Disease relevance of MDD1

• It is possible to determine the specific abnormality in most patients, but it can sometimes be difficult to decide whether the patient has hypercortisolism and whether it is primary or due to major depressive disorder or to the stress of other diseases [1].
• OBJECTIVE: To evaluate the safety and efficacy of sertraline treatment of MDD in patients hospitalized for acute myocardial infarction (MI) or unstable angina and free of other life-threatening medical conditions [2].
• PATIENTS: Eighty-one outpatients meeting Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria for major depressive disorder and with documented ischemic heart disease [3].
• PATIENTS: A total of 369 patients with MDD (64% male; mean age, 57.1 years; mean 17-item Hamilton Depression [HAM-D] score, 19.6; MI, 74%; unstable angina, 26%) [2].
• The results indicated that the SCID can be employed reliably to differentiate MDD from GAD [4].

Psychiatry related information on MDD1

• However, the lifetime prevalence of major depressive disorder, posttraumatic stress disorder, and substance use disorders was overrepresented compared to the general female population [5].
• To determine the prevalence rates of major depressive disorder and of depressive symptoms and their relationship to mortality in nursing homes, research psychiatrists examined 454 consecutive new admissions and followed them up longitudinally for 1 year [6].
• Risk of relapse into an affective episode was high in the months immediately after recovery from a major depressive disorder (MDD) in 141 subjects with nonbipolar depression, without a preexisting dysthymic disorder [7].
• The typical patient was a polydrug-abusing girl with a borderline personality disorder and a superimposed major depressive disorder [8].
• Of 104 cases, 41% had anxiety disorders in conjunction with their index depression, which was more likely with MDD and DD than with ADDM [9].

High impact information on MDD1

• METHODS: We randomly assigned 681 adults with a chronic nonpsychotic major depressive disorder to 12 weeks of outpatient treatment with nefazodone (maximal dose, 600 mg per day), the cognitive behavioral-analysis system of psychotherapy (16 to 20 sessions), or both [10].
• The CGI-I responder rates for sertraline were significantly higher than for placebo in the total sample (67% vs 53%; P =.01), in the group with at least 1 prior episode of depression (72% vs 51%; P =.003), and in the more severe MDD group (78% vs 45%; P =.001) [2].
• OBJECTIVE: To compare the 6-month efficacy and safety of a flexible dosage of venlafaxine XR in outpatients with GAD without associated MDD [11].
• Women are twice as likely as men to be diagnosed with major depressive disorder, yet no known risk factors can account for this sex difference [12].
• We aimed to assess whether lowering of brain serotonin activity by depletion of its amino acid precursor, tryptophan, could provoke a short-term relapse of clinically significant symptoms in women vulnerable to major depressive disorder [13].

Chemical compound and disease context of MDD1

• The lack of effect of fluoxetine on depressive symptoms in CFS suggests that processes underlying the presentation of depressive symptoms in CFS may differ from those in patients with major depressive disorder [14].
• INTERPRETATION: We conclude that rapid lowering of brain serotonin function can precipitate clinical depressive symptoms in well, untreated individuals who are vulnerable to major depressive disorder [13].
• Women with PTSD and comorbid MDD had higher cortisol levels [15].
• RESULTS: Tryptophan depletion induced a transient return of depressive symptoms in patients with remitted MDD but not in controls (P<.001) [16].
• METHODS: Outpatients with DSM-III-R major depressive disorder and atypical features (N = 108) were treated in a 10-week, double-blind, randomized, controlled trial comparing acute-phase cognitive therapy or clinical management plus either phenelzine sulfate or placebo [17].

Biological context of MDD1

• CONCLUSION: Dopamine-related neuroanatomical substrates are involved in altered reward processing in MDD, shedding light on the neurobiology of the anhedonic symptoms in MDD and suggesting these substrates as future therapeutic targets [18].
• Epidemiology of major depressive disorder: results from the National Epidemiologic Survey on Alcoholism and Related Conditions [19].
• We measured regional cerebral blood flow with the xenon 133 inhalation technique in 41 patients with major depressive disorder and 40 matched, normal controls during an eyes-closed, resting condition [20].
• Our data are also suggestive of the association between SNPs in other PDE genes and MDD [21].
• We show here that PDE11A haplotype GAACC is significantly associated with MDD [21].

Anatomical context of MDD1

• RESULTS: At baseline, subjects with MDD had higher normalized metabolism than controls in the prefrontal cortex (and caudate and thalamus), and lower metabolism in the temporal lobe [22].
• Larger reductions in mu-opioid system BP during sadness were obtained in patients with MDD in the anterior insular cortex, anterior and posterior thalamus, ventral basal ganglia, amygdala, and periamygdalar cortex [23].
• CONCLUSION: These findings suggest that there is reduced frontal cortical glial cell density and neuronal size in major depressive disorder [24].
• Lymphocyte function in major depressive disorder [25].
• OBJECTIVE: To test the hypothesis that neuritic plaques and neurofibrillary tangles are more pronounced in the hippocampus of patients with AD with a lifetime history of major depressive disorder, as compared with patients with AD without depression history [26].

Associations of MDD1 with chemical compounds

• METHODS: Fifty-one patients diagnosed as having comorbid major depressive disorder and alcohol dependence were randomized to receive fluoxetine (n = 25) or placebo (n = 26) in a 12-week, double-blind, parallel-group trial [27].
• Cortisol secretion in prepubertal children with major depressive disorder. Episode and recovery [28].
• Between scans, subjects with MDD were treated with either paroxetine or interpersonal psychotherapy (based on patient preference), while controls underwent no treatment [22].
• CONCLUSIONS: The SRI sertraline was more effective in reducing MDD and OCD symptoms than the primarily norepinephrine reuptake inhibitor desipramine for patients with concurrent OCD and MDD [29].
• Patients who were nonsuppressors in the dexamethasone suppression test had significantly higher 60-minute cortisol concentrations and cortisol increases than did normal subjects and patients with MDD who were suppressors [30].

Physical interactions of MDD1

• Decreased hippocampal 5-HT2A receptor binding in major depressive disorder: in vivo measurement with [18F]altanserin positron emission tomography [31].
• Glucocorticoid receptor binding in three different cell types in major depressive disorder: lack of evidence of receptor binding defect [32].

Enzymatic interactions of MDD1

• In this study, we examined the amounts of cAMP-responsive element binding protein (CREB) and its phosphorylated form in homogenate preparations from postmortem orbitofrontal cortices of antidepressant drug-free patients with major depressive disorder and age-matched controls by immunoblotting [33].

Regulatory relationships of MDD1

• In the present study, thyroid functions (TFTs) and thyrotropin-releasing hormone (TRH) stimulation of thyroid-stimulating hormone (TSH) were measured before and after treatment with desipramine (DMI) in 13 men with a diagnosis of major depressive disorder [34].
• In a preliminary, prospective pilot study, five patients with major depressive disorder and eleven age and sex matched normal controls received intravenous human growth hormone releasing factor (hGRF) (1 microgram/kg in 5 cc of normal saline infused over five minutes) and placebo [35].
• Thirteen of thirty-nine patients (33%) developed IFN-alpha-induced major depressive disorder (MDD) [36].
• In order to test the serotonin hypothesis of depression, the authors compared 20 outpatients with major depressive disorder to 20 normal control subjects using prolactin response to D-fenfluramine as a measure of central serotonergic (5-HT) functioning [37].
• To test whether this also occurs in patients receiving AD treatment, G-protein-activated-AC activity and the levels of alpha s and alpha i were measured in mononuclear leukocytes (MNLs) from 12 subjects with major depressive disorder (MDD) at baseline and after a 5 week trial of AD treatment [38].

Other interactions of MDD1

• Association between COMT (Val158Met) functional polymorphism and early onset in patients with major depressive disorder in a European multicenter genetic association study [39].
• Twenty-four subjects (12 patients with major depressive disorder and 12 controls matched for sex and age) received 100 micrograms synthetic human corticotropin-releasing hormone (hCRH) as an iv bolus dose [40].
• Growth hormone response to growth hormone releasing hormone and to clonidine stimulation in peripubertal patients with major depressive disorder [41].
• Estrogen receptor alpha mRNA levels were reduced in the basomedial nucleus in major depressive disorder and bipolar disorder [42].
• Before treatment, productions of IL-2 and IFN-gamma were markedly decreased in PD patients compared to patients with major depressive disorder and healthy controls [43].

Analytical, diagnostic and therapeutic context of MDD1

• CONTEXT: Intense debate persists about the need for placebo-controlled groups in clinical trials of medications for major depressive disorder (MDD) [44].
• METHODS: We undertook a case-control study to assess the association between violent victimisation early in life and major depressive disorder in women [12].
• RESULTS: The mean anterior cingulate cortex distribution volume differed across groups (F55 = 3.4; P = .04), and this difference was accounted for by significantly lower binding in bipolar disorder compared with both major depressive disorder and control groups [45].
• Major depressive disorder and immunity. Role of age, sex, severity, and hospitalization [46].
• We examined the correlates of recovery in a "mega-analysis," or meta-analysis of original data, of 595 patients with major depressive disorder enrolled in 6 standardized treatment protocols [47].

References