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Gene Review

MDD1  -  Major depressive disorder

Homo sapiens

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Disease relevance of MDD1


Psychiatry related information on MDD1


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


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


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


Enzymatic interactions of MDD1


Regulatory relationships of MDD1


Other interactions of MDD1


Analytical, diagnostic and therapeutic context of MDD1


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  20. Regional cerebral blood flow in mood disorders. I. Comparison of major depressives and normal controls at rest. Sackeim, H.A., Prohovnik, I., Moeller, J.R., Brown, R.P., Apter, S., Prudic, J., Devanand, D.P., Mukherjee, S. Arch. Gen. Psychiatry (1990) [Pubmed]
  21. Phosphodiesterase genes are associated with susceptibility to major depression and antidepressant treatment response. Wong, M.L., Whelan, F., Deloukas, P., Whittaker, P., Delgado, M., Cantor, R.M., McCann, S.M., Licinio, J. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
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