ライフサイエンスコーパス: MDD

1 MDD group showed reduced GBCr in the prefrontal cortex (

2 MDD patients often suffer from lifelong recurring episod

3 MDD patients received a single infusion of ketamine and

4 MDD patients with early age at onset and higher symptom

5 MDD subjects exhibited abnormal negative task-related (p

6 MDD subjects then received 8 wk of standardized pharmaco

7 MDD-PRS were based on a discovery sample of approximatel

8 e longitudinal sample (cohort B) included 16 MDD patients who underwent MRI at baseline then 24 h fol

9 ty-two unipolar, drug-free rrMDD patients (2 MDD episodes) and 41 healthy controls (HCs) were recruit

10 etic resonance imaging (MRI) scans from 2148 MDD patients and 7957 healthy controls were analysed wit

11 Data were combined from 3024 MDD cases and 2741 control subjects from nine cohorts co

12 rt A included a cross-sectional sample of 34 MDD and 26 healthy control (HC) subjects, with high-reso

13 status using pre-ECT gray matter (GM) in 38 MDD patients and validate in two independent data sets.

14 ith current (n = 1062) or remitted (n = 711) MDD and healthy control subjects (n = 497).

15 In addition, MDD participants with greater attenuation of connectivit

16 These data show how recent stressors and an MDD history can reverberate through metabolic alteration

17 This study aims to meta-analyze MDD-PRS x CT interaction results across these two and ot

18 pressive disorder suicides (MDD-S, N=21) and MDD non-suicides (MDD, N=9) in the dorsal lateral prefro

19 To examine whether AD and MDD overlap genetically, using a polygenic score approac

20 patients with non-dialysis-dependent CKD and MDD, treatment with sertraline compared with placebo for

21 depressive symptoms in patients with CKD and MDD.

22 ng from chronic inflammatory conditions, and MDD patients exhibit higher levels of circulating pro-in

23 h comorbid posttraumatic stress disorder and MDD.

24 underlying mechanism connecting obesity and MDD with atypical features.

25 Atypical MDD (B = 0.41 (standard error, 0.15); P = 0.007) was a s

26 Atypical MDD (odds ratio (OR) = 1.68, 95% confidence interval (CI

27 Race/ethnicity was a moderator; atypical MDD was a stronger predictor of incident obesity in Hisp

28 gher leptin was associated with the atypical MDD subtype both for remitted (n = 144, odds ratio = 1.5

29 The atypical MDD subtype, and only this subtype, was prospectively as

30 US adults with atypical MDD are at particularly high risk of weight gain and obe

31 bolic consequences in patients with atypical MDD.

32 (n = 4), and offspring with missing baseline MDD data (n = 2) were excluded.

33 Association between MDD PRS and AD.

34 ferences in ketamine-induced changes between MDD and control groups at either time point (P=0.8).

35 Association analyses were conducted between MDD polygenic risk score (PRS) and AD case-control statu

36 No interaction was found between MDD-PRS and the two-domain and five-domain CT measure (O

37 ta-analytic evidence for interaction between MDD-PRS and CT was found.

38 ity (that is, [(11)C]ABP688 binding) in both MDD and control subjects (average of 14+/-9% and 19+/-22

39 espectively, were significantly regulated by MDD-associated SNPs within this region.

40 Pathological states such as CHF, MDD, and PD are associated with an increased complexity

41 RS using MDD GWAS data sets without comorbid MDD-AD cases, significant evidence was observed for an a

42 The degree to which major depression (MDD) and bipolar disorder (BD) are associated with commo

43 of patients with major depressive disorder (MDD) achieve remission with their first antidepressant.

44 nce suggests that major depressive disorder (MDD) affects multiple large-scale brain networks.

45 outpatients with major depressive disorder (MDD) and 20 matched controls completed two runs of the m

46 Major depressive disorder (MDD) and alcohol dependence (AD) are heritable disorders

47 een implicated in major depressive disorder (MDD) and in the actions of antidepressants.

48 sociation between major depressive disorder (MDD) and obesity may stem from shared immunometabolic me

49 Major depressive disorder (MDD) and other mood disorders remain difficult to effect

50 Major depressive disorder (MDD) and schizophrenia (SZ) are considered two distinct

51 cal substrates of major depressive disorder (MDD) are still not well understood, despite many neuroim

52 sed likelihood of major depressive disorder (MDD) as well as suicidal thoughts and behaviours.

53 c risk scores for major depressive disorder (MDD) calculated from the results of the most recent anal

54 sant treatment in major depressive disorder (MDD) cannot be predicted currently, leading to uncertain

55 brain networks in major depressive disorder (MDD) during a depressive episode and following treatment

56 s and symptoms of major depressive disorder (MDD) have been closely associated with impairments in re

57 tter structure in Major Depressive Disorder (MDD) have been inconsistent.

58 Patients with major depressive disorder (MDD) have clinically relevant, significant decreases in

59 of patients with major depressive disorder (MDD) have consistently reported reduced hippocampal volu

60 tudies (GWASs) of major depressive disorder (MDD) have identified few significant associations.

61 (cAMP) cascade in major depressive disorder (MDD) have noted that the cAMP cascade is downregulated i

62 Major depressive disorder (MDD) in the elderly is a risk factor for dementia, but t

63 abnormalities in major depressive disorder (MDD) in two cohorts.

64 Major depressive disorder (MDD) is a debilitating condition that affects over 14 mi

65 Major depressive disorder (MDD) is a debilitating mental illness and a major cause

66 Major depressive disorder (MDD) is a leading cause of disease burden worldwide.

67 Major depressive disorder (MDD) is a prevalent psychiatric condition with limited t

68 Major depressive disorder (MDD) is associated with deficits in representing reward

69 Major depressive disorder (MDD) is associated with reduced concentrations of gamma-

70 dysregulation in major depressive disorder (MDD) is conflicting.

71 Major depressive disorder (MDD) is predicted to be the second leading cause of glob

72 Major depressive disorder (MDD) is prevalent among patients with chronic kidney dis

73 Major depressive disorder (MDD) is the second largest cause of global disease burde

74 sorders including major depressive disorder (MDD) largely ignore biological factors in favor of behav

75 enetic effects on major depressive disorder (MDD) may be partly attributable to moderation of genetic

76 gene finding for major depressive disorder (MDD) may be partly due to phenotypic heterogeneity.

77 and a history of major depressive disorder (MDD) on inflammatory responses to high-fat meals.

78 iteria for either major depressive disorder (MDD) or bipolar disorder I/II and who were currently exp

79 the treatment of major depressive disorder (MDD) over 12 weeks.

80 Major depressive disorder (MDD) patients display a common but often variable set of

81 l connectivity in major depressive disorder (MDD) patients with suicidal ideation are poorly understo

82 all patients with major depressive disorder (MDD) treated with currently available antidepressants (A

83 outpatients with major depressive disorder (MDD) was examined in a 3-site, 8-week, randomized, doubl

84 50 patients with major depressive disorder (MDD), 50 patients with post-traumatic stress disorder (P

85 n associated with major depressive disorder (MDD), and immunological biomarkers of depression remain

86 orders, including major depressive disorder (MDD), bipolar disorder, anxiety disorders, and schizophr

87 ipal diagnosis of major depressive disorder (MDD), bipolar disorder, or schizoaffective disorder.

88 ers, particularly major depressive disorder (MDD), highlighting insights from positron emission tomog

89 d as treatment of major depressive disorder (MDD), their comparative efficacy and acceptability is un

90 d heritability of major depressive disorder (MDD), there has been limited success in identifying repl

91 ts diagnosed with major depressive disorder (MDD).

92 individuals with major depressive disorder (MDD).

93 mon treatment for major depressive disorder (MDD).

94 ch as anxiety and major depressive disorder (MDD).

95 e for dopamine in major depressive disorder (MDD).

96 l connectivity in major depressive disorder (MDD).

97 disorder (BD) and major depressive disorder (MDD).

98 individuals with major depressive disorder (MDD).

99 ly in adults with major depressive disorder (MDD); however, results have been inconsistent regarding

100 r (s.e.) = 0.03), major depressive disorder (MDD; r g = 0.69, s.e. = 0.07) and subjective well-being

101 R spectroscopy ((1)H MRS) was used to divide MDD subjects into two subgroups: glutamate-based depress

102 opsychiatric Interview was used to establish MDD.

103 ured Clinical Interview for DSM-IV evaluated MDD.

104 The FEP, MDD, and PTSD groups showed reductions in intranetwork c

105 f MDD variance and 1.1% (p = 1.30e(-05)) for MDD with age at onset <18 years.

106 MDD variance, and 1.5% (p = 4.23e(-09)) for MDD endorsing nine DSM symptoms.

107 ) of MDD variance, 2.6% (p = 2.88e(-10)) for MDD with higher symptom severity, and 2.3% (p = 2.26e(-1

108 ptom severity, and 2.3% (p = 2.26e(-13)) for MDD endorsing nine DSM symptoms.

109 In analyses adjusted for MDD status in 3 AD GWAS data sets, similar patterns of a

110 get for drug development and a biomarker for MDD pathogenesis.

111 Results support a complex etiology for MDD and highlight the value of analyzing components of h

112 Genomic profile risk scores (GPRSs) for MDD, bipolar disorder, and SCZ were based on meta-analys

113 This study highlights the value of HRHM for MDD and provides an important target within TOX2 for fur

114 way is identified as a candidate pathway for MDD and should be explored in further large population s

115 Individuals with elevated polygenic risk for MDD may also be at risk for AD.

116 or WM microstructure, and polygenic risk for MDD, SCZ or BP.

117 novel rTMS interventions as a treatment for MDD.

118 safety of 3 common alternate treatments for MDD.

119 small RNA-sequencing in paired samples from MDD patients enrolled in a large, randomized placebo-con

120 GPRS-MDD explained 1.0% (p = 4.19e(-09)) of MDD variance, and

121 [9.1] years), 30 (58%) were women and 32 had MDD.

122 10.3] years), 44 (59%) were women and 54 had MDD.

123 % CI, 0.11-0.79) compared with those who had MDD (RR, 0.53; 95% CI, 0.26-0.81).

124 Higher MDD PRS was associated with a significantly increased ri

125 analyses in a pipeline designed to identify MDD-associated pathways.

126 ts, and may be more powerful for identifying MDD-associated genomic regions.

127 ting-state functional brain abnormalities in MDD has been inconsistent.

128 es showed widespread cortical alterations in MDD patients as compared to controls and suggests that M

129 Group on cortical structural alterations in MDD.

130 regions implicated in this research, and in MDD more generally, include the nucleus accumbens (NAcc)

131 ophenotypic predictor of response to BATD in MDD.

132 otes improving approach-related behaviors in MDD.

133 e PFC/subcortex and the rest of the brain in MDD, which appeared to normalize postketamine.

134 ure-to-function correlations in the brain in MDD.

135 l lateral PFC (vlPFC) and local circuitry in MDD.

136 idence that their function is compromised in MDD.

137 capacity to actively avoid negative cues in MDD, which could lead to excessive negative focus.

138 This pattern was significantly different in MDD subjects, for whom habenula activation decreased sig

139 ed that the cAMP cascade is downregulated in MDD and upregulated by antidepressant treatment.

140 ve and motivational circuitry dysfunction in MDD.

141 has not yet shown antidepressant efficacy in MDD and bipolar disorder.

142 metabolic mechanisms particularly evident in MDD with atypical features, characterized by increased a

143 r normalizing altered inhibitory function in MDD and other disorders with reduced SST cell and GABA f

144 e 75 genes underexpressed (or DOWN genes) in MDD were associated with the adaptive immune response an

145 ariance in MDD risk, and the heritability in MDD explained by each chromosome was proportional to its

146 h thalamic regions with suicidal ideation in MDD were inversely proportional to the severity of suici

147 the functional dysconnectivity identified in MDD and the swift and robust normalization following tre

148 d their responses to IV ketamine infusion in MDD patients and HCs were measured at four time points:

149 cision-making and information integration in MDD patients with suicidal ideation.

150 ence for disrupted white matter integrity in MDD.

151 l dimorphism at the transcriptional level in MDD and highlight the importance of studying sex-specifi

152 ort either no differences or lower mGluR5 in MDD, potentially reflecting MDD heterogeneity.

153 it and state progressive neuropathologies in MDD using both unbiased approaches and tests of a priori

154 strate that reduced Slc6a15 in NAc occurs in MDD individuals and that Slc6a15 reduction in NAc D2-neu

155 rearrangement of transcriptional patterns in MDD, with limited overlap between males and females, an

156 d regulation of oxidative phosphorylation in MDD patients.

157 uggest intact and stable value processing in MDD during risky decision-making.

158 eficits across disorders and specifically in MDD.

159 of voxel-based morphometry (VBM) studies in MDD and BD.

160 varied with severity of clinical symptoms in MDD.

161 ained between 20% and 29% of the variance in MDD risk, and the heritability in MDD explained by each

162 ed reduced hippocampal grey matter volume in MDD and reduced white matter integrity in several brain

163 cohort A, we found larger left NAc volume in MDD compared to controls (Cohen's d=1.05), but no signif

164 Interestingly, MDD is highly prevalent in patients suffering from chron

165 Patients (n = 1539) with a DSM-IV MDD diagnosis and control subjects (n = 1792) were from

166 d the secondary outcome was the total DSM-IV MDD symptom score.

167 Lifetime DSM-IV MDD was diagnosed using structured diagnostic instrument

168 re collected on 32 individuals with moderate MDD and 20 control participants who performed a probabil

169 uctuation (ALFF) in first-episode drug-naive MDD patients, using the Seed-based d Mapping method (SDM

170 andard error, 0.21); P = 0.142), nonatypical MDD (B = 0.007 (standard error, 0.06); P = 0.911), and n

171 rs of incident obesity than were nonatypical MDD (OR = 1.11, 95% CI: 1.01, 1.22; P = 0.027) and no hi

172 Outpatients with nonpsychotic MDD (n=202) based on DSM-IV criteria and a 17-item Hamil

173 centers who were diagnosed with nonpsychotic MDD, unresponsive to at least 1 antidepressant course me

174 disorder explained 0.6% (p = 2.97e(-05)) of MDD variance and 1.1% (p = 1.30e(-05)) for MDD with age

175 GPRS-MDD explained 1.0% (p = 4.19e(-09)) of MDD variance, and 1.5% (p = 4.23e(-09)) for MDD endorsin

176 GPRS-SCZ explained 2.0% (p = 6.15e(-16)) of MDD variance, 2.6% (p = 2.88e(-10)) for MDD with higher

177 erapeutics to adequately treat the 30-50% of MDD patients who are unresponsive to traditional antidep

178 Results from a meta-analysis of MDD (9240 patients with MDD and 9519 controls) from the

179 thods to clarify the genetic architecture of MDD by estimating and partitioning heritability by chrom

180 gnitive, behavioral, and clinical aspects of MDD, the current study provides important new evidence t

181 cidal ideation in functional connectivity of MDD patients.

182 Diagnoses of MDD and subtypes were based on DSM-IV symptoms.

183 pocampal tail volumes and (i) a diagnosis of MDD, and (ii) clinical remission to anti-depressant medi

184 ited 50 subjects with a current diagnosis of MDD, not currently treated with psychotropic medication,

185 iction was used to investigate the effect of MDD-associated SNPs within the regions.

186 To detect consistent effects of MDD and its modulators on cortical thickness and surface

187 eline (n = 27), offspring with an episode of MDD that had remitted by follow-up (n = 4), and offsprin

188 hers) had experienced at least 2 episodes of MDD (recruited through primary care) and among whom ther

189 y suggests that the genetic heterogeneity of MDD is not attributable to genome-wide moderation of gen

190 ings may be attributable to heterogeneity of MDD, aggregating biologically different subtypes.

191 s support a neurodevelopmental hypothesis of MDD wherein dysfunctional self-regulation is potentially

192 INTERPRETATION: The increased likelihood of MDD and suicidal ideation in frequent cannabis users can

193 These data suggest that, in the CMS model of MDD, the ILPFC is the primary driver of diminished dopam

194 A large number of MDD patients do not respond to the currently available m

195 factors that influence the co-occurrence of MDD and AD have been sought in family, twin, and adoptio

196 tion of miR-124-3p in the pathophysiology of MDD and suggests that this miRNA may serve as a novel ta

197 Prevalence of MDD ranged from 901 (20.3%) people in sample 1 to 1773 (

198 e insights into the vulnerability profile of MDD.

199 by examining the impact of polygenic risk of MDD, SCZ, and BP on subcortical brain volumes and white

200 from two independent case-control studies of MDD: the GlaxoSmithKline-High-Throughput Disease-specifi

201 cal, melancholic and unspecified subtypes of MDD with changes of fasting glucose, high-density lipopr

202 our results further support the subtyping of MDD and highlight the particular need for prevention and

203 ile the incidence, symptoms and treatment of MDD all point toward major sex differences, the molecula

204 se approaches in the short-term treatment of MDD.

205 icated in two independent clinical trials of MDD, a well-characterized animal model of depression, an

206 s and CILD experts, emphasizing the value of MDD in ILD diagnosis.

207 The primary outcome was new-onset offspring MDD, and the secondary outcome was the total DSM-IV MDD

208 that lead to first-episode adolescent-onset MDD (incident cases) in those at high familial risk and

209 ferent pathways to incident adolescent-onset MDD composed of contributions from familial/genetic and

210 clinical antecedents of new adolescent-onset MDD, but disruptive behavior (beta = -0.08, P = .14) and

211 risk exists between earlier and adult-onset MDD with commonly comorbid disorders of schizophrenia, b

212 hrenia and bipolar disorder than adult-onset MDD.

213 c score analyses, we show that earlier-onset MDD is genetically more similar to schizophrenia and bip

214 MDD differs between adult- and earlier-onset MDD, with earlier-onset cases having a greater genetic o

215 ators directly influenced risk for new-onset MDD rather than indirectly through acting on dimensional

216 wenty (6 males and 14 females) had new-onset MDD, with a mean (SD) age at onset of 14.4 (2.0) years (

217 reened 763 original genetic studies of BD or MDD that investigated genes encoding targets of the path

218 nt to TMS, posttraumatic stress disorder, or MDD (subgenual anterior cingulate cortex [sgACC], left d

219 ssociation with leptin was found for overall MDD or the typical subtype.

220 the results provide evidence for persistent MDD effects across current episodes or remission, in the

221 chiatric Genomics Consortium (PGC), the PGC2-MDD (Major Depression Dataset).

222 e that shares some individuals with the PGC2-MDD.

223 MDD was created, and its accuracy to predict MDD, using area under the curve, logistic regression, an

224 After recalculating MDD PRS using MDD GWAS data sets without comorbid MDD-AD

225 ing criteria for single episode or recurrent MDD and with a history of inadequate treatment response.

226 Genetic risk for liability to recurrent MDD was partitioned using sparse whole-genome sequencing

227 llected data on 5278 patients with recurrent MDD from 58 provincial mental health centers and psychia

228 lower mGluR5 in MDD, potentially reflecting MDD heterogeneity.

229 ities, in the pathophysiology of early-stage MDD.

230 , DSM-IV major depressive disorder suicides (MDD-S, N=21) and MDD non-suicides (MDD, N=9) in the dors

231 suicides (MDD-S, N=21) and MDD non-suicides (MDD, N=9) in the dorsal lateral prefrontal cortex (Brodm

232 Further analyses demonstrated that MDD showed decreased amygdala-VPFC FC and SZ had reducti

233 These results suggest that MDD and BD are characterised by both common and distinct

234 , consistent with prior work suggesting that MDD may alter functional network development.

235 ts as compared to controls and suggests that MDD may impact brain structure in a highly dynamic way,

236 was observed for an association between the MDD PRS and AD in the meta-analysis of 3 GWAS AD samples

237 Consistently, the MDD patients with overexpression of UP genes also had un

238 er [(11)C]ABP688 binding was detected in the MDD as compared with the control group.

239 e, hippocampal tail volume was larger in the MDD cohort compared to control subjects.

240 ved following ketamine administration in the MDD group (P<0.001), which was associated with the chang

241 icantly different, with higher levels in the MDD group at baseline.

242 ACC and the cerebellum were observed in the MDD group.

243 o-function correlation in the PFC/ACC in the MDD group.

244 bjects from nine cohorts contributing to the MDD Working Group of the Psychiatric Genomics Consortium

245 he central executive network relative to the MDD, PTSD, and HC groups (p<0.05 corrected); therefore,

246 In addition, within the MDD group, gray matter Pi, a regulator of oxidative phos

247 In contrast to MDD, there has been much less investigation of mGluR5 in

248 and astrocytic cell functions contribute to MDD and suicide, and identify putative pathways and mech

249 netic susceptibility contributes modestly to MDD and AD comorbidity.

250 treatment on any outcome measures related to MDD.

251 s suggest that the genetic susceptibility to MDD differs between adult- and earlier-onset MDD, with e

252 o not support the use of sertraline to treat MDD in patients with non-dialysis-dependent CKD.

253 ors of sex-specific gene networks underlying MDD and confirm their sex-specific impact as mediators o

254 ge phosphodiesterase-4 (PDE4) in unmedicated MDD patients and after 8 weeks of treatment with a sele

255 c studies, PDE4 was decreased in unmedicated MDD patients and increased after SSRI treatment.

256 We found in unmedicated MDD patients widespread, 20% reductions in (11)C-(R)-ro

257 ssociations between aspects of cannabis use, MDD, and suicidal thoughts and behaviours and examine wh

258 After recalculating MDD PRS using MDD GWAS data sets without comorbid MDD-AD cases, signif

259 ons across gray matter and white matter when MDD subjects were compared with controls.

260 We examined whether MDD is characterized by reduced myelin at the whole-brai

261 tively intact elderly patients (N = 28) with MDD and age- and gender-matched healthy controls (N = 18

262 networks) in 42 unmedicated adolescents with MDD and 53 well-matched healthy controls.

263 mpared to matched controls, adolescents with MDD had lower total surface area (but no differences in

264 Adults with MDD had thinner cortical gray matter than controls in th

265 ale transcriptional profiles associated with MDD across six brain regions.

266 le in the bone abnormalities associated with MDD and, if so, whether ketamine treatment corrected the

267 he pathway most consistently associated with MDD was created, and its accuracy to predict MDD, using

268 pathways were significantly associated with MDD, and two of these explained a significant amount of

269 ups when searching for genes associated with MDD.

270 e serious bone abnormalities associated with MDD.

271 showed the most consistent association with MDD across the two samples.

272 ding of neuroticism and its association with MDD.

273 matic stress disorder is often comorbid with MDD, and symptoms of both disorders can be alleviated wi

274 ed genes influence risk for BD compared with MDD.

275 ods to differentiate patients diagnosed with MDD from HCs.

276 en GPRSs with characteristics and GPRSs with MDD subgroups stratified according to the most relevant

277 ordinating Center (NDCC; Jaipur, India) with MDD, and experienced ILD experts at the Center for ILD (

278 Additionally, individuals with MDD had significantly lower whole-brain intrinsic functi

279 Offspring with MDD before the study or at baseline (n = 27), offspring

280 Data included 11837 participants with MDD and 14791 control individuals, for a total of 26 628

281 onance imaging after which participants with MDD received up to 15 sessions of BATD.

282 ures of value sensitivity, participants with MDD were comparable to non-psychiatric controls.

283 Among participants with MDD, 5347 (45.2%) were classified in the decreased A/W a

284 tivity to reward values in participants with MDD: 'risk preference,' indicating how objective values

285 = 1.7) and 26 medication-free patients with MDD (HDRS-24 = 24.8) underwent PET scanning using (11)C-

286 (k = 33) samples including 912 patients with MDD and 894 HCs were included in the meta-analysis.

287 m a meta-analysis of MDD (9240 patients with MDD and 9519 controls) from the Psychiatric Genomics Con

288 Medication-free patients with MDD and healthy control subjects (HC) completed baseline

289 that accurately differentiate patients with MDD from healthy control subjects (HCs).

290 Patients with MDD had significant decreases in baseline OPG/RANKL rati

291 Patients with MDD in a current major depressive episode (N=104) with a

292 determine whether subgroups of patients with MDD stratified according to the A/W criterion had a diff

293 Across all studies, patients with MDD were separated from HCs with 77% sensitivity and 78%

294 Patients with MDD were stratified into subgroups according to change i

295 , (11)C-McN5652, we found that patients with MDD who did not achieve remission after 12 mo of natural

296 ared with healthy subjects and patients with MDD.

297 pathophysiologic mechanisms in patients with MDD.

298 the Center for ILD (CILD; Seattle, WA) with MDD.

299 e meta-analysis of 3 GWAS AD samples without MDD cases (best P = .007).

300 ocus associated with adult-onset (>27 years) MDD (rs7647854, odds ratio: 1.16, 95% confidence interva