The presence of a mental disorder produces great difficulty in the daily life of those who suffer from it. Schizophrenia, bipolarity, anxiety, depression… all of them generate a high level of suffering and induce changes at a cognitive and behavioral level.
However, the effects of some psychopathologies are not limited to these aspects, but rather produce great changes at a physiological and cerebral level In the case of depression, recent research suggests that suffering from this pathology could be associated with a shrinkage of some brain areas.
The results of these investigations have been obtained through the analysis of neuroimaging techniques applied to a large number of volunteers with and without depression. as well as through the analysis of donated brain tissues.
In many mental disorders, changes occur at the brain level. These modifications in brain structure and functionality explain the symptoms present in the disorders. But it is necessary to take into account a fundamental consideration: the fact that there is a correlation between brain modifications and mental disorders does not indicate in which direction said relationship occurs. In a large number of disorders, research shows that Brain alterations cause or facilitate the appearance of the disorder and its symptoms
In the case of depression, however, the latest research indicates that the observed reductions occur after the appearance of symptoms, being an effect derived from the persistence of the symptoms.
That is, in the brains of depressed people, measures and structural modifications are observed that are not present in subjects without this disorder. For this reason, the research carried out reinforces the idea of the importance of early intervention, in order to avoid not only the persistence of symptoms but also the degradation of brain structures.
Brain changes produced during depression
These studies indicate that the main effects occur in the hippocampus, which is a very important brain structure when it comes to ensuring that certain memories are stored in long-term memory. Depression is associated with a reduction in neuronal density in this part of the brain, causing in turn deficits in memory, attention and retention of information (something that can also be observed in the depressive process itself). This hippocampal atrophy, according to studies, increases as the depressive episodes are repeated and as their duration is prolonged.
On the other hand, research carried out to date indicates that the brain is compressed, losing internal neuronal connections and not only in the hippocampus.
Other changes in the brain during depression
In addition to the neurons themselves, glial cells are affected during depression, especially in the frontal cortex. Blood flow to the brain is slightly altered, which, together with a slowdown in glucose metabolism in the prefrontal cortex, means that the supply of oxygen and nutrients is reduced, producing a long-term reduction in this area as well. In the same way, the cerebellar amygdala also shrinks.
Finally, as occurs with other disorders such as schizophrenia, the lateral ventricles undergo dilation, occupying the space left by neuronal loss
The reason for this reduction in the brain is due to the activation of a transcription factor known as GATA1 which prevents the expression of a series of genes essential for the creation of synaptic connections This transcription factor interrupts cognitive functions and emotions.
Likewise, other data reflect that recurrent depressive states, as well as stress, cause hypercortisolemia, which if maintained produces neurotoxicity that ends up affecting the neurons of the hippocampus, reducing their number and their interconnection. With that, the hippocampus is reduced, its functions also being affected For this reason, it is essential to treat depressive states early, especially in the case of depression in adolescents, whose brain is not yet fully developed.
In the long run, this reduction of the brain causes a decrease in processing speed and the ability to organize and work with the information obtained from the environment, making it difficult to find an adaptive response to life situations. Likewise, depressive symptoms worsen, both due to the direct effect of the reduction in abilities and due to knowledge of the decrease in ability.
Reasons for hope: the alterations are partly reversible
However, the fact that research has reflected this phenomenon does not imply that depressed people have a permanent deterioration, and treatment (both psychologically and pharmacologically) and the improvement of depressive symptoms may be motivated by neurogenesis and neuronal strengthening. Thus, treating depression can motivate the creation of new neurons, recovering the functionality lost during the course of the depressive disorder.
At a clinical level, the alterations discovered may contribute to clarifying the reason for the delay between the start of antidepressant consumption and their therapeutic effects, requiring slow changes not only in the availability of neurotransmitters but also at a structural level. This research may contribute to the development of new antidepressant drugs, which could be dedicated to inhibiting the GATA1 factor, as well as encouraging the search for professional help before the problem becomes consolidated.
