Major depressive disorder (MDD) (also known as clinical depression, major depression, unipolar depression, or unipolar disorder; or as recurrent depression in the case of repeated episodes) is a mental disorder characterized by a pervasive and persistent low mood that is accompanied by low self-esteem and by a loss of interest or pleasure in normally enjoyable activities. The term “depression” is used in a number of different ways. It is often used to mean this syndrome but may refer to other mood disorders or simply to a low mood. Major depressive disorder is a disabling condition that adversely affects a person's family, work or school life, sleeping and eating habits, and general health. In the United States, around 3.4% of people with major depression die by suicide, and up to 60% of people who die by suicide had depression or another mood disorder.
The diagnosis of major depressive disorder is based on the patient's self-reported experiences, behavior reported by relatives or friends, and a mental status examination. There is no laboratory test for major depression, although physicians generally request tests for physical conditions that may cause similar symptoms. The most common time of onset is between the ages of 20 and 30 years, with a later peak between 30 and 40 years.
The subcallosal cingulate gyrus CG25 which consists of BA25 as well as parts of BA24 and BA32 has been implicated as playing an important role in major depression and has been the target of deep brain stimulation to treat the disorder.
One study found that BA25 is metabolically overactive in treatment resistant depression.
A different study found that metabolic hyperactivity in this area is associated with poor therapeutic response of persons with Major Depressive Disorder to cognitive-behavioral therapy and venlafaxine.
In 2005 Helen S. Mayberg and collaborators described how they successfully treated a number of depressed people — individuals virtually catatonic with depression despite years of talk therapy, drugs, and electroconvulsive therapy — with pacemaker-like electrodes (deep brain stimulation) in area 25.
A recent study found that Transcranial magnetic stimulation is more clinically effective treating depression when targeted specifically to Brodmann area 46, because this area has intrinsic functional connectivity (negative correlation) with area 25.
Another recent study has found that the responses of area 25 to viewing sad stimuli are affected by cortisol.
This suggests that depression related changes in the activity in area 25 could be due to Hypothalamic–pituitary–adrenal axis dysregulation 1).
A study examined, for the first time, olfactory memory and discrimination in the Flinders Sensitive Line (FSL) rodent model of depression. Male FSL rats and controls were trained on an Olfactory Discrimination (OD) and a Social Interaction (SI) test. On the OD test, the FSL and controls performed similarly at the shortest inter-trial interval (5min), however, with extended delay of 30min, the FSLs had a recall and odor discrimination deficit. At the longest delay (60min) both groups performed poorly. The FSL rats i.) had a deficit in olfactory discrimination suggesting impairment in olfactory memory and recall; ii.) were less likely to socialize with unfamiliar rats. The data suggests that FSL animals have an impaired olfactory information processing capacity 2).
A study of Sorri et al. from the Tampere University Hospital in Finland, included thirty patients suffering from major depressive disorder (MDD). Their serum and plasma brain derived neurotrophic factor (BDNF) levels were examined before electroconvulsive therapy (ECT) (baseline) and after the first, fifth, and last ECT session. The severity of the depression and the response to ECT were measured with Montgomery-Asberg Depression Rating Scale (MADRS).
Electroconvulsive therapy caused no significant changes in serum BDNF levels. Plasma BDNF levels decreased during the fifth ECT session between the baseline and the 2-hr samples (p = 0.019). No associations were found between serum or plasma BDNF levels and remission. The correlations between plasma and serum BDNF levels in each measurement varied between 0.187 and 0.636.
Neither serum nor plasma BDNF levels were systematically associated with the clinical remission. However, the plasma BDNF levels somewhat varied during the ECT series. Therefore, the predictive value of BDNF for effects of ECT appears to be at least modest 3).