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The biology of depression is the attempt to identify a biochemical origin of depression, as opposed to theories that emphasize psychological or situational causes. Scientific studies have found that different brain areas show altered activity in humans with major depressive disorder (MDD) . [ 1 ]
NHS figures show that the number of people in England taking antidepressants continues to rise, with 8.3m patients receiving them in 2021/22.
Depression is commonly attributed to a deficiency in monoamines, such as serotonin. The monoamine hypothesis of depression suggests that depression is primarily caused by a deficiency of several monoamines, namely serotonin, dopamine and norepinephrine. [2] This hypothesis is widely accepted due to its simplicity. [3]
This article needs to be updated. The reason given is: Many outdated sources and information (older than five years). Please help update this article to reflect recent events or newly available information. (July 2024) Medical condition Major depressive disorder Other names Clinical depression, major depression, unipolar depression, unipolar disorder, recurrent depression Specialty Psychiatry ...
There may also be imbalances in mood-regulating neurotransmitters (brain chemicals) like dopamine and serotonin. But this isn’t well understood, either. But this isn’t well understood, either.
Physical activity has been shown to boost mood, decrease symptoms of depression, and reduce stress. If it gets darker outside earlier in the winter, try to take short walks throughout the day to ...
[12] [13] [14] One interpretation is that depression manifests due to an imbalance of neurotransmitters in the brain, resulting in feelings of worthlessness and despair. Magnetic resonance imaging shows that the brains of people diagnosed with depression may have a hippocampus up to 10% smaller than those who do not exhibit signs of depression.
Serotonin in the brain is not usually degraded after use, but is collected by serotonergic neurons by serotonin transporters on their cell surfaces. Studies have revealed nearly 10% of total variance in anxiety-related personality depends on variations in the description of where, when and how many serotonin transporters the neurons should deploy.
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