Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atypical depression has been linked to low hypothalamic-pituitary-adrenocortical axis activity and exhibits physical and affective symptoms resembling those of glucocorticoid deficiency. Because atypical depression has also been defined by preferential responsiveness to monoamine oxidase inhibitors (MAO-I), we hypothesized that MAO-I reverse these abnormalities by interfering with glucocorticoid feedback and increasing hypothalamic-pituitary-adrenocortical activity. To test this hypothesis, we measured plasma hormones and ACTH secretagogue gene expression in male C57BL/6 mice treated chronically with saline vehicle or phenelzine, a representative MAO-I. Changes in glucocorticoid feedback were evaluated using adrenalectomized (ADX) mice with and without corticosterone replacement. Antidepressant efficacy was confirmed by decreased immobility during forced swim testing. Phenelzine significantly increased circadian nadir and postrestraint plasma corticosterone levels in sham-operated mice, an effect that correlated with increased adrenocortical sensitivity to ACTH. Phenelzine increased circadian nadir, but not poststress ACTH in ADX mice, suggesting that phenelzine augmented corticosterone secretion in sham-operated mice by increasing stimulation and decreasing feedback inhibition of hypothalamic-pituitary activity. Consistent with the latter possibility, phenelzine significantly increased plasma ACTH and paraventricular hypothalamus CRH mRNA in ADX, corticosterone-replaced mice. Phenelzine did not increase paraventricular hypothalamus CRH or vasopressin mRNA in ADX mice lacking corticosterone replacement. We conclude that chronic phenelzine treatment induces sustained increases in glucocorticoids by impairing glucocorticoid feedback, increasing adrenocortical responsiveness to ACTH, and increasing glucocorticoid-independent stimulation of hypothalamic-pituitary activity. The resulting drive for adrenocortical activity could account for the ability of MAO-I to reverse endocrine and psychiatric symptoms of glucocorticoid deficiency in atypical depression.
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PMID:Chronic treatment with the monoamine oxidase inhibitor phenelzine increases hypothalamic-pituitary-adrenocortical activity in male C57BL/6 mice: relevance to atypical depression. 1556 36

Leptin is thought to be related to vegetative symptoms of depression such as alterations in food intake and weight. Fifty-seven drug-free patients and 26 healthy controls were enrolled in this study. We have found that the serum leptin levels were higher in patients with atypical depressive disorder than in controls, but not in patients with non-atypical depressive disorder, however, body mass index, age, and gender were not significantly different between these groups. Probably, these findings seem to be associated with some features of the atypical depressive disorders such as weight gain, a result of hyperphagia.
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PMID:High serum leptin levels in depressive disorders with atypical features. 1640 Dec 52

Atypical depression, with features of hypersomnia, hyperphagia, anergia, and rejection sensitivity, is a common presentation of major depressive disorder. There are few available effective therapies for this disorder. We test modafinil, a novel wake-promoting agent, as monotherapy for atypical depression in a double-blind, placebo-controlled, relapse prevention trial after open-label treatment. We found that modafinil significantly improved atypical depression symptoms during 12 weeks of open-label treatment (mean +/- SD Hamilton Depression Scale (29-item version) score changed from 34 +/- 8.2 at baseline to 9.7 +/- 9.3, P < 0.0001), and that benefits were maintained alike in both the continuation and placebo arms during the double-blind treatment phase (P = 0.92). Modafinil was well tolerated and the drug was associated with significant weight loss compared with placebo (P = 0.01).
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PMID:Modafinil for atypical depression: effects of open-label and double-blind discontinuation treatment. 1685 54

Atypical depression, one of the 4 historically important ways of subdividing depression, was first used by West and Dally to describe a patient subgroup that was nonresponsive to imipramine but responsive to iproniazid. The definition was later refined to include reverse vegetative and hysteroid dysphoria symptoms, presaging adoption of the current DSM definition in 1984. However, focusing on hysteroid dysphoria symptoms drew attention away from anxiety symptoms, some of which are more strongly linked to atypical depression. Studies that have attempted to validate atypical depression have reinforced reverse vegetative symptoms criteria and have shown that atypical depression is probably more common than melancholia. Studies suggest that atypical depression is not preferentially responsive to monoamine oxidase inhibitors, but rather less responsive to tricyclic antidepressants.
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PMID:New directions in the treatment of atypical depression. 1720 Oct 29

Atypical depression is defined as a type of depression that responds preferentially to monoamine oxidase inhibitors. In addition to mood reactivity, symptoms of atypical depression include hypersomnia, hyperphagia or weight gain, leaden paralysis, and a long-standing pattern of rejection sensitivity or interpersonal sensitivity. Over the years, atypical depression has been associated with or identified as nonendogenous depression, anxiety, reverse vegetative shift, chronic pain, bipolar disorder, and rejection sensitivity. This presentation discusses the history of the identification of atypical depression, starting with its initial identification in 1959, and describes the important studies of atypical depression and its treatment by various research groups during the past 50 years. The presentation concludes by differentiating between typical and atypical depression and detailing of some of the clinical characteristics of atypical depression.
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PMID:A history of the concept of atypical depression. 1733 11

The concept of atypical depression emerged in the 1950s to describe individuals who experienced unusual characteristics of depression and responded better to treatment with monoamine oxidase inhibitors than with tricyclic antidepressants. Over the next 50 years, research refined the criteria for atypical depression, which led to the establishment of the criteria outlined by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. These criteria, however, appear to be in need of revision. Newer research downplays the role of mood reactivity and instead emphasizes rejection sensitivity. Atypical depression appears to be a multiaxial condition that ranges across Axis I symptom states to Axis II personality styles, is a nonmelancholic spectrum disorder, and is associated with self-consolatory strategies that are homeostatic and symptomatic.
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PMID:Atypical depression: a valid subtype? 1738 2

Evaluating whether certain subtypes of Major Depressive Disorder (MDD) are more strongly associated with Substance Use Disorders (SUDs) may help clarify reasons for MDD-SUD relations. Therefore, this study compared DSM-IV-defined non-atypical/non-melancholic depression (undifferentiated depression; n=365), atypical depression (n=117), melancholic depression (n=245), and atypical-melancholic depression (n=68) in the prevalence of current SUDs, while controlling for relevant demographic and clinical variables. Psychiatric outpatients with a current diagnosis of unipolar MDD were assessed using the Structured Clinical Interview for DSM-IV, supplemented by questions from the Schedule for Affective Disorders and Schizophrenia. Results showed that compared with patients with undifferentiated depression, melancholic patients had higher rates of current nicotine dependence (34% vs. 26%) and drug abuse/dependence (8% vs. 3%), Ps<0.05. These differences were explained by the association between specific melancholic features (marked psychomotor agitation and weight loss/decreased appetite) and nicotine and drug use disorders. Atypical depression, atypical-melancholic depression, and other subtype symptoms were not significantly associated with any SUDs. Although this study is limited by low prevalence of alcohol and drug use disorders, the present findings suggest that different symptomatic expressions of MDD differentially associate with some SUDs.
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PMID:Associations between depression subtypes and substance use disorders. 1878 40

The authors conducted Pubmed searches to examine the epidemiological characteristics, symptoms, association with bipolar disorder, personality and temperament features, biology, and pharmacotherapy response of atypical depression and significance of current knowledge about this subtype of depression in treatment planning. Atypical depression has a high prevalence rate, starts early in life, tends to last longer, is more likely to occur in people with bipolar disorder, has high comorbidity of anxiety disorders, carries more risk of suicidal behavior, and has distinct personality psychopathology and biological traits. Atypical depression is an important specifier with significance in terms of predicting clinical course of depression, and hence in treatment planning and service use.
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PMID:Atypical depression. 2110 69

Depression is a clinically heterogenous condition defined by sub-types that can have diametrically opposed features, such as sleep and appetite. Within the same individual these features may change over time, and different symptom clusters may respond selectively to different treatments. It has been hypothesized that different pathophysiological processes may be operating in the different sub-types of depression and specifically that Melancholic depression may be associated with relative overactivity, and Atypical depression with relative hypoactivity, of the hypothalamic drive of the HPA axis. A consistent finding that emerges from the literature is that the experience of depression alters over the course of the illness with the features of Atypical depression dominating a more chronic clinical picture. This suggests that different stress states characterize the different profiles of depression as the illness becomes more chronic. There is evidence that the corticotropin-releasing hormone (CRH) control of HPA axis output is reduced in Atypical, compared to Melancholic, sub-types, but there is no convincing evidence that overall HPA activity, i.e., cortisol output, reduces. We suggest that there is a "switch" in the regulation of the HPA system from CRH to arginine vasopressin (AVP) control as stress becomes more sustained or repeated; resulting in an altered homeostasis within the HPA system. Cortisol, and the neuropeptides CRH and AVP, have different neurobiological, behavioural and experiental effects. The "switch" process should result in different neuropeptide/cortisol combinations and ratios and may explain the changing profile of depression over time. The heuristic merit in making a distinction between the different clinical states of depression will be discussed.
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PMID:A review of Atypical depression in relation to the course of depression and changes in HPA axis organization. 2249 86

Growing evidence suggests immune and metabolic dysregulation among depressed persons, possibly restricted to specific subgroups. This study explores the association between depressive disorders and characteristics with immunometabolic functioning among older persons. Data are from the baseline assessment of the Netherlands Study of Depression in Older Persons, including 131 non-depressed and 358 depressed (6-month DSM-IV major depressive disorder) persons (60-93 years). Immune (C-reactive protein, interleukin [IL]-6) and metabolic (waist circumference, triglycerides, high-density lipoprotein cholesterol, blood pressure, fasting glucose) factors were measured. Depression characteristics included severity, age of onset, symptom profile (atypical/melancholic) and antidepressant use. Depressed persons showed lower IL-6 levels compared with non-depressed persons. Depressed persons, except those with atypical depression, had lower waist circumference, lower glucose levels and scored lower on an overall index including all immunometabolic factors. Low waist circumference was more pronounced among those with less severe depression and those with a later age of onset, whom also had lower blood pressure levels. Atypical depression was associated with higher triglyceride levels. Antidepressant use was not clearly associated with immunometabolic functioning. To conclude, contrary to our expectations, we found overall immunometabolic downregulation in older depressed persons, in particular among those with less severe symptoms and those with late-life onset. However, persons with atypical depression presented with metabolic upregulation compared with other depressed persons. Taking depression symptom profiles into account is important when examining biological dysregulation in late-life depression.
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PMID:Late-life depression symptom profiles are differentially associated with immunometabolic functioning. 2483 21


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