ライフサイエンスコーパス: MDD

1 MDD and HV groups also differed with respect to the corr

2 MDD GRS was associated with 22 distinct diseases in the

3 MDD patients were characterized by higher levels of asym

4 MDD patients who responded to antidepressant treatment h

5 MDD was associated with disorders of lipid metabolism (O

6 CBF) was calculated and compared between 106 MDD and 36 HC EMBARC participants (whole-brain Discovery

7 41 healthy controls (HC) (sample 1) and 124 MDD participants and 148 HCs (sample 2).

8 dorsolateral prefrontal cortex (dlPFC) of 15 MDD and 15 matched non-psychiatric control subjects.

9 163 MDD and 62 healthy individuals underwent functional MRI

10 Depressed individuals with BD (n = 18), MDD (n = 23), and HC (n = 23) were scanned while perform

11 participants (whole-brain Discovery); and 58 MDD EMBARC participants and 58 HC from the DLBS study (r

12 ated blood DNA methylation profiles from 581 MDD patients at baseline with MDD status 6 years later.

13 yptophan and kynurenine are decreased across MDD, BD, and SZ; kynurenic acid and the kynurenic acid t

14 ifferences in a smaller sample of adolescent MDD patients and controls did not survive correction for

15 d, lower fractional anisotropy (FA) in adult MDD patients compared with controls in 16 out of 25 WM t

16 ined potential advanced brain aging in adult MDD patients, and whether this process is associated wit

17 ad differences in WM microstructure in adult MDD, which may suggest structural disconnectivity in MDD

18 system may interact with the brain to affect MDD susceptibility.

19 ne and is associated with protection against MDD, mainly in women.

20 a-3 PUFA (380 mg/day) was associated with an MDD decrease of 5 cases/1000 people and a PTB decrease o

21 (naMCI), MDD+naMCI, amnestic MCI (aMCI), and MDD+aMCI.

22 at5 (pY694) responses in B cells from BD and MDD patients.

23 s in relatives of patients with SCZ, BD, and MDD in PubMed and Embase identified 33 studies with 2292

24 s in relatives of patients with SCZ, BD, and MDD to identify overlapping and discrete brain structura

25 orted trauma exposure, body composition, and MDD.

26 y in four datasets of patients with PTSD and MDD, and show that the subtypes are transferable across

27 between extracellular matrix regulation and MDD.SIGNIFICANCE STATEMENT Reduced excitatory neurotrans

28 Disease stage, tumor response, and MDD at diagnosis did not demonstrate thresholds that res

29 show that PRSs were associated with SCZ and MDD diagnostics, and with cognition in SCZ and pathology

30 dal cell arborization occurs with stress and MDD, and may diminish excitatory neurotransmission.

31 On average, MDD patients showed a higher brain-PAD of +1.08 (SE 0.22

32 th depression under stress than at baseline (MDD-PRS x stress interaction beta = 0.036, P = 0.005).

33 muli contributes to discrimination among BD, MDD, and healthy controls (HC).

34 ubstantially less of the association between MDD-PRS and depression when under stress than at baselin

35 ver and replicate differences in CBF between MDD participants and healthy controls (HC) as part of th

36 The biological connection between MDD and AD is still unclear.

37 bserved that the genetic correlation between MDD and waist circumference was only significant in indi

38 ositive genetic correlation observed between MDD and reported trauma exposure.

39 a also suggest a role for astrocytes in both MDD and antidepressant action.

40 f(-/-) mice displayed several characteristic MDD traits such as augmented microglial numbers, increas

41 h other conditions than for strictly defined MDD.

42 or developing dementia- remitted depression (MDD), non-amnestic MCI (naMCI), MDD+naMCI, amnestic MCI

43 sk scores of MDD significantly discriminated MDD cases from controls in an independent dataset and ma

44 adolescents with major depressive disorder (MDD) (age mean [SD] = 14.9 +/- 1.5, 56 girls) and 47 hea

45 ts diagnosed with Major Depressive Disorder (MDD) (n = 64) to healthy controls (n = 64) using a compr

46 rrent and chronic major depressive disorder (MDD) accounts for a substantial part of the disease burd

47 Major depressive disorder (MDD) and Alzheimer's disease (AD) reciprocally elevate t

48 ve been linked to major depressive disorder (MDD) and preterm birth (PTB), and prenatal depression as

49 isorder (BD), and major depressive disorder (MDD) are heritable psychiatric disorders with partially

50 ications to treat major depressive disorder (MDD) are not equally effective across patients.

51 in subjects with major depressive disorder (MDD) as compared with age- and sex-matched healthy contr

52 s of olfaction of major depressive disorder (MDD) before and after medical treatment, and to prelimin

53 is effective for major depressive disorder (MDD) but its effects on memory limit its widespread use.

54 been examined in major depressive disorder (MDD) despite the presence of inflammation and impaired v

55 analyses between major depressive disorder (MDD) genetic risk score (GRS) and 925 disease outcomes.

56 Major depressive disorder (MDD) has an enormous impact on global disease burden, af

57 of patients with major depressive disorder (MDD) has been demonstrated using functional near-infrare

58 Major depressive disorder (MDD) is a leading cause of disability worldwide, yet cur

59 vere anhedonia in major depressive disorder (MDD) is a negative predictor of antidepressant response.

60 Major depressive disorder (MDD) is a serious mental illness, characterized by high

61 Major depressive disorder (MDD) is a serious, heterogeneous disorder accompanied by

62 Major depressive disorder (MDD) is associated with alterations of GABAergic interne

63 Although major depressive disorder (MDD) is associated with altered functional coupling betw

64 Major depressive disorder (MDD) is associated with altered global brain connectivit

65 Major depressive disorder (MDD) is associated with an increased risk of brain atrop

66 in patients with major depressive disorder (MDD) is challenging, in part because of poor reproducibi

67 s have shown that major depressive disorder (MDD) is characterized by abnormal neural activity and co

68 isorder (BD) from major depressive disorder (MDD) is clinically challenging, especially during depres

69 ological basis of major depressive disorder (MDD) is derived from studies of chronic stress models in

70 Although major depressive disorder (MDD) is highly prevalent, its pathophysiology is poorly

71 sorder (PTSD) and major depressive disorder (MDD) on the basis of robust and distinct functional conn

72 of never-treated major depressive disorder (MDD) patients who exhibit inflammation remains to be cla

73 s (65 melancholic major depressive disorder (MDD) patients, 65 healthy controls) were included to bui

74 ndard of care for major depressive disorder (MDD) pharmacotherapy, but only approximately half of the

75 ) from the ENIGMA Major Depressive Disorder (MDD) working group.

76 27 subjects with major depressive disorder (MDD), 29 subjects with bipolar disorder (BD), and 33 hea

77 n-responders with major depressive disorder (MDD), a systematic search of Pubmed/Medline was conducte

78 ar disorder (BD), major depressive disorder (MDD), and schizophrenia (SCZ; n = 25 each), alongside ma

79 correlations with Major Depressive Disorder (MDD), Bipolar Disorder (BD), Schizophrenia, anxiety, and

80 ted and recurrent major depressive disorder (MDD), bipolar disorder and schizophrenia would enhance s

81 een identified in major depressive disorder (MDD), but findings have been variable and inconsistent.

82 seases, including major depressive disorder (MDD), has been postulated.

83 ses, particularly major depressive disorder (MDD), remains largely unknown.

84 e) nasal spray in major depressive disorder (MDD), we performed a genome-wide association study (GWAS

85 a from a study of major depressive disorder (MDD), we show that NPDR with covariate adjustment remove

86 bitory balance in major depressive disorder (MDD), which afflicts ~14%-20% of individuals.

87 in patients with major depressive disorder (MDD).

88 isorder (BD), and major depressive disorder (MDD).

89 cal challenge for major depressive disorder (MDD).

90 sed treatment for major depressive disorder (MDD).

91 of life (QoL) in major depressive disorder (MDD).

92 e pathogenesis of major depressive disorder (MDD).

93 in patients with major depressive disorder (MDD).

94 e pathogenesis of major depressive disorder (MDD).

95 individuals with major depressive disorder (MDD).

96 I) in adults with major depressive disorder (MDD).

97 tive treatment of major depressive disorder (MDD).

98 athophysiology of major depressive disorder (MDD).

99 for treatment of major depressive disorder (MDD).

100 of patients with major depressive disorder (MDD).

101 in patients with major depressive disorder (MDD).

102 n associated with major depressive disorder (MDD).

103 patitis-C develop major depressive disorder (MDD).

104 strictly defined major depressive disorder (MDD): the former has a lower genotype-derived heritabili

105 ine, for treating major depressive disorder (MDD); however, its neural mechanism of action remains po

106 10,395 controls), major depressive disorder (MDD, 1,475 cases and 2,144 controls), and height (5,974

107 g 6 risk factors (major depressive disorder [MDD], attention deficit/hyperactivity disorder [ADHD], b

108 ratio are decreased in mood disorders (i.e., MDD and BD), whereas kynurenic acid is not altered in SZ

109 a-3 PUFA and its precursors may be elevating MDD and PTB rates in 85% of the countries studied.

110 ale and 1236 female controls from the ENIGMA MDD working group.

111 ion findings may stem in part from examining MDD patients with varied interventions.

112 formational changes in Enterococcus faecalis MDD that describe sequential steps in an induced fit enz

113 (95% CI 1.16 to 1.23, q = 1.33 x 10-35) for MDD.

114 er fluency task is a promising biomarker for MDD.

115 ing LC omega-3 PUFA, up to ~ 1000 mg/day for MDD and up to ~ 550 mg/day for PTB.

116 The genetic liabilities for MDD and schizophrenia were associated with self-harm ind

117 respond to an antidepressant medication for MDD.

118 tage, with the strongest signal observed for MDD diagnosis and related co-morbidities including anxie

119 themselves associated with SSRI response for MDD patients enrolled in the Mayo Clinic PGRN-AMPS SSRI

120 for BD, and in right striatum with risk for MDD.

121 sample sizes rather than by specificity for MDD.

122 may be an attractive therapeutic target for MDD.

123 resent promising new therapeutic targets for MDD.

124 ranscranial magnetic stimulation therapy for MDD.

125 of these processes in discriminating BD from MDD remains unexplored.

126 ant biological marker distinguishing BD from MDD.

127 ing neuropsychiatric spectrum extending from MDD on one end, through BD and SCZ, to ASC on the other

128 l cell disinhibition and with remission from MDD.

129 unmedicated patients with first-episode GAD, MDD, respectively, and n = 35 healthy controls).

130 w Omega-3 intake would associate with higher MDD and PTB rates on the country-level.

131 rontal cortex and nucleus accumbens in human MDD and the 3 mouse chronic stress models, with each of

132 ional organization of gene networks in human MDD.

133 ts of the broad molecular pathology of human MDD, with no one mouse model apparently better than anot

134 roduce gene networks characteristic of human MDD.

135 In MDD cases, we found a significant upregulation of CX3CR1

136 ated 4 up and 13 downregulated; p < 0.05) in MDD subjects.

137 rmalities in resting-state brain activity in MDD.

138 uman adult hippocampal neurogenesis (AHN) in MDD and AD.

139 r regional cortical thickness alterations in MDD, mainly involving increased cortical thickness in th

140 hat neural response to rewards is altered in MDD and given that reward-related circuitry is modulated

141 medication, to investigate biosignatures in MDD.

142 and an in-depth profiling of those cells in MDD is lacking.

143 rthermore, increased peripheral blood CRP in MDD has been associated with altered reward circuitry an

144 proportion of microstate D was decreased in MDD and rMDD compared to the HC group (Cohen's d = 0.63

145 nic acid to kynurenine ratio is decreased in MDD and SZ, and the kynurenine to tryptophan ratio is in

146 to 3-hydroxykynurenine ratio is decreased in MDD but not SZ.

147 CBF differences have been detected in MDD, and may reveal biosignatures of disease-state.

148 ch may suggest structural disconnectivity in MDD.

149 enic acid were consistently downregulated in MDD patients, regardless of antidepressant exposure.

150 t microglia enhance homeostatic functions in MDD but are not immune activated.

151 ple brain regions thought to be important in MDD, and (2) highlight the potential role of using perfu

152 nurenine to tryptophan ratio is increased in MDD and SZ.

153 increased hippocampal network inhibition in MDD is linked to hippocampal serotonergic dysfunction wh

154 and of GBCr as a potential imaging marker in MDD.

155 n AHN as a potential converging mechanism in MDD and AD.

156 in the human genome, we assay methylation in MDD cases and controls from both blood (N = 1132) and po

157 e the phenotype and function of microglia in MDD.

158 ed with antidepressant treatment outcomes in MDD.

159 8%]) showed increased expression patterns in MDD subjects.

160 Both samples also revealed increased rCBF in MDD relative to HC in both the left and right inferior p

161 s at the synapse and their possible roles in MDD pathogenesis.

162 nnate immune toll-like receptor signaling in MDD.

163 RNAs and their functioning at the synapse in MDD by examining miRNA processing machinery at synapse a

164 ological mechanisms and treatment targets in MDD and GAD.

165 istics on variation in cortical thickness in MDD.

166 The MRS explained 1.75% of the variance in MDD (beta = 0.338, p = 1.17 x 10(-7)) and remained assoc

167 SSRI treatment outcomes in four independent MDD trials.

168 country-level estimates for omega-3 intake, MDD prevalence, PTB rate, and per capita income for 184

169 g empirical information about the likelihood MDD is chronic or will recur in the future.

170 Finally, we found that low MDD-PRS may have particular use in identifying individua

171 ntrols) were included to build a melancholic MDD classifier, and 10 FCs were selected by our sparse m

172 drug-free independent cohort of melancholic MDD, and did not generalize to other MDD subtypes or oth

173 Forty-eight medicine-naive MDD patients plus 33 healthy controls (HC) matched on ge

174 depression (MDD), non-amnestic MCI (naMCI), MDD+naMCI, amnestic MCI (aMCI), and MDD+aMCI.

175 ealthy controls, medicated, and nonmedicated MDD patients.

176 and gephyrin mRNA in the NAc of nonmedicated MDD patients is paralleled by decreased inhibitory synap

177 We both replicated and identified novel MDD-methylation associations in human brain and blood sa

178 1 collection of blood samples (N = 1132) of MDD cases and controls, we used epigenomic deconvolution

179 ay bias views of the genetic architecture of MDD and impede the ability to identify pathways specific

180 ress paradigms capturing distinct aspects of MDD abnormalities.

181 been implicated in QoL, the neural basis of MDD, and the mechanisms of ADM response.

182 role of using perfusion as a biosignature of MDD.

183 ssive symptoms in those without diagnosis of MDD.

184 diverse approaches to analyse the effect of MDD and AD on human AHN and analyse different studies im

185 he behavioral and neuroendocrine features of MDD, the extent to which they reproduce the molecular pa

186 The olfactory function of MDD appears to be correlated negatively with the age and

187 a responding phenotype of brain function of MDD rather than the emotional responding.

188 ways, overlapped with genes found in GWAS of MDD disease status, autoimmune disease and inflammation,

189 The SNP-based heritability of MDD with reported trauma exposure (24%) was greater than

190 pattern recognition analyses independent of MDD diagnosis.

191 Early detection and management of MDD is important, and treatment strategies should be sel

192 replicated regions and clinical measures of MDD chronicity.

193 es play a key role in the pathophysiology of MDD and alterations in peripheral cytokine levels are as

194 stently implicated in the pathophysiology of MDD, potentially driven in part by excessive hippocampal

195 ctors that are relevant to the prediction of MDD.

196 After the remission of MDD, the olfactory dysfunction was improved, which might

197 In addition to confirming the role of MDD, we demonstrate that ADHD and schizophrenia likely p

198 DNAm-based risk scores of MDD significantly discriminated MDD cases from controls

199 Longitudinal studies of MDD and somatic health outcomes are needed to further as

200 Past molecular studies of MDD employed bulk homogenates of postmortem brain tissue

201 chronic social stress model for the study of MDD and performed metabolomic, lipidomic, and proteomic

202 ed findings from a past methylation study of MDD.

203 acid metabolism, in the peripheral system of MDD patients.

204 markers for the pharmacological treatment of MDD.

205 A) receptor as a target for the treatment of MDD.

206 We contrasted genetic influences on MDD stratified by reported trauma exposure (final sample

207 ncholic MDD, and did not generalize to other MDD subtypes or other psychiatric disorders.

208 ed a methylation risk score (MRS) to predict MDD status 6 years later.

209 scores created using a set of five putative MDD biomarkers, genome-wide SNP data, and 27 clinical, d

210 depression with self-reported MDD, recurrent MDD, bipolar disorder and schizophrenia were 0.79 +/- 0.

211 depression with self-reported MDD, recurrent MDD, bipolar disorder and schizophrenia.

212 ared to be driven by patients with recurrent MDD and an adult age of onset of depression.

213 s with MDD, and 30 individuals with remitted MDD (rMDD) were included.

214 Older individuals with remitted MDD and naMCI did not have the same white or gray matter

215 road depression phenotype with self-reported MDD and ZNF804A, MIR3143, PSORS1C2, STK19, SPATA31D1, RT

216 - SE) of broad depression with self-reported MDD, recurrent MDD, bipolar disorder and schizophrenia w

217 tions of broad depression with self-reported MDD, recurrent MDD, bipolar disorder and schizophrenia.

218 ategorical and dimensional analyses revealed MDD-specific decreased whole-brain connectivity profiles

219 or depressive disorder polygenic risk score (MDD-PRS) derived from the most recent Psychiatric Genomi

220 A subset (MDD n = 368, TD n = 200) also completed neuroimaging.

221 orted trauma exposure (24%) was greater than MDD without reported trauma exposure (12%).

222 s (beta = 0.095, P = 4.7 x 10(-16)) and that MDD-PRS was more strongly associated with depression und

223 to 5,227 training physicians, we found that MDD-PRS predicted depression under training stress (beta

224 Penalized splines indicated that MDD and PTB rates decreased linearly with increasing LC

225 Together, these findings suggest that MDD-PRS holds promise in furthering our ability to predi

226 der stress than at baseline, suggesting that MDD-PRS adds unique predictive power in depression predi

227 Among the MDD group, proportion and duration of microstate D were

228 nsition probabilities were nonrandom and the MDD group, relative to the HC and the rMDD groups, exhib

229 the lowest in the BD group, followed by the MDD and healthy control groups.

230 ccurrence of microstate D was reduced in the MDD group compared to the HC group (Cohen's d = 0.43 and

231 55-3p, and miR-337-3p were also noted in the MDD group.

232 ly increased in the BD group compared to the MDD group.

233 lts suggest that the genetic contribution to MDD is greater when reported trauma is present, and that

234 microglial phenotype and its contribution to MDD.

235 biological functions of likely importance to MDD etiology.

236 The findings are limited to MDD patients ranging between moderate to severe depressi

237 ATP, have been shown to bind sequentially to MDD.

238 ppocampal inhibition network was specific to MDD but not HV.

239 lly identifies loci that are not specific to MDD, and, although it generates highly predictive polyge

240 the ability to identify pathways specific to MDD.

241 zed medicine strategies to effectively treat MDD.

242 vated MMP-9 levels in antidepressant-treated MDD patients compared with controls.

243 However, the molecular mechanisms underlying MDD remain unclear.

244 the dynamics of brain mechanisms underlying MDD.

245 During negative picture viewing, MDD subjects demonstrated significant hippocampal inhibi

246 n, and a random forest classifier for BD vs. MDD classification.

247 BD vs. MDD were classified with 70.7% accuracy (p < 0.01) based

248 table source of neuropathology in vulnerable MDD patients.

249 ents (193 with SZ, 171 with BD, and 217 with MDD) and 363 healthy controls (HC).

250 A total of 222 unmedicated adults with MDD randomized to receive sertraline (n = 110) or placeb

251 d SI were consistently linked in adults with MDD.

252 ts that regulate transcripts associated with MDD and demonstrate NPDR's utility for GWAS and continuo

253 d replicated methylated loci associated with MDD that are involved in biological functions of likely

254 in the peripheral blood were associated with MDD, particularly decreased L-tryptophan and kynurenic a

255 ofiles in peripheral tissues associated with MDD.

256 tly, our findings involved associations with MDD in human samples that implicated many closely relate

257 files from 581 MDD patients at baseline with MDD status 6 years later.

258 omisation (MR) analyses were conducted, with MDD, ADHD, and schizophrenia emerging as the most plausi

259 cortex and nucleus accumbens-of humans with MDD and of 3 chronic stress models in mice: chronic vari

260 l prefrontal cortex of male individuals with MDD (n = 17) and of healthy controls (n = 17).

261 GBC was analyzed in 28 individuals with MDD and 22 healthy controls (HCs) at baseline, post-plac

262 t samples consisting of 179 individuals with MDD and 41 healthy controls (HC) (sample 1) and 124 MDD

263 Eighteen medication-free individuals with MDD currently in a major depressive episode were enrolle

264 9 healthy controls (HC), 63 individuals with MDD, and 30 individuals with remitted MDD (rMDD) were in

265 l lines were generated from individuals with MDD.

266 currently unmedicated adult outpatients with MDD.

267 HV) and 27 medication-free participants with MDD underwent positron emission tomography (PET) using [

268 om post-mortem brain tissue of patients with MDD (n = 13-19) and control donors (n = 12-25).

269 In Study 2, a second cohort of patients with MDD (N = 14) completed the same scanning protocol at bas

270 e imaging (MRI) scans from 196 patients with MDD and 110 healthy participants were obtained as part o

271 SAM as adjunctive treatment in patients with MDD and an inadequate response to antidepressant therapy

272 oth in the peripheral blood of patients with MDD and in the two depressive-like mouse models: the chr

273 tion in depressive symptoms in patients with MDD and produced minimal cognitive impairment.

274 , MIP-1alpha, and Eotaxin-1 in patients with MDD based on validated depression scales both before and

275 d sgACC activity was higher in patients with MDD compared to controls and to determine whether this a

276 the current trial, consecutive patients with MDD consented to receive MST applied over the prefrontal

277 sent work aimed to distinguish patients with MDD from HCs, using haemodynamic response measured durin

278 In addition, patients with MDD had higher resting-state functional connectivity bet

279 Patients with MDD had smaller changes in oxy-haemoglobin in the fronta

280 hology of attempted suicide in patients with MDD involves multiple brain networks and their interacti

281 rty patients were screened; 86 patients with MDD received a minimum of eight treatments and were deem

282 Patients with MDD showed higher sgACC activation to positive and negat

283 e hundred and five HCs and 105 patients with MDD took part in this study.

284 75.2% and 76.5% of patients with MDD were correctly classified using frontal and temporal

285 esting-state brain networks in patients with MDD who had or did not have a history of suicide attempt

286 dge, we analyzed data from 128 patients with MDD who participated in the iSPOT-D trial and were asses

287 Medication-free patients with MDD, relative to HCs, showed a complex pattern of increa

288 l thickness in medication-free patients with MDD, using a newly developed meta-analytic mask compatib

289 pies targeting TNF and IL-6 in patients with MDD.

290 uitry and clinical symptoms in patients with MDD.

291 to antidepressant treatment in patients with MDD.

292 pressant treatment outcomes in patients with MDD.

293 etabolite concentrations between people with MDD, BD, or SZ, and controls, presented as Hedges' g wit

294 , and their associate ratios) in people with MDD, SZ, or BD, compared to controls.

295 function of the CD300f immune receptor with MDD in humans, depressive-like and anhedonic behaviors i

296 AM(+) exosomes were greater in subjects with MDD and were associated with suicidality and anhedonia.

297 IRS-1) in L1CAM(+) exosomes in subjects with MDD as compared with age- and sex-matched HC.

298 ssment of IR in HC, but not in subjects with MDD.

299 IRS-1 in L1CAM(+) exosomes in subjects with MDD.

300 as the left and right insula, for those with MDD relative to HC.

301 nced stimuli) is a consistent finding within MDD; can predict treatment efficacy and reverses followi