There depression It is a psychic disorder characterized mainly by one mood deviation With states of accentuated sadness, dissatisfaction, lack of pleasure and negative thoughts regarding oneself and one’s life. Should not be confused with the sadness: while the latter is a physiological and adaptive reaction to a stress or a threatdepression is a pathological condition in which negative emotional responses become spontaneoussevere, persistent and disabling.
In addition to the emotional and behavioral aspects, numerous research have shown that this condition is accompanied by marked alterations in the cerebral level and the regulation of some neurotransmittersin particular serotonin, dopamine And norepinephrine. Depression can also be influenced by stress and chronic inflammation and becomes pathological When dysphoric mood, that is, characterized by discomfort and discouragement, and negative thoughts persist for weeks or even yearsaccompanied by disorders of motivated and psychomotor behavior, sleep, appetite, energy and libido.
Disclaimer: The information contained in this article is purely for popular purposes, they do not constitute diagnoses or prescriptions. We strongly reiterate, as always, the need to contact your doctor for any problem.
What happens in the brain when depression appears
Numerous imaging studies have highlighted neurological and functional differences between depressed subjects and healthy individuals. In particular, in depressed subjects there is often one volume reduction in some areas key, such as the hippocampus and parts of the front lobe. A decrease in the hippocampal mass is associated with the deficit of memory and emotional regulation, a mirror of an emotional life denoted by lowering of the mood and poor ability to find the motivation.
In parallel, the prefrontal regions, fundamental for planning and cognitive control, show a reduced activation During executive tasks, suggesting in depressed subjects a compromise of those mechanisms that regulate emotions. If normally the activity of these areas helps us not to succumb to situations that seem, at first glance, too hard and unsurpassed, in depressed subjects this mechanism of rational downsizing seems to work less.
Also in the cingolated cortexin particular the subgenual nucleusand theamigdalatwo other crucial structures in the management of emotions, there are dysfunctions. Neuroimaging studies detected one Hyperactivity of the amygdalawhich seems to respond excessively to negative stimuli, thus promoting the development of a pessimistic vision of reality. In depressed subjects, the subgenual nucleus of the tracked cortex is also hyperactive, and the degree of this hyperactivity has been related to the severity of the depressive symptoms. These discoveries have even led to the use of techniques of neuromodulationlike deep brain stimulation, aimed at restoring balance in these dysfunctional neural networks.
Dysfunctions in the neural circuits characteristic of depression
Recent research have oriented towards an analysis not so much of specific areas of the brain, as brain networkshighlighting how depression is not the result of an isolated alteration of individual regions, but of one connections dysfunction among them.
The more a network is activated, the more it creates and consequently the easier to activate future activation. Like a plant that extends its roots when it is watering, neural networks are strengthened and expanding more are activated. In many depressed patients the so -called is hyperactive Default Mode Networkinvolved in processes of auto-reflexion and mobble: this hyperactivation contributes to a tendency to rumination (i.e. a persistent and depressive form of thought) and to the focus on negative thoughts.
At the same time, the communication between the default Mode Network and the networks responsible for cognitive control, such as the front-parietalis altered, with negative consequences on the ability to effectively regulate emotions.
Neurotransmitters and synaptic plasticity
For decades, the “monoamine theory” has provided a basis to understand the role of serotoninfrom the norepinephrine and of the dopamine in depression. Although the simple imbalance of these neurotransmitters cannot explain by the complexity of the disorder, recent studies underline how therapies with antidepressants can act not only on the neurotransmitters themselves, but also by promoting synaptic plasticity processes (the ability to modify the interactions between neurons) And neurogenesisthat is, the formation of new neurons. For example, it is assumed that the promotion of neurogenesis in the hippocampus can represent one of the mechanisms through which antidepressants improve the symptoms of the disease.
The neurotransmitter who enjoys the greatest consideration for the fight against depression is the serotonin. Little serotonergic transmission implies a poor regulation of emotions and a tendency to converge towards negative emotions. The antidepressants of the class of Ricapation inhibitors of serotonin They aim precisely to ensure that there is more availability of this neurotransmitter in the synaptic space between two neurons, to facilitate nervous transmission, with consequent increase in neuroplasticity and improvement of the mood tone.
There norepinephrinesummarized mainly in the locus coeruleus, it is particularly important for the attention managementthe supervision and the answer to stress. The problem presents itself when there is a chronic activation of this neurotransmitter, which can lead to irritability, anxiety And difficulty concentration, symptoms often observed in depressed subjects.
Finally the dopaminethe neurotransmitter of the reward processing, motivation and pleasure. In depression, dopaminergic transmission is reduced and this is related to anedoniathat is, the inability to feel pleasure, and to the strong lack of motivation.
These three systems they do not work is isolated: The activity of serotonin often influences the liberation of dopamine, and norepinephrine has modular impact on both streets. There are therefore complex interactions that modulate the overall neurochemical balance and contribute to giving rise to More common symptoms of this disorder, including mood deviation, loss of attention, interest and motivation.
Stress, inflammation and immune response
Another fundamental aspect concerns the Response to stress. The axis Hypotalam-pituitary-free-length regulates the production of cortisolthe stress hormone, and its chronic activation can have deleterious effects on the brain. Excessive production too protracted in cortisol time is associated with neuronal damage and one reduction of synaptic plasticityparticularly in the hippocampus.
Parallel, more recent studies have highlighted one inflammatory component in a subgroup of depressed patients. The massive presence of Proinflammatory cytokines It suggests that even an activation of the immune system can interfere with normal brain functioning, further contributing to the pathogenesis of depression.
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