Depression research paper introduction
This finding is particularly interesting because MD incidence in women is about twice that for men .
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In addition to neuroanatomical changes, MD is also associated with severe vegetative and biological disturbances, including sleep and eating disorders, body weight changes, and neuroendocrine abnormalities. Most animal models including several discussed in the present Collection  ,  —  describe stress-associated weight loss, which has long being considered a face-validity criterion for a valid animal model of MD .
- Introduction Published in May 2011 the paper entitled “The relation of depression and anxiety in;
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Until recently there was a paucity of animal models of chronic stress-induced weight gain. Bartolomucci and coworkers  now report a mouse model of social subordination stress with behavioral depression-like responses and neuroendocrine disturbances, which also determine hyperphagia, weight gain, and increased vulnerability to obesity. In addition, another study in the present Collection  reports that maternal deprivation determined increased weight gain in juvenile rats when compared with undisturbed controls.
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These data offer new experimental tools to investigate the link between mood disorders and metabolic functions. In this respect it is remarkable that obesity is often found in comorbidity with MD and particularly so with the atypical depression subtype  , while clinical efficacy of antidepressants is reduced in obese individuals .
Accordingly, there is a great need to rule out the mechanism responsible for stress-induced positive or negative energy balance in different animal models as well as in MD patients.
The notion that stress may cause depression has been an underlying concept in the choice of papers included in the PLoS ONE Collection discussed here. The link between stress and depression is not novel, and several authors have aimed at identifying new subtypes of depression based on their functional link with stress exposure e.
Follow up showed that STRID tended to have a prolonged course, and that the patients often remained in a state of exhaustion after the depressive symptoms had remitted. Typically, the remaining clinical picture was one of deep mental and physical fatigue, disturbed and non-restorative sleep, irritability, perceptual hypersensitivity, emotional liability, and pronounced cognitive disturbances mainly memory and concentration problems.
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A closer examination of the case histories revealed that a majority was clearly induced by psychosocial stress, either at the workplace or often in combination with stress factors in the family. This was confirmed by data obtained in a cohort of almost 5, Swedish workers on long-term sick leave with a psychiatric diagnosis . Findings are consistent with the life event stress literature showing that specific, enduring work-related stressful experiences contribute to depression . From an endocrine standpoint, disturbances of the HPA axis may be distinctive pathophysiological features of this depression subtype.
HPA-axis hyper-reactivity has long been known and considered a classical feature of depression, particularly with the severe, melancholic type. An opposite situation, i. In addition to the HPA-axis disturbance, the STRID subtype of MD is expected to be linked to different neurobiological, immunological  , and metabolic features, thus requiring joint forces between preclinical and clinical research.
Both preclinical and clinical research will be pivotal in clarifying the validity of this new subtype of MD, in improving predictors for treatment response, and in providing a better basis for genetic studies, as well as in stimulating new drug discovery processes. Competing Interests: The authors have declared that no competing interests exist. Funding: The authors have no support or funding to report.
Stress and Depression: Preclinical Research and Clinical Implications
National Center for Biotechnology Information , U. PLoS One. Published online Jan Bernhard Baune, Editor. Author information Article notes Copyright and License information Disclaimer.
Received Dec 5; Accepted Jan 7. Copyright Bartolomucci, Leopardi. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. This article has been cited by other articles in PMC. Introduction Major depression MD is a severe, life-threatening, and widespread psychiatric disorder having an incidence of about million cases worldwide. The Problematic Diagnosis of Major Depression Presently accepted diagnostic criteria for MD  are five or more specific symptoms having been present during the same two-week period and representing a change from previous functioning; at least one of the symptoms should be either depressed mood or loss of interest or pleasure.
Genetic Predisposition Although no single gene could be responsible for a complex and multifactorial disorder like MD, association and pharmacogenetic studies identified a number of loci associated with vulnerability to MD or antidepressant efficacy  ,  ,  — . Molecular Neuroscience In the postgenomic era, high-throughput techniques allow the identification of genes overexpressed or downregulated in selected brain regions after chronic stress exposure or in MD.
Metabolic Functions In addition to neuroanatomical changes, MD is also associated with severe vegetative and biological disturbances, including sleep and eating disorders, body weight changes, and neuroendocrine abnormalities. Footnotes Competing Interests: The authors have declared that no competing interests exist. References 1. World Health Organization. WHO global report: Preventing chronic diseases: A vital investment.
Geneva: World Health Organization. Accessed 8 January Mathers CD, Loncar D. Projections of global mortality and burden of disease from to PLoS Medicine. The genetics of major depressive disorder. Curr Psychiatry Rep. Binder EB, Holsboer F. Pharmacogenomics and antidepressant drugs. Ann Med. Future antidepressants: what is in the pipeline and what is missing? CNS Drugs. Greden JF. Unmet need: what justifies the search for a new antidepressant? J Clin Psychiatry. Serotonin 4 5-HT 4 receptor agonists are putative antidepressants with a rapid onset of action.
Holsboer F. How can we realize the promise of personalized antidepressant medicines? Nat Rev Neurosci. A neurotrophic model for stress-related mood disorders. Biol Psychiatry. Lesch KP. Gene-environment interaction and the genetics of depression. J Psychiatry Neurosci. Preclinical models: status of basic research in depression.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th ed. Krishnan V, Nestler EJ. The molecular neurobiology of depression.
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Parker G. Beyond major depression. Psychol Med. Antonijevic IA. Depressive disorders—is it time to endorse different pathophysiologies? Rush AJ. The varied clinical presentations of major depressive disorder. There is also a need to study the course of depressive disorders in India so as to determine the need and duration of continuation treatment. Studies should also evaluate the cost-effective models of treatment which can be easily used in the primary care setting to effectively treat depression. Source of Support: Nil.
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Conflict of Interest: None declared. National Center for Biotechnology Information , U. Journal List Indian J Psychiatry v. Indian J Psychiatry. Author information Copyright and License information Disclaimer. Address for correspondence: Dr.