He did not receive any financial compensation for his work on this manuscript. Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2. Received Jun; Accepted Sep.
Abstract Introduction or background Depressive disorder is a long term, relapsing condition associated with high levels of disability and mortality. It has a neurobiological basis and is associated with functional and structural brain abnormalities. Sources of data The data discussed have been obtained mainly from meta-analyses, randomized controlled clinical trials and key review papers as well as animal studies.
Areas of agreement Genetic vulnerability and stress are key factors in its aetiopathogenesis. Dysregulation of the hypothalamo-pituitary-adrenal HPA axis reduces hippocampal volumes and prefrontal cortex PFC activity in depressed patients and disrupts homeostasis within the neurocircuit of depression.
Antidepressant drugs increase brain-derived neurotrophin, restoring neuronal growth and activity and modulate interactions between the neurocircuit anatomical structures.
Areas of controversy It remains to be confirmed whether structural changes in the brain are purely abnormalities in neuroplasticity and are fully reversible, whether they predate depression and whether they increase in the long term.
Growing points Investigation of the molecular mechanisms mediating gene and environment interaction is a growing and potentially fruitful area of research in the neurobiology of depression.
Further elucidation of the neuroanatomical and physiological connections between the limbic structures and PFC may help identify key areas to target in treatment. The role of the dysregulation of the HPA axis and identifiable stressors in the recent or remote past which are not always present in depression need further study.
Areas timely for developing research Prospective studies examining the interaction between changes in brain function and structure in relation to stress and identified relevant genes and how these may be influenced by antidepressant drug treatment and the long-term course of depression would help clarify their role in the pathophysiology of this disorder.
However, in the last decade or so, thanks to technological advances, major leaps have been made in our understanding of the workings of the brain, particularly, its significant capacity for plasticity in interacting with the environment physical and psychological.
It has become increasingly clear that both psychosocial and biological factors are highly relevant and far from contradicting each other, they are inextricably linked in the genesis of this multifaceted condition.
The pathophysiology will be discussed in relation to the clinical presentation and course of the depressive illness and how it can inform the clinical management of this disorder and help optimize its long-term outcome. The World Health Organization global burden of disease study places unipolar affective disorder amongst the 10 leading medical causes of disability in the world and second only to ischaemic heart disease.
Three quarters of the patients experience more than one episode of depression and the risk of recurrence is higher if the first episode occurs at a younger age and if there is a family history of depression.
Maintenance treatment for several months during remission is essential after an acute episode of depression to prevent relapse 7 as well as long-term treatment to prevent recurrence in patients with more than one episode. In addition to the number of episodes, the prognosis is influenced by the duration of illness remaining untreated.
The more protracted this is, the poorer the response to treatment and the lower the likelihood of achieving remission. Subsyndromal states encourage relapse 9 and progression to chronicity. Long-term over 2 years depression is common; it is clinically more serious than episodic depression and is associated with more functional impairment and high comorbidity cardiac and respiratory syndromes.
Such patients suffer significantly more from social phobia and benzodiazepine abuse and both their somatic and psychological well-being are impaired. Pre-existing anxiety is a risk factor for later depression; individuals with anxiety states tend to develop either depression alone or comorbid anxiety and depression as they progress through adulthood.
Depression alone and depression comorbid with anxiety is more persistent than anxiety alone over time and this applies to both threshold and subthreshold disorders. He understood this circuit to form a functional route of communication between the above structures enabling cortical control of emotion as well as playing a role in the storing of memory.
In the absence of appropriate technology, further study to elucidate the connection between brain structures and human experience and behaviour was limited to clinical observations of the effects of localized neurological disorders, such as strokes or tumours and accidental trauma.
These brain sites and their connections, which have been widely studied, are responsible for maintaining emotional stability and their malfunction is considered central to the pathophysiology of depression.
It is divided into three major sections: The VMPFC is necessary for the normal generation of emotions, in particular social emotions 12 and it regulates autonomic and neuroendocrine responses, pain modulation, aggression and sexual and eating behaviours.
The DLPFC has been implicated in cognitive control, solving complex tasks, maintenance and manipulation of information in working memory. The PFC, the amygdala and particularly the hippocampus are the brain structures most widely studied in relation to depression.
Magnetic resonance studies show a reduction in the brain volume of depressed patients compared with healthy controls, with large volume reductions in the anterior cingulate and orbitofrontal cortex and moderate reductions in the hippocampus, the putamen and the caudate.
Response to treatment is associated with a decrease in metabolic activity, and chronic antidepressant drug treatment reduces metabolism in the amygdala and ACC in subjects with persistent, positive treatment response.
Abnormal activation of the amygdala correlates with the severity of the depression. They have been implicated in the tendency to ruminate and may also play a role in bipolar depression and anxiety.
A recent meta-analysis of MRI studies, which took into account the possible role of medication on the size of the amygdala, demonstrated that this is actually reduced in unmedicated depressed patients.
Whether and how much neurogenesis occurs in other brain regions in adulthood is not known. The new neurons arising from neural progenitor cells, which are maintained throughout adult life, project to the CA3 hippocampal region, receive afferents and exhibit electrophysiological properties very similar to those of mature dentate granule neurons.Neurobiology of depression: an integrated view of key findings V Maletic, 1 M Robinson, 2 T Oakes, 2 S Iyengar, 2 S G Ball, 2, 3 and J Russell 2 1 School of Medicine, University of .
Depression is one of the most common psychiatric disorders worldwide, affecting at least 12% of American women and 8% of American men in their lifetime. Prevalence rates are higher in some countries, for example, a 19% rate of depression has been reported for Lebanon. Women are affected approximately twice as often as men.
Investigation of the molecular mechanisms mediating gene and environment interaction is a growing and potentially fruitful area of research in the neurobiology of depression.
Further elucidation of the neuroanatomical and physiological connections between the limbic structures and PFC may help identify key areas to target in treatment.
Traditional treatments have had impressive results in children with depression. But, why does efficacy of treatment vary in children? Host Dr. Peter Jensen welcomes Dr.
Paul Croarkin, Assistant Professor of Psychiatry at Mayo Clinic, to answer these questions and discuss recent clinical trials, child and adolescent psychopharmacology and transcranial magnetic stimulation (TMS) and brain stimulation .
Behavioral Neurobiology of Depression and Its Treatment (Current Topics in Behavioral Neurosciences): Medicine & Health Science Books @ attheheels.com Basic Information Depression is a common mental illness, mainly for depression, interest reduction, pessimistic, thinking slow, lack of initiative, self-blame from the offense, diet, sleep is poor, worried about their suffering from various diseases, many feel that the body discomfort, serious suicidal thoughts and behavior can occur.