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1 scale (range, 0-60; >=16 indicates possible depressive disorder).
2 2 (PHQ-2; range, 0-6; >=3 indicates possible depressive disorder).
3 r for ACS in combination with a diagnosis of depressive disorder.
4 S to real RNA-Seq data from a study of major depressive disorder.
5 No significant difference was found in major depressive disorder.
6 aluated oral NSI-189 as monotherapy in major depressive disorder.
7 in a clinical setting in patients with major depressive disorder.
8 ngly with recurrent and single-episode major depressive disorder.
9 d with other mental disorders, such as major depressive disorder.
10 to affect-related illnesses, including major depressive disorder.
11 are also implicated in the etiology of major depressive disorder.
12 marker of inflammation associated with major depressive disorder.
13 administration in treatment-resistant major depressive disorder.
14 ve in bipolar disorder but negative in major depressive disorder.
15 in particular for treatment-resistant major depressive disorder.
16 els lower than the threshold indicative of a depressive disorder.
17 has a closer genetic association with major depressive disorder.
18 biomarker of stress vulnerability and major depressive disorder.
19 d with psychiatric disorders including major depressive disorder.
20 tidepressant approved for treatment of major depressive disorder.
21 trial of sertraline versus placebo for major depressive disorder.
22 is in development for the treatment of major depressive disorder.
23 ding posttraumatic stress disorder and major depressive disorder.
24 e in neuroticism, psychological distress, or depressive disorder.
25 to BDNF expression is associated with major depressive disorder.
26 lammation pathways in the treatment of major depressive disorder.
27 of stress-related disorders, including major depressive disorder.
28 rget the underlying pathophysiology of major depressive disorder.
29 eatment-seeking adult outpatients with major depressive disorder.
30 s in women not formally diagnosed with major depressive disorder.
31 s an effective add-on intervention for major depressive disorder.
32 these interventions for prevention of major depressive disorder.
33 ior studies indicate is hyperactive in major depressive disorder.
34 anging from 9,529 with autism to 88,182 with depressive disorder.
35 re a particularly disabling feature of major depressive disorder.
36 order is more strongly correlated with major depressive disorder.
37 icipants consisted of adults with persistent depressive disorder.
38 trimental effect of BMI on the risk of major depressive disorder.
39 sants are similar in BD as in unipolar major depressive disorder.
40 l cortex (mPFC) has been implicated in major depressive disorder.
41 cores for behavioral disinhibition and major depressive disorder.
42 t stress, modeling multiple aspects of major depressive disorder.
43 able response for a drug treatment for major depressive disorder.
44 ively representing 2,928 patients with major depressive disorder.
45 otherapy practice, CBT, in adults with major depressive disorder.
46 n between the Netrin-1/DCC pathway and major depressive disorder.
47 nisms of maladaptive learning in anxiety and depressive disorders.
48 edisposes individuals to develop anxiety and depressive disorders.
49 ed genetic variants of SIRT1 linked to major depressive disorders.
50 sian BD multiplex families (166 BD, 78 major depressive disorder, 151 unaffected) as well as 438 subj
51 visit were anxiety disorders (20.0%), major depressive disorder (16.9%), and substance use disorders
52 0.05 for other income quintiles), those with depressive disorders (28.78 [20.04-41.33]; p<0.0001) and
53 ttempters and 8,786 nonattempters with major depressive disorder; 3,264 attempters and 5,500 nonattem
54 ntrol, and conduct disorders; 11% (9-13) for depressive disorders; 9% (7-10) for obsessive-compulsive
55 r schizophrenia, alcohol use disorder, major depressive disorder, a combined bipolar disorder-schizop
56 tic resonance imaging in patients with major depressive disorder, a disease associated with an altere
58 s is a primary objective when treating major depressive disorder-a disease that afflicts ~20% of the
62 ter puberty, females are more prone to major depressive disorder and anxiety disorders compared to ma
63 der, along with the increased rates of major depressive disorder and anxiety disorders in one or more
64 the shared molecular genetic basis of major depressive disorder and bipolar disorder and to highligh
65 c associations, and genetic studies of major depressive disorder and bipolar disorder can be combined
69 were compared with those of women with major depressive disorder and chronic widespread pain (MD-P) a
70 R to real RNA-Seq data from a study of major depressive disorder and discuss STIR's straightforward e
71 s of brain anatomy between people with major depressive disorder and healthy control subjects, but fe
72 % confidence interval = 1.04-1.23), and both depressive disorder and high severity predicted higher I
74 in disorders (including, among others, major depressive disorder and obsessive-compulsive disorder, a
75 ed neuropsychiatric disorders, such as major depressive disorder and posttraumatic stress disorder, e
76 ere collected for 28 patients (20 with major depressive disorder and seven with bipolar II disorder;
77 ct, the bidirectional relation between major depressive disorder and sleep has been well-documented.
78 e durability and safety of SAGE-217 in major depressive disorder and to compare SAGE-217 with availab
79 vidence to suggest that cannabinoids improve depressive disorders and symptoms, anxiety disorders, at
80 tional disorders, including addiction, major depressive disorder, and autism (Cousins et al., 2002; K
81 motional face processing, diagnosis of major depressive disorder, and greater self-reported depressio
82 citatory neurotransmission occurs with major depressive disorder, and may be normalized by antidepres
83 with schizophrenia, bipolar disorder, major depressive disorder, and obsessive-compulsive disorder.
86 ion, FMRP targets were associated with major depressive disorder, and we present novel evidence of as
87 ing enhancing memory and learning, reversing depressive disorders, and modulating cognitive functions
88 In sibling analyses, we found that men with depressive disorder, anxiety disorder, alcohol use disor
89 n-6 (IL-6) and C-reactive protein with major depressive disorder are well established, evidence for l
90 perationalize depression severity, and major depressive disorder as defined in the Diagnostic and Sta
91 morphometry studies in schizophrenia, major depressive disorder, bipolar disorder, addiction, and an
92 mpt, using cohorts of individuals with major depressive disorder, bipolar disorder, and schizophrenia
93 rge genetic studies of six phenotypes: major depressive disorder, bipolar disorder, attention-deficit
95 rimary psychiatric disorders including major depressive disorder, bipolar disorder, schizophrenia, ob
96 hest deletion burdens were observed in major depressive disorder brain, at levels greater than Kearns
97 t-line antidepressants for adults with major depressive disorder, but success is limited and patients
98 icrobiota dysbiosis has been linked to major depressive disorder, but the mechanisms whereby the micr
99 nd bipolar disorder, and an additional major depressive disorder cohort from UK Biobank (total: 185,2
102 ders (schizophrenia, bipolar disorder, major depressive disorder, cross disorder, attention-deficit/h
103 c correlation was found between PD and major depressive disorder, depressive symptoms, and neuroticis
104 tic risk for behavioral disinhibition, major depressive disorder, depressive symptoms, autism spectru
106 al design, 36 patients with first onset of a depressive disorder (Diagnostic and Statistical Manual o
107 Almost two-thirds of patients with major depressive disorder do not achieve remission with initia
109 tal depression, which is the occurrence of a depressive disorder during pregnancy or following childb
113 types analysed in UK Biobank only were major depressive disorder, generalised anxiety disorder, bipol
114 atients who had a primary diagnosis of major depressive disorder, had a score >=18 on the 17-item Ham
115 icacy of dopamine agonists in treating major depressive disorder has been hypothesized to stem from e
117 a higher likelihood of remission from major depressive disorder in children undergoing PCIT-ED (B =
118 rt study of 53,034 patients diagnosed with a depressive disorder in fiscal year 2017 in the U.S. Vete
120 a higher likelihood of remission from major depressive disorder in the PCIT-ED group (B = 0.14; SE =
123 dication-free 18- to 65-year-olds with major depressive disorder, insomnia, and suicidal ideation.
138 We compare participants diagnosed with Major Depressive Disorder (MDD) (n = 64) to healthy controls (
140 alance in 35 unmedicated subjects with major depressive disorder (MDD) and 25 healthy controls enroll
144 contribute to symptoms associated with major depressive disorder (MDD) and post-traumatic stress diso
145 (LC omega-3 PUFA) have been linked to major depressive disorder (MDD) and preterm birth (PTB), and p
146 The UK Biobank concurrently assessed Major Depressive Disorder (MDD) and self-reported lifetime exp
147 Early life adversity (ELA) increases major depressive disorder (MDD) and suicide risk and potential
148 enia (SCZ), bipolar disorder (BD), and major depressive disorder (MDD) are heritable psychiatric diso
150 pressed in the brain, in subjects with major depressive disorder (MDD) as compared with age- and sex-
151 nvestigate the changes of olfaction of major depressive disorder (MDD) before and after medical treat
152 vulsive therapy (ECT) is effective for major depressive disorder (MDD) but its effects on memory limi
153 V) and HCMV has never been examined in major depressive disorder (MDD) despite the presence of inflam
154 nome-wide association analyses between major depressive disorder (MDD) genetic risk score (GRS) and 9
157 ontotemporal cortices of patients with major depressive disorder (MDD) has been demonstrated using fu
158 Subcortical volumetric changes in major depressive disorder (MDD) have been purported to underli
160 nal interventions on the prevention of major depressive disorder (MDD) in overweight adults are unkno
171 ct treatment response in patients with major depressive disorder (MDD) is challenging, in part becaus
172 Neuroimaging studies have shown that major depressive disorder (MDD) is characterized by abnormal n
173 tinguishing bipolar disorder (BD) from major depressive disorder (MDD) is clinically challenging, esp
174 r knowledge of the biological basis of major depressive disorder (MDD) is derived from studies of chr
178 t-traumatic stress disorder (PTSD) and major depressive disorder (MDD) on the basis of robust and dis
179 wever, the proportion of never-treated major depressive disorder (MDD) patients who exhibit inflammat
180 ata of 130 individuals (65 melancholic major depressive disorder (MDD) patients, 65 healthy controls)
182 itors (SSRIs) are standard of care for major depressive disorder (MDD) pharmacotherapy, but only appr
184 me-wide association studies (MWAS) for major depressive disorder (MDD) to identify sites of potential
186 udy participants were 27 subjects with major depressive disorder (MDD), 29 subjects with bipolar diso
187 ssant partial- and non-responders with major depressive disorder (MDD), a systematic search of Pubmed
188 ondition (ASC), bipolar disorder (BD), major depressive disorder (MDD), and schizophrenia (SCZ; n = 2
189 fferences in kynurenine metabolites in major depressive disorder (MDD), bipolar disorder (BD), and sc
190 f major psychiatric disorders, such as major depressive disorder (MDD), bipolar disorder (BD), and sc
191 s identified genetic correlations with Major Depressive Disorder (MDD), Bipolar Disorder (BD), Schizo
192 a-GWASs of self-reported and recurrent major depressive disorder (MDD), bipolar disorder and schizoph
193 ical thickness have been identified in major depressive disorder (MDD), but findings have been variab
194 otonergic dysfunction is implicated in major depressive disorder (MDD), but the mechanisms of this re
195 ansmission has long been implicated in major depressive disorder (MDD), for which selective serotonin
197 ings in stress disorders, particularly major depressive disorder (MDD), highlighting insights from po
198 e adversity (ELA) is a risk factor for major depressive disorder (MDD), however the underlying mechan
201 S-ketamine (esketamine) nasal spray in major depressive disorder (MDD), we performed a genome-wide as
202 Using RNA-Seq data from a study of major depressive disorder (MDD), we show that NPDR with covari
203 al excitatory to inhibitory balance in major depressive disorder (MDD), which afflicts ~14%-20% of in
204 adjunctive treatment of patients with major depressive disorder (MDD), who did not respond adequatel
236 nimal phenotyping and strictly defined major depressive disorder (MDD): the former has a lower genoty
237 tor antagonist, ketamine, for treating major depressive disorder (MDD); however, its neural mechanism
238 Endothelial dysfunction is evident in major depressive disorder (MDD); however, the molecular mediat
239 (MS, 4,888 cases and 10,395 controls), major depressive disorder (MDD, 1,475 cases and 2,144 controls
240 n models, PSs indexing 6 risk factors (major depressive disorder [MDD], attention deficit/hyperactivi
241 We analyzed data from outpatients with major depressive disorder (n = 124) randomized to receive esci
243 autism spectrum disorder (N = 126), or major depressive disorder (N = 398; total N = 2937 from 12 sit
244 We recruited unmedicated patients with major depressive disorder (N = 71 approached; N = 39 randomise
245 a diagnosis of major depressive disorder or depressive disorder not otherwise specified and no prior
246 ere made from 2007 to 2012, including DSM-IV depressive disorder, NR3C1 methylation, and various demo
247 ible novel treatment for diseases like major depressive disorder, obesity, chronic pain, and certain
248 ant enrichments of the heritability of major depressive disorder, obsessive-compulsive disorder and s
249 ribute to the heritability of anxiety, major depressive disorder, obsessive-compulsive disorder, schi
250 ly in clinical trials for treatment of major depressive disorder, offers the opportunity for the deve
252 one associated with suicide attempt in major depressive disorder, one associated with suicide attempt
253 67,807 individuals with a diagnosis of major depressive disorder or depressive disorder not otherwise
254 about the role(s) of these neurons in major depressive disorder or in mediating the delayed behavior
255 insically linked to the development of major depressive disorder, originate in part from the dysregul
256 nnectivity at 1-week post treatment in major depressive disorder patients randomized to 8 weeks of se
260 ession, and many prominent theories of major depressive disorder propose a role for abnormal cortico-
261 tly associated with suicide attempt in major depressive disorder (R(2)=0.25%), bipolar disorder (R(2)
262 negatively genetically correlated with major depressive disorder (r(g)=-0.24) and ADHD (r(g)=-0.10).
263 elated with schizophrenia (r(g)=0.22), major depressive disorder (r(g)=0.26), and attention deficit h
266 nment interaction hypotheses regarding major depressive disorder remains strong despite controversy s
267 ), bipolar disorder (BD) and recurrent major depressive disorder (rMDD) are common psychiatric illnes
269 oactivity and right parietal hypoactivity in depressive disorders, so aspects of lateralized anatomy
272 lity is an important symptom domain of major depressive disorder that is not fully reflected in depre
273 arched for all case-control studies on major depressive disorder that reported microarray or RNA sequ
274 sing real RNA-seq data from a study of major depressive disorder.The cnCV method has similar training
275 samples of SSRI-treated patients with major depressive disorder: the MARS (n = 253, P = 0.0169) and
279 outpatients with epilepsy and current major depressive disorder to sertraline or weekly CBT for 16 w
281 3 individuals with treatment-resistant major depressive disorder (TRD) and 25 healthy volunteers (HVs
282 e FDA for treating treatment-resistant major depressive disorder (TRD) in 2019, almost 50 years after
284 f 41 subjects with treatment-resistant major depressive disorder underwent one [(18)F]FEPPA positron
286 studies linking transcriptional profiles to depressive disorder, we examined whether post-endotoxin
287 sing independent microarray studies of major depressive disorder, we find that including prior knowle
289 al of Mental Disorders IV criteria for major depressive disorder were eligible and consented to take
291 een schizophrenia/bipolar disorder and major depressive disorder were found in the limbic system, whi
293 -type potassium channel-for the treatment of depressive disorders, which may exert a therapeutic effe
294 xpression are associated with risk for major depressive disorder while those of higher expression are
295 ge 2 sample comprised 87 patients with major depressive disorder who switched medication and 38 healt
297 erm prognosis of ACS only in the presence of depressive disorder with significant synergistic interac
298 om the Psychiatric Genomics Consortium Major Depressive Disorder Working Group and the UK Biobank.
299 an effective treatment for refractory major depressive disorder, yet no studies have characterized t