Depression

What is Depression?

Depression is a clinically heterogeneous disorder. The common feature of depression is the presence of sad, empty, or irritable mood, accompanied by somatic and cognitive changes that significantly affect the individual’s capacity to function. A diagnosis based on a single episode is possible, although the disorder is a recurrent one in the majority of cases.

Major depressive disorder (MDD) is characterized by discrete episodes of at least 2 weeks’ duration (although most episodes last considerably longer) involving clear-cut changes in affect, cognition, and neurovegetative functions and inter-episode remissions.

Depression often has a remitting and relapsing course, and symptoms may persist between episodes. Severity of the disorder is determined by both the number and severity of symptoms, as well as the degree of functional impairment.

Get an introduction to depression or dive into details on the subject by going through our slide decks. Our slide decks encompass various subjects, including functional impairment in Major Depressive Disorder (MDD), the prevalence of MDD in patients with chronic conditions, and the global significance of MDD as a leading cause of burden.

Comorbidity

This slide deck includes graphic illustrations of a retrospective analysis of patient data performed to compare the prevalence of chronic conditions in patients with MDD. Go to the slide deck.

Epidemiology and burden

This slide deck presents the essential components of the epidemiology and burden of MDD. Go to the slide deck.

Definitions and Diagnosis

This slide deck offers opportunities to discuss the core definitions of MDD as well as a presentation of the key components of its diagnosis, signs and symptoms. Go to the slide deck.

Course, Natural History and Prognosis

This slide deck covers the course, natural history, and prognosis of MDD. This includes the definition of depression based on WHO’s ICD-10 classification system or the American Psychiatric Association’s DSM-IV and DSM-5 system. Go to the slide deck.

Neurobiology and Aetiology

This slide deck includes the key components of neurosynaptic transmission, neurotransmitters and hypotheses about the underlying causes of depression. Go to the slide deck.

Treatment Principles

This slide deck includes infographic slides and figures illustrating the treatment principles of MDD, such as pharmacotherapy and non-pharmacological therapies. Go to the slide deck.

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The various comorbidities of Major Depressive Disorder (MDD) adversely affect patients’ quality of life. MDD frequently occurs alongside substance-related and anxiety disorders, as well as a host of other physical conditions such as type 2 diabetes. This slide deck includes graphic illustrations of a retrospective analysis of patient data performed to compare the prevalence of chronic conditions in patients with MDD.

This slide deck has been developed in collaboration with the former Lundbeck International Neuroscience Foundation.

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Selected articles on Depression

Access essential articles on depression, covering topics like polygenic risk, reducing untreated illness duration for better long-term outcomes, achieving full remission over partial response, strategies for recurrence prevention, suicide prevention, and personalized treatment through inflammatory mechanisms

Polygenic Scores in Psychiatry: The Example of Depression

Psychiatric disorders are greatly influenced by multiple genes, making them highly polygenic, with common gene variations contributing significantly to their heritability. Recent research shows a substantial genetic overlap among different disorders and medical conditions, suggesting vulnerability is not specific to one disorder. Studying the genetic susceptibility of psychiatric conditions like major depressive disorder (MDD) sheds light on similarities and differences with other conditions and risk factors, challenging our understanding of depression. Polygenic risk scores (PRS), derived from large-scale studies, can help predict risk and outcomes in clinical psychiatry, incorporating data from various factors. This article discusses the latest advances in psychiatric genetics, focusing on MDD, the use of PRS in research, and potential future clinical practice applications.

Depression: Cognitive Function the Next Frontier

The involvement of inflammatory mechanisms may one day help us to identify biological subtypes of mood disorders and so tailor treatment more effectively to individual needs. However, the biology is likely to be highly complex. While the treatment of mood disorders with agents that can broadly be described as anti-inflammatory has shown some preliminary evidence of effect, a high degree of caution is warranted moving forward.

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Depression may be Neurotoxic

Evidence shows that neurotoxicity is clinically and therapeutically relevant. To improve the long-term prognosis of a major depressive episode, clinicians should aim to reduce the duration of untreated illness (treat faster), focus on the quality of remission without tolerating partial response (treat better), and prevent recurrence (treat longer).

Download and use images on depression in your teaching

Discover illustrations and explanations on relevant topics such as Noradrenergic and Specific Serotonergic Antidepressants, the Effects of a Noradrenaline Antagonist, Specific Noradrenaline Re-Uptake Inhibitors, and much more.

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Hypothalamic Pituitary Adrenal (HPA) Axis in Depression

In depression, the hypothalamic-pituitary-adrenal (HPA) axis is upregulated with a down-regulation of its negative feedback controls. Corticotropin-releasing factor (CRF) is hypersecreted from the hypothalamus and induces the release of adrenocorticotropin hormone (ACTH) from the pituitary. ACTH interacts with receptors on adrenocortical cells and cortisol is released from the adrenal glands; adrenal hypertrophy can also occur. Release of cortisol into the circulation has a number of effects, including elevation of blood glucose. The negative feedback of cortisol to the hypothalamus, pituitary and immune system is impaired. This leads to continual activation of the HPA axis and excess cortisol release. Cortisol receptors become desensitized leading to increased activity of the pro-inflammatory immune mediators and disturbances in neurotransmitter transmission.

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