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1 No significant difference was found in major depressive disorder.
2 ial evaluated oral NSI-189 as monotherapy in major depressive disorder.
3 s strongly with recurrent and single-episode major depressive disorder.
4 ation in a clinical setting in patients with major depressive disorder.
5 omorbid with other mental disorders, such as major depressive disorder.
6 evant to affect-related illnesses, including major depressive disorder.
7 level are also implicated in the etiology of major depressive disorder.
8 te biomarker of inflammation associated with major depressive disorder.
9 ecoxib administration in treatment-resistant major depressive disorder.
10 positive in bipolar disorder but negative in major depressive disorder.
11 utics, in particular for treatment-resistant major depressive disorder.
12 which has a closer genetic association with major depressive disorder.
13 8 as a biomarker of stress vulnerability and major depressive disorder.
14 ociated with psychiatric disorders including major depressive disorder.
15 dal antidepressant approved for treatment of major depressive disorder.
16 nical trial of sertraline versus placebo for major depressive disorder.
17 that is in development for the treatment of major depressive disorder.
18 including posttraumatic stress disorder and major depressive disorder.
19 ration to BDNF expression is associated with major depressive disorder.
20 ng inflammation pathways in the treatment of major depressive disorder.
21 nesis of stress-related disorders, including major depressive disorder.
22 eby target the underlying pathophysiology of major depressive disorder.
23 studies in women not formally diagnosed with major depressive disorder.
24 in treatment-seeking adult outpatients with major depressive disorder.
25 d it is an effective add-on intervention for major depressive disorder.
26 use of these interventions for prevention of major depressive disorder.
27 ich prior studies indicate is hyperactive in major depressive disorder.
28 ents are a particularly disabling feature of major depressive disorder.
29 II disorder is more strongly correlated with major depressive disorder.
30 ong detrimental effect of BMI on the risk of major depressive disorder.
31 depressants are similar in BD as in unipolar major depressive disorder.
32 gn chronopharmacological strategies to treat major depressive disorder.
33 termediate in bipolar disorder, and least in major depressive disorder.
34 a continuum between depressive symptoms and major depressive disorder.
35 decreased glutamate levels in patients with major depressive disorder.
36 frontal cortex (mPFC) has been implicated in major depressive disorder.
37 arly scores for behavioral disinhibition and major depressive disorder.
38 defeat stress, modeling multiple aspects of major depressive disorder.
39 favorable response for a drug treatment for major depressive disorder.
40 ollectively representing 2,928 patients with major depressive disorder.
41 psychotherapy practice, CBT, in adults with major depressive disorder.
42 ciation between the Netrin-1/DCC pathway and major depressive disorder.
43 POT-FSS to real RNA-Seq data from a study of major depressive disorder.
44 entified genetic variants of SIRT1 linked to major depressive disorders.
45 Andalusian BD multiplex families (166 BD, 78 major depressive disorder, 151 unaffected) as well as 43
46 at the visit were anxiety disorders (20.0%), major depressive disorder (16.9%), and substance use dis
47 cide attempters and 8,786 nonattempters with major depressive disorder; 3,264 attempters and 5,500 no
48 res for schizophrenia, alcohol use disorder, major depressive disorder, a combined bipolar disorder-s
49 magentic resonance imaging in patients with major depressive disorder, a disease associated with an
51 ynapses is a primary objective when treating major depressive disorder-a disease that afflicts ~20% o
54 ly, after puberty, females are more prone to major depressive disorder and anxiety disorders compared
55 disorder, along with the increased rates of major depressive disorder and anxiety disorders in one o
56 larify the shared molecular genetic basis of major depressive disorder and bipolar disorder and to hi
57 genetic associations, and genetic studies of major depressive disorder and bipolar disorder can be co
61 Data were compared with those of women with major depressive disorder and chronic widespread pain (M
62 ly STIR to real RNA-Seq data from a study of major depressive disorder and discuss STIR's straightfor
63 erences of brain anatomy between people with major depressive disorder and healthy control subjects,
65 al brain disorders (including, among others, major depressive disorder and obsessive-compulsive disor
66 -related neuropsychiatric disorders, such as major depressive disorder and posttraumatic stress disor
67 tive ability, neuroticism, bipolar disorder, major depressive disorder and schizophrenia (standardise
68 data were collected for 28 patients (20 with major depressive disorder and seven with bipolar II diso
69 In fact, the bidirectional relation between major depressive disorder and sleep has been well-docume
70 ine the durability and safety of SAGE-217 in major depressive disorder and to compare SAGE-217 with a
71 motivational disorders, including addiction, major depressive disorder, and autism (Cousins et al., 2
72 ring emotional face processing, diagnosis of major depressive disorder, and greater self-reported dep
73 ced excitatory neurotransmission occurs with major depressive disorder, and may be normalized by anti
74 ipants with schizophrenia, bipolar disorder, major depressive disorder, and obsessive-compulsive diso
77 and subjects with SZ, bipolar disorder, and major depressive disorder, and the messenger RNA was sub
78 variation, FMRP targets were associated with major depressive disorder, and we present novel evidence
79 rleukin-6 (IL-6) and C-reactive protein with major depressive disorder are well established, evidence
80 and operationalize depression severity, and major depressive disorder as defined in the Diagnostic a
81 -based morphometry studies in schizophrenia, major depressive disorder, bipolar disorder, addiction,
82 e attempt, using cohorts of individuals with major depressive disorder, bipolar disorder, and schizop
83 on large genetic studies of six phenotypes: major depressive disorder, bipolar disorder, attention-d
84 tive primary psychiatric disorders including major depressive disorder, bipolar disorder, schizophren
86 he highest deletion burdens were observed in major depressive disorder brain, at levels greater than
87 s first-line antidepressants for adults with major depressive disorder, but success is limited and pa
89 dMe) and bipolar disorder, and an additional major depressive disorder cohort from UK Biobank (total:
92 NRG3 class I was increased in bipolar and major depressive disorder, consistent with observations
93 disorders (schizophrenia, bipolar disorder, major depressive disorder, cross disorder, attention-def
94 genetic correlation was found between PD and major depressive disorder, depressive symptoms, and neur
95 d genetic risk for behavioral disinhibition, major depressive disorder, depressive symptoms, autism s
96 ecular profiles of individuals with PTSD and major depressive disorder despite their high comorbidity
102 phenotypes analysed in UK Biobank only were major depressive disorder, generalised anxiety disorder,
103 t outpatients who had a primary diagnosis of major depressive disorder, had a score >=18 on the 17-it
104 he efficacy of dopamine agonists in treating major depressive disorder has been hypothesized to stem
106 dicted a higher likelihood of remission from major depressive disorder in children undergoing PCIT-ED
108 dicted a higher likelihood of remission from major depressive disorder in the PCIT-ED group (B = 0.14
111 ere medication-free 18- to 65-year-olds with major depressive disorder, insomnia, and suicidal ideati
124 teristics, the biological characteristics of major depressive disorder may be close to those of HCS.
128 atic balance in 35 unmedicated subjects with major depressive disorder (MDD) and 25 healthy controls
133 ed to contribute to symptoms associated with major depressive disorder (MDD) and post-traumatic stres
134 acids (LC omega-3 PUFA) have been linked to major depressive disorder (MDD) and preterm birth (PTB),
137 izophrenia (SCZ), bipolar disorder (BD), and major depressive disorder (MDD) are heritable psychiatri
140 tly expressed in the brain, in subjects with major depressive disorder (MDD) as compared with age- an
141 d to investigate the changes of olfaction of major depressive disorder (MDD) before and after medical
142 troconvulsive therapy (ECT) is effective for major depressive disorder (MDD) but its effects on memor
144 me (GMV) and HCMV has never been examined in major depressive disorder (MDD) despite the presence of
145 udy investigated intrinsic brain networks in major depressive disorder (MDD) during a depressive epis
146 ee phenome-wide association analyses between major depressive disorder (MDD) genetic risk score (GRS)
149 the frontotemporal cortices of patients with major depressive disorder (MDD) has been demonstrated us
150 f altered grey and white matter structure in Major Depressive Disorder (MDD) have been inconsistent.
153 tritional interventions on the prevention of major depressive disorder (MDD) in overweight adults are
166 predict treatment response in patients with major depressive disorder (MDD) is challenging, in part
168 Distinguishing bipolar disorder (BD) from major depressive disorder (MDD) is clinically challengin
170 of our knowledge of the biological basis of major depressive disorder (MDD) is derived from studies
175 of post-traumatic stress disorder (PTSD) and major depressive disorder (MDD) on the basis of robust a
177 However, the proportion of never-treated major depressive disorder (MDD) patients who exhibit inf
178 erations of brain functional connectivity in major depressive disorder (MDD) patients with suicidal i
179 fMRI data of 130 individuals (65 melancholic major depressive disorder (MDD) patients, 65 healthy con
181 inhibitors (SSRIs) are standard of care for major depressive disorder (MDD) pharmacotherapy, but onl
183 ethylome-wide association studies (MWAS) for major depressive disorder (MDD) to identify sites of pot
186 The study participants were 27 subjects with major depressive disorder (MDD), 29 subjects with bipola
187 ty in 50 patients with FEP, 50 patients with major depressive disorder (MDD), 50 patients with post-t
188 idepressant partial- and non-responders with major depressive disorder (MDD), a systematic search of
189 trum condition (ASC), bipolar disorder (BD), major depressive disorder (MDD), and schizophrenia (SCZ;
190 the differences in kynurenine metabolites in major depressive disorder (MDD), bipolar disorder (BD),
191 logy of major psychiatric disorders, such as major depressive disorder (MDD), bipolar disorder (BD),
192 nalyses identified genetic correlations with Major Depressive Disorder (MDD), Bipolar Disorder (BD),
193 om meta-GWASs of self-reported and recurrent major depressive disorder (MDD), bipolar disorder and sc
194 n cortical thickness have been identified in major depressive disorder (MDD), but findings have been
195 Serotonergic dysfunction is implicated in major depressive disorder (MDD), but the mechanisms of t
196 eurotransmission has long been implicated in major depressive disorder (MDD), for which selective ser
197 glia in neuropsychiatric diseases, including major depressive disorder (MDD), has been postulated.
198 5 findings in stress disorders, particularly major depressive disorder (MDD), highlighting insights f
199 ly life adversity (ELA) is a risk factor for major depressive disorder (MDD), however the underlying
200 rcRNAs in psychiatric diseases, particularly major depressive disorder (MDD), remains largely unknown
202 cy of S-ketamine (esketamine) nasal spray in major depressive disorder (MDD), we performed a genome-w
204 cortical excitatory to inhibitory balance in major depressive disorder (MDD), which afflicts ~14%-20%
205 or the adjunctive treatment of patients with major depressive disorder (MDD), who did not respond ade
238 by minimal phenotyping and strictly defined major depressive disorder (MDD): the former has a lower
239 receptor antagonist, ketamine, for treating major depressive disorder (MDD); however, its neural mec
240 have been observed frequently in adults with major depressive disorder (MDD); however, results have b
242 rosis (MS, 4,888 cases and 10,395 controls), major depressive disorder (MDD, 1,475 cases and 2,144 co
243 (r g = 0.82, standard error (s.e.) = 0.03), major depressive disorder (MDD; r g = 0.69, s.e. = 0.07)
244 ression models, PSs indexing 6 risk factors (major depressive disorder [MDD], attention deficit/hyper
247 211), autism spectrum disorder (N = 126), or major depressive disorder (N = 398; total N = 2937 from
249 s possible novel treatment for diseases like major depressive disorder, obesity, chronic pain, and ce
250 y contribute to the heritability of anxiety, major depressive disorder, obsessive-compulsive disorder
251 gnificant enrichments of the heritability of major depressive disorder, obsessive-compulsive disorder
252 urrently in clinical trials for treatment of major depressive disorder, offers the opportunity for th
254 ound: one associated with suicide attempt in major depressive disorder, one associated with suicide a
255 luded 67,807 individuals with a diagnosis of major depressive disorder or depressive disorder not oth
256 known about the role(s) of these neurons in major depressive disorder or in mediating the delayed be
257 e intrinsically linked to the development of major depressive disorder, originate in part from the dy
258 CFP connectivity at 1-week post treatment in major depressive disorder patients randomized to 8 weeks
262 s depression, and many prominent theories of major depressive disorder propose a role for abnormal co
263 ificantly associated with suicide attempt in major depressive disorder (R(2)=0.25%), bipolar disorder
264 antly negatively genetically correlated with major depressive disorder (r(g)=-0.24) and ADHD (r(g)=-0
265 y correlated with schizophrenia (r(g)=0.22), major depressive disorder (r(g)=0.26), and attention def
268 environment interaction hypotheses regarding major depressive disorder remains strong despite controv
270 a (SCZ), bipolar disorder (BD) and recurrent major depressive disorder (rMDD) are common psychiatric
271 A total of 154 medication-free patients with major depressive disorder seeking treatment at two unive
273 non-psychiatric controls (CON, N=29), DSM-IV major depressive disorder suicides (MDD-S, N=21) and MDD
274 antly associated with a greater reduction in major depressive disorder symptoms (r = -.12, p > .4).
275 P was associated with a greater reduction in major depressive disorder symptoms (r = -.24, p = .05).
276 ritability is an important symptom domain of major depressive disorder that is not fully reflected in
277 We searched for all case-control studies on major depressive disorder that reported microarray or RN
278 hods using real RNA-seq data from a study of major depressive disorder.The cnCV method has similar tr
279 armacologic Treatment of Adult Patients with Major Depressive Disorder." The evidence review done for
280 ective samples of SSRI-treated patients with major depressive disorder: the MARS (n = 253, P = 0.0169
281 r predicting the response of 894 adults with major depressive disorder to cognitive behavior therapy.
282 adult outpatients with epilepsy and current major depressive disorder to sertraline or weekly CBT fo
284 e in 33 individuals with treatment-resistant major depressive disorder (TRD) and 25 healthy volunteer
285 by the FDA for treating treatment-resistant major depressive disorder (TRD) in 2019, almost 50 years
287 otal of 41 subjects with treatment-resistant major depressive disorder underwent one [(18)F]FEPPA pos
290 l Manual of Mental Disorders IV criteria for major depressive disorder were eligible and consented to
292 s between schizophrenia/bipolar disorder and major depressive disorder were found in the limbic syste
294 low expression are associated with risk for major depressive disorder while those of higher expressi
296 he stage 2 sample comprised 87 patients with major depressive disorder who switched medication and 38
298 ies from the Psychiatric Genomics Consortium Major Depressive Disorder Working Group and the UK Bioba
299 MS) is an effective treatment for refractory major depressive disorder, yet no studies have character