybin in the treatment of depression and cancer-related anxiety.

70 sex differences in the comorbidity of major depression and cardiovascular disease.

71 ogical fitness through metabolic and aerobic depression and changes to anti-predator behavior, with i

72 a range of brain disorders, including major depression and cognitive deficits.

73 social ties in communities, which can reduce depression and contribute to healthy aging.

74 ocessing speed, executive function, anxiety, depression and disease severity.

75 re the proportion of participants with major depression and function scores at 6 months post-treatmen

76 COVID-19 lockdown and expressing feelings of depression and health anxiety.

77 nd inconsistent condom use with clients, and depression and HIV infection.

78 behaviour, illicit drug use and depression, depression and inconsistent condom use with clients, and

79 es examining the prospective associations of depression and inflammatory biomarkers.

80 ning new prevention or treatment avenues for depression and its associated cardiometabolic comorbidit

81 Our understanding of depression and its treatment has advanced with the adven

82 ty, global brain connectivity) correlates of depression and negative affect across three population-i

83 rders like depression.SIGNIFICANCE STATEMENT Depression and other mental disorders can be induced by

84 ch signaling can underlie conditions such as depression and Parkinson's disease.

85 ent-caregiver dyads (beta=0.47 and 0.44, for depression and perceived stress models, respectively, P<

86 d view of the circuit mechanisms surrounding depression and potential mechanistic targets for develop

87 ession and schizophrenia to be used to treat depression and psychotic symptoms in HD.

88 sociation between known risk factors such as depression and quality of life (QOL) in stroke survivor-

89 vide a rationale for treatments effective in depression and schizophrenia to be used to treat depress

90 Higher volumes of depression and schizophrenia tweets were associated with

91 ey priorities for future research into major depression and schizophrenia, including studies of the m

92 psychiatric symptomatology, including major depression and schizophrenia.

93 This model tested whether each person's depression and stress predicted their own decisional con

94 ate of reduced inhibitory tone in the NAc in depression and stress susceptibility.SIGNIFICANCE STATEM

95 determined the association between maternal depression and stress symptom trajectories and infant fe

96 ntify core behavioral pathology of late-life depression and targets it with simple interventions, co-

97 rs in rodents are widely used to model human depression and to test the efficacy of novel anti-depres

98 In three cohorts of individuals with depression and treated with serotonin-norepinephrine reu

99 activity represent a trait-like indicator of depression and which represent a current depressed state

100 e for PTSD (7.9%, N = 42), all had co-morbid depression and/or anxiety.

101 present in the prevalence estimates of PTSD, depression, and anxiety, and limited covariates were rep

102 Self-reported anxiety, depression, and bodily pain levels were significantly hi

103 entanil-induced antinociception, respiratory depression, and bradycardia in mice and rats.

104 Risk of diabetes mellitus, depression, and cardiovascular disease was significantly

105 , with symptoms similar to anxiety and major depression, and is associated with differential sensitiv

106 ical activity during pregnancy and perinatal depression, and it is limited for different physical act

107 GluA3 slows and attenuates synaptic depression, and makes it less dependent on the presynapt

108 d to underlie motivational disorders such as depression, and many prominent theories of major depress

109 in is a key mediator of stress, anxiety, and depression, and novel therapeutic targets within seroton

110 ssociated with Alzheimer's disease, clinical depression, and other disorders may begin to clarify how

111 g cardiovascular disease, sleep disturbance, depression, and psychosocial stress.

112 gnition, presurgical function, postoperative depression, and the development of postoperative complic

113 is effective for the treatment of recurrent depression, and the MRI-guided method of coil targeting

114 The lateral habenula (LHb) is hyperactive in depression, and thus potentiating inhibition of this str

115 r cognitive problems (eg, cognitive decline, depression, anxiety).

116 adolescent-emergent disorders, specifically depression, anxiety, and deliberate self-harm (nonsuicid

117 Changes in depression, anxiety, and pain catastrophizing were not s

118 Rates of depression, anxiety, and post-traumatic stress disorder

119 ngs to a specific mental disorder, including depression, anxiety, bipolar, borderline personality dis

120 led prevalence estimates were calculated for depression, anxiety, post-traumatic stress disorder (PTS

121 creased medical co-morbidities, a history of depression, anxiety, substance use disorder, and chronic

122 Differential effects of inbreeding depression are also observed between study sites with di

123 stic targets for development and reversal of depression associated circuit abnormalities.

124 (MDD) and preterm birth (PTB), and prenatal depression associates with PTB.

125 n of MORs from KF neurons also relieved rate depression at near-maximal respiratory depressant doses

126 lleles or C4 haplotypes were associated with depression at the region-wide threshold.

127 ronic social defeat stress, a mouse model of depression, at both the level of synaptic function and p

128 ood allergy were associated with anxiety and depression, atopic dermatitis was associated with suicid

129 r for adult internalizing (i.e., anxiety and depression, beta = 0.20) psychopathology, rather than a

130 ma exposure as an environmental influence on depression, both gene-environment correlations and gene-

131 reased inflammatory proteins and more severe depression but differed in terms of myeloid and lymphoid

132 mine improves motivation-related symptoms in depression but simultaneously elicits similar symptoms i

133 apses of the brain involves potentiation and depression capable of branching and is essential for sur

134 ta-driven analysis identified 4 subgroups of depression cases, 2 of which (n = 38 and n = 100; 67% co

135 opment, yet the relationships among prenatal depression, child behavior, and children's brain structu

136 Mindfulness groups showed reduced depression compared to control groups (g=.14, 95%CI[.01-

137 veloped or showed exacerbated pituitary dome depression compared with baseline.

138 entia, non-smoking, low alcohol consumption, depression, daytime somnolence, epilepsy and earlier men

139 differences in genetic architecture between depression defined by minimal phenotyping and strictly d

140 ent suicidal behaviour, illicit drug use and depression, depression and inconsistent condom use with

141 ls (69% female, 10-35 years old at the first depression diagnosis) from the iPSYCH Danish case-cohort

142 magnetic stimulation (TMS) for treatment of depression (discovery sample, N=30; active replication s

143 hs later demonstrated low levels of anxiety, depression, distress, and uncertainty and high levels of

144 that any HLA or C4 variants associated with depression either are rare or have very modest effect si

145 part because the clinical diagnosis of major depression encompasses biologically heterogeneous condit

146 n the VITAL-DEP (Vitamin D and Omega-3 Trial-Depression Endpoint Prevention) ancillary study to VITAL

147 etabolites, 21 were significantly related to depression (false discovery rate q < .05).

148 ll average daily gain, delayed the FI and BW depression for ~ 2 weeks and had transiently higher ener

149 acebo-controlled clinical trial of AV-101 in depression found negative results.

150 erview of our current understanding of major depression, from pathophysiology to treatment.

151 The dispersive undulating depression front and its subsequent whelps act as a bump

152 n trajectories and brain volume changes with depression, generalized anxiety, and hyperactivity sympt

153 hosocial factors (ie, education, symptoms of depression), grip strength, and household and ambient po

154 Depression has been associated with increased inflammato

155 Although a genetic basis of depression has been well established in twin studies, id

156 The cognitive model of depression has significantly influenced the understandin

157 ially those designed for treatment-resistant depression, has been sorely needed.

158 few studies on the neurobiology of psychotic depression have been pursued.

159 tabolic dysregulations vary as a function of depression heterogeneity by illustrating that such biolo

160 and Abeta deposition was not associated with depression history characteristics.

161 hecklist Individual Strength-8), anxiety and depression (Hospital Anxiety and Depression Scale), cogn

162 ng of distorted cognitive processes in major depression; however, this model's conception of cognitio

163 in the Study of Pharmacotherapy of Psychotic Depression II randomized controlled trial.

164 , we find that transcriptional correlates of depression imaging phenotypes track gene down-regulation

165 cation in 1.3 and 1.5 mM calcium and lead to depression in 1.8 mM.

166 n is a well-known correlate and predictor of depression in adults and adolescents, with depressed ind

167 t study (iPSYCH2012) who were diagnosed with depression in Danish psychiatric hospitals from 1994 to

168 ed phase change in addition to melting-point depression in deformed or damaged crystals relative to t

169 neighborhood-level social capital relates to depression in different welfare-state contexts.

170 sociated specifically with increased risk of depression in HD, as was schizophrenia risk score with p

171 al interventions as first-line treatment for depression in low-income and middle-income countries.

172 The study of depression in mothers in relation to transmission of ris

173 dern genomic tools to investigate inbreeding depression in nature have been limited to single populat

174 n reward processing may mitigate the risk of depression in nondepressed older adults, especially olde

175 ratory depression (OIRD), a life-threatening depression in respiratory rate thought to be caused by s

176 LANDD EPSPs show little depression in response to tetanic stimulation and, there

177 le is known about the dynamics of inbreeding depression in subdivided populations over time.

178 to identify factors associated with incident depression in the full sample and among at-risk individu

179 creased risk of daily hospital admission for depression in the general urban population in China, whi

180 on through blocking the function of Pdcd4 in depression, indicating that Pdcd4 might be a new potenti

181 that PV(+) cell-mediated short-term synaptic depression influences the experimentally reported dynami

182 imer disease, amyotrophic lateral sclerosis, depression, insomnia, intelligence, neuroticism, and sch

183 pressive mood states examined using the Beck Depression Inventory-II, and general distress assessed u

184 nxiety Inventory], depressive symptoms [Beck Depression Inventory-II], and cognition [Montreal Cognit

185 Depression is a leading cause of disability.

186 Depression is a seriously disabling psychiatric disorder

187 Given that depression is associated with altered dopamine (DA) and

188 ity between coronary heart disease (CHD) and depression is evident, it is unclear whether the two dis

189 The prevalence of depression is higher in individuals with autoimmune dise

190 Depression is more frequent among individuals exposed to

191 Depression is one of the most common comorbidities of ma

192 ogical states including stress, anxiety, and depression-is a substantial prenatal exposure.

193 actor, with high loadings across anxiety and depression items, were linked to impoverished adjustment

194 ow that E2 add-back induces anxiety-like and depression-like behavior in Het-Met mice, but not in WT

195 gic neuron-selective Ahnak KO mice display a depression-like behavioral phenotype similar to that of

196 e nucleus accumbens (NAc) is associated with depression-like behaviors and synaptic plasticity.

197 CF mice also exhibit depression-like behaviors compared to WT mice in an age

198 mPFC confers resilience or susceptibility to depression-like behaviors in adult mice, using the chron

199 cumbal MFN2 on the regulation of anxiety and depression-like behaviors through actions on mitochondri

200 l roles for RhoA and Rho-kinase in mediating depression-like behaviors via dendritic remodeling of NA

201 Highly anxious animals showed increased depression-like behaviors, as well as reduced expression

202 been linked to increased stress-related and depression-like behaviors.

203 of circulating proinflammatory cytokines and depression-like behaviors.

204 chizophrenia, whereas adult stress induced a depression-like hypodopaminergic state.

205 PL)-M1 before and after inducing a long term depression-like plastic change to dIPL node with continu

206 Late-life depression (LLD) is a prevalent and disabling condition

207 estion for NMDA receptor-dependent long-term depression (LTD) in the hippocampus.

208 rigger metaplastic facilitation of long-term depression (LTD) induction at hippocampal CA1 synapses.

209 n (HFS) of cortical inputs induced long-term depression (LTD) mediated by adenosine A1 receptor (A1R)

210 neuronal communication by inducing long-term depression (LTD) of excitatory transmission at hippocamp

211 hether BNST group I mGluR-mediated long-term depression (LTD) was disrupted at these timepoints.

212 ative orientation, internet memes related to depression may be beneficial for individuals experiencin

213 Conversely, symptoms of depression may decrease adherence to treatment of both d

214 ologic antagonism of NMDARs in patients with depression may reduce excitability in A25, mimicking the

215 Apathy, but not depression, may be a prodromal symptom of dementia in SV

216 MD -7.29; 95% CI -8.23 to -6.35) and anxiety/depression (MD -3.08; 95% CI -4.41 to -1.75) and improve

217 ygenic scores (PGSs) were computed for major depression (MD) at different GWAS p value thresholds usi

218 phrenia (SCZ), bipolar disorder (BIP), major depression (MD), attention-deficit hyperactivity disorde

219 80 was ineffective in the cortical spreading depression model of migraine aura in conditional knockou

220 The Patient Health Questionnaire depression module (PHQ-9) is a 9-item self-administered

221 ile several therapeutic strategies exist for depression, most antidepressant drugs require several we

222 e depressive symptom on the EURO-D scale for depression (N =8,557).

223 binoid-receptor 1 (CB(1))-mediated long-term depression of inhibitory transmission (iLTD), a form of

224 OXTR-mediated excitation of CeL neurons and depression of Kir channels.

225 We demonstrate that Hip14 regulates depression of sensory inputs onto an identified hindbrai

226 henylacetate 3-hydroxylase (HPAH), revealing depression of the pK(a) of 3-fluoro-4-hydroxyphenylaceta

227 , MBL, C3b and C5b-9 terminal C complex, and depressions of CR1 and CD59 relative to those of control

228 dose and death is opioid-induced respiratory depression (OIRD), a life-threatening depression in resp

229 rting a role for healthy dietary patterns in depression onset and symptom management.

230 brain (MGB) axis changes are associated with depression onset, but the mechanisms underlying this obs

231 A history of depression or anxiety (HR = 6.87, 95%CI 3.97-11.90); man

232 The primary outcomes were the risk of depression or clinically relevant depressive symptoms (t

233 es for psychosis; patients with recent-onset depression or psychosis; and healthy volunteers.

234 motional interpretation of social signals in depression or schizophrenia by providing the missing lin

235 nce outside of the Northeast, and history of depression or substance abuse.

236 t way forward to accelerate gene finding for depression, or psychiatric disorders in general.

237 icipants of Combining Medications to Enhance Depression Outcomes (CO-MED, n = 665), Establishing Mode

238 the availability of effective treatments for depression, patients with co-occurring substance use dis

239 sitive subjects had higher levels of current depression, performed worse on the Rey Auditory Verbal L

240 ssociation studies (meta-GWASs) of the broad depression phenotype with those from meta-GWASs of self-

241 CU patients may have high levels of anxiety, depression, posttraumatic stress disorders, and/or compl

242 irculating lipid metabolites associated with depression, potentially opening new prevention or treatm

243 that MDD-PRS adds unique predictive power in depression prediction.

244 eration of an internal dispersive undulating depression produced during the initial acceleration of t

245 ted Olfactory Scale (SROS), 17-item Hamilton Depression Rating Scale (HAMD-17), Hamilton Anxiety Rati

246 task [SRET]) and clinical ratings (Hamilton Depression Rating Scale [HAM-D], Symptom Checklist-90 Re

247 uded Hamilton Anxiety Rating Scale, Hamilton Depression Rating Scale, World Health Organization Quali

248 ty-two participants with treatment-resistant depression received open-label SAINT.

249 map quantitative trait loci for respiratory depression, recovery time and survival time.

250 lity and synaptic transmission and regulates depression-related behaviors in a sex-specific manner.

251 blockade in the adult influenced anxiety- or depression-related behaviors.

252 at adiponectin acts in the brain to regulate depression-related behaviors.

253 literature concerning age, alcohol use, and depression-related changes in brain volume.

254 stress paradigms-procedures that mediated a depression-related phenotype (along with a ketamine anti

255 urbance of sleep continuity in patients with depression, revealing not only a decrease in Slow Wave S

256 isease was associated with a 20% increase in depression risk (95% confidence interval [CI] 16-24%, p

257 was assessed using the Edinburgh Postpartum Depression Scale (EPDS; cut-off score 9).

258 , Hamilton Anxiety Scale (HAMA) and Hamilton Depression Scale (HAMD) before and after the treatment.

259 t least a 50% reduction in Symptom Checklist Depression Scale (SCL-20) scores (range, 0-4; higher sco

260 scores (8-item Patient Health Questionnaire depression scale [PHQ-8]; score range, 0 points [least s

261 e SF12v2 score, and the hospital anxiety and depression scale questionnaire.

262 anxiety and depression (Hospital Anxiety and Depression Scale), cognitive functioning (Cognitive Fail

263 ress assessed using the Hospital Anxiety and Depression Scale.

264 nt and postpartum women (Edinburgh Postnatal Depression Scale: sensitivity, 74%; specificity, 64%), a

265 An increase of DASS-depression score negatively influenced PD >5 mm (OR = 1.

266 that identified significant association with depression severity of two modules, TPOT-FSS corroborate

267 with stronger links between neighborhood and depression, should focus on improving the physical envir

268 treatments for stress-related disorders like depression.SIGNIFICANCE STATEMENT Depression and other m

269 erides are likely to be causally linked with depression, so could be targets for treatment and preven

270 e functions and emotion regulation represent depression-specific neurofunctional markers and treatmen

271 Prevalence rates of positive depression status were 24.4% (WHI-OS), 25.7% (WHI-HT), a

272 -dose testosterone has been shown to improve depression symptom severity, fatigue, and sexual functio

273 rain regions and the periphery contribute to depression symptomatology and a more complete understand

274 h and the trajectories of children's anxiety-depression symptoms between ages 3 to 8 years (adjusted

275 ges may contribute to subsequent anxiety and depression symptoms in childhood.

276 ing theory were associated with lower week-8 depression symptoms in the sertraline versus placebo arm

277 After adjusting for depression symptoms, the PTSD findings in left and right

278 reductions (i.e., less placebo response) in depression than those who did not receive the PCRS (n =

279 considerable beneficial effects in treating depression that may exceed CBT.

280 resynaptic H(3) receptor-dependent long-term depression that requires G(betagamma)-directed Akt-GSK3b

281 ng at least one biological parent with major depression, the authors identified a Swedish National Sa

282 1-MSNs and may prove a useful target for new depression therapeutics.

283 lieved to be a link between inflammation and depression through effects on brain glutamate receptors.

284 direct effect of peer problems on adolescent depression through nucleus accumbens (NAcc) volume alter

285 stimates the number of people suffering from depression to be over 264 million.

286 of mothers in the antepartum and persistent depression trajectories (6% and 2% of women, respectivel

287 iduals (ages 18-65) with treatment-resistant depression (TRD) who received a single ketamine infusion

288 less likely to receive guideline-concordant depression treatment.

289 C has been proposed as an explicit target of depression treatments, this suggest that the limited eff

290 sizes (ESs) of mindfulness interventions on depression using standardized mean differences (Hedge's

291 associations between violence experience and depression, violence experience and recent suicidal beha

292 Postpartum depression was assessed using the Edinburgh Postpartum D

293 Polygenic risk score for major depression was associated specifically with increased ri

294 rajectories of maternal perceived stress and depression were based on scored scales administered in p

295 Genes differentially expressed in depression were identified with the TWAS FUSION method,

296 less of the association between MDD-PRS and depression when under stress than at baseline, suggestin

297 presence of GluA3 reduces and slows synaptic depression, which is achieved by lowering the probabilit

298 brain were enriched for genes for long-term depression; while those in adult brain involved genes en

299 ontrolled trial, 105 patients with recurrent depression who exhibited no responses to at least one ad

300 o estimate the genetic correlations of broad depression with self-reported MDD, recurrent MDD, bipola