Disease relevance of Depressive Disorder

• RESULTS: Hyperhomocysteinemia, vitamin B(12) deficiency, and to a lesser extent, folate deficiency were all related to depressive disorders [1].
• METHOD: Geriatric patients with unipolar depression (N = 43) and elderly comparison subjects (N = 24) were assessed for depressive symptoms, cognitive functions, risk factors for vascular disease, and P300 latency [2].
• DST in bulimia without endogenous depression [3].
• Abnormalities within the serotonin metabolic pathway have been observed in depressed patients with Parkinson's disease and may help to explain why this form of depressive disorder is so common and persistent [4].
• Amitriptyline and phenelzine have limited use (if any) in depression with melancholia after minor closed head injury [5].

Psychiatry related information on Depressive Disorder

• Prolactin response to electroconvulsive therapy (E.C.T.)was investigated in nine patients with endogenous depression [6].
• Cerebral metabolic rates for glucose were examined in patients with unipolar depression (N = 11), bipolar depression (N = 5), mania (N = 5), bipolar mixed states (N = 3), and in normal controls (N = 9) using positron emission tomography and fluorodeoxyglucose F 18 [7].
• Plasma norepinephrine level in affective disorders. Relationship to melancholia [8].
• RESULTS: Fifty women were enrolled in the study; 26 met DSM-IV criteria for major depressive disorder, 11 for dysthymic disorder, and 13 for minor depressive disorder [9].
• Depressive symptoms present in 43 patients with unipolar nondelusional melancholia were studied to determine which symptoms were the best measures of response to desipramine hydrochloride [10].

High impact information on Depressive Disorder

• It has been suggested that there are altered levels of norepinephrine or other neurotransmitters at functionally important receptors in patients with depressive disorders [11].
• We found that drug-free inpatients with endogenous depression had lower isoproterenol-stimulated cyclic AMP levels in intact lymphocytes than did healthy control subjects (3.9 +/- 0.5 vs. 7.4 +/- 1.0 pmol per 10(6) cells, P less than 0.01) [11].
• The finding suggests the existence of a biochemical subgroup of depressive disorder, characterized by a disturbance of serotonin turnover [12].
• Attempts to correlate plasma concentrations with clinical response to amitriptyline hydrochloride and nortriptyline hydrochloride failed, probably because of the heterogeneity of depressive syndromes being treated [13].
• Central regulation of CRH by glucocorticoids is important for adaptive and sustained fear-related behaviors, and its aberration is associated with anxiety and depressive disorders [14].

Chemical compound and disease context of Depressive Disorder

• In a group of 30 patients with major unipolar depressive disorder urinary excretion of tyramine sulphate was measured after an oral dose of tyramine [15].
• Neuroendocrine aspects of primary endogenous depression. I. Cortisol secretory dynamics in patients and matched controls [16].
• beta-Endorphin/beta-lipotropin immunoreactivity in endogenous depression. Effect of dexamethasone [17].
• We examined the effect of lithium carbonate addition in 39 patients with unipolar depression whose conditions were not improved by at least three weeks' TCA drug administration [18].
• Afternoon continuous plasma levels of 3-methoxy-4-hydroxyphenylglycol and age. Distinctive biologic subgroups of endogenous depression [19]?

Biological context of Depressive Disorder

• If CRF is chronically hypersecreted in depressed patients, then, due to down-regulation, a reduced number of CRF receptor binding sites should be present in patients with profound depressive disorder [20].
• Twenty-three short tandem repeat markers were investigated in 57 families containing 103 individuals with bipolar I disorder (BPI), 26 with bipolar II disorder (BPII), nine with schizoaffective disorder of the bipolar type (SA/BP), and 38 individuals with recurrent unipolar depression (UPR) [21].
• Cortisol suppression and circadian rhythm in endogenous depression: a preliminary report [22].
• All the subjects were Japanese. RESULTS: There was statistically no difference between normal control subjects and patients with depressive disorders in Apo E genotype or allele frequency [23].
• Plasma ACTH and serum cortisol levels were measured at 20-min intervals for 24 h in six young women with unipolar endogenous depression and in eight normal women during the early follicular phase of the menstrual cycle [24].

Anatomical context of Depressive Disorder

• RESULTS: Prefrontal cortex and cerebellar expression of RELN mRNA, GAD(67) protein and mRNA, and prefrontal cortex RELN-positive cells was significantly decreased by 30% to 50% in patients with schizophrenia or bipolar disorder with psychosis, but not in those with unipolar depression without psychosis when compared with nonpsychiatric subjects [25].
• Erythrocyte membrane Na+-K+ ATPase and Ca++ATPase levels were investigated in 11 women treated with ECT for endogenous depression and 11 age-matched normal control subjects [26].
• Venlafaxine but not bupropion decreases cerebrospinal fluid 5-hydroxyindoleacetic acid in unipolar depression [27].
• Kynurenine in blood plasma and DST in patients with endogenous anxiety and endogenous depression [28].
• The very marked decrease in plasma 5-HT levels may be in accord with the central nervous system changes reported in depression and suggests the possibility of using plasma 5-HT as a peripheral indicator of abnormal serotonin function in melancholia [29].

Gene context of Depressive Disorder

• Sequence variations in CREB1 cosegregate with depressive disorders in women [30].
• Higher levels of NR2C subunit implicate altered glutamatergic input to the LC in depressive disorders [31].
• Given the role of MAP kinases in various physiological functions and gene expression, alterations in p44/42 MAP kinase activation and expression of ERK1/2 may contribute significantly to the pathophysiology of depressive disorders [32].
• No correlation was found between the changes in COMT activity and the psychopathological picture of depression or the severity of endogenous depressive syndrome [33].
• The blunted growth hormone response in endogenous depression could be explained by inhibitory influences such as increased somatomedin-C concentrations or a hyperactivity of central beta-adrenergic-receptors [34].

Analytical, diagnostic and therapeutic context of Depressive Disorder

• METHOD: One hundred sixty-two patients with minor depressive disorder were randomly assigned to receive fluoxetine or placebo in a 12-week, double-blind study; 73% (59 of 81) of the patients in each treatment group completed the study [35].
• The results indicate considerable descriptive validity of the syndrome in childhood and its independence from obsessional traits; however, all of the children had a history of major depressive disorder, and their sleep EEG measures resembled those of young adults with primary depressive disorder [36].
• We propose that withdrawal from chronic cocaine in rats may serve as a useful animal model of depressive disorders [37].
• d-Amphetamine response and dexamethasone suppression test as predictors of treatment outcome in unipolar depression [38].
• Prolactin, cortisol, growth hormone and TSH serum levels (before and 15 minutes after treatment) were measured in 62 patients with endogenous depression randomly allocated to real or pseudo-ECT [39].

References