Although there are a number of symptoms that can be used to identify depression, such as a lack of energy or a loss of interest in life, it is not clear what happens in the brain when someone becomes depressed. Despite the emergence of techniques such as functional magnetic resonance imaging (fMRI), which measures changes in blood flow in the brain and relates them to different functions, no significant differences have been found in the structure or connections of this organ between healthy and depressed people. If the characteristics of sick people could be identified, it is reasoned, it would be possible to better understand what causes the disease and how to cure it.
Today, the magazine Nature publish the work An international team of scientists led by Charles Lynch and Conor Liston of Cornell University (USA) has identified a series of brain regions that are almost twice as large in people with depression. These regions are grouped into what is known as the frontostriatal salience network, which connects more superficial areas of the brain, such as the prefrontal cortex, which we need for reasoning, with regions below that are essential for regulating mood or processing information collected by our senses. Together, this network plays a crucial role in identifying and processing relevant stimuli (those that are salient), such as the smell of a food we like or signs of a dangerous situation, and is involved in regulating goal-directed behavior, decision-making, and adapting to changes in the environment.
Until now, fMRI studies had made comparisons between groups of depressed and healthy people, averaging between them, and had not found significant differences between them. Lynch and Liston’s team obtained their novel result thanks to an innovative technique, precision functional mapping, with which they observed a few patients during many spaced sessions, in order to reconstruct what happens at the brain level during the good and bad times of someone with depression. “Traditional studies look at two moments in time and do not give you a complete perspective of what is happening. In this study, we looked at a few subjects and characterized the evolution over time very well,” explains Cesar Caballero-Gaudes, researcher at the Basque Center for Cognition, Brain and Languagein San Sebastian. His team provided measurements of the same quality and taken with the same method of healthy people with whom the Cornell group could compare their depressed subjects.
With this follow-up, the scientists wanted to see if the size of the network was different when the person was well and when they were in a low mood. They discovered that it does not change and that it cannot be modified with antidepressant treatments such as transcranial magnetic stimulation, which applies magnetic fields to the scalp to modulate brain activity. In all cases, the size of the network remained stable. In addition, the authors write, neither the severity of the depressive crisis nor the number of episodes could be related to differences in the size of these brain regions. According to Caballero-Gaudes, this stability “could have diagnostic utility,” because, “in children, it was observed that those who later developed depressive symptoms already presented an expansion of the salience network before showing them.”
The size, shape, or location of the brain’s functional networks has been shown to be controlled in part by genetics, but also by our experiences or environmental influences. “An extreme example of an environmental influence that helps illustrate this idea is that different parts of the body have a certain amount of dedicated space in the primary motor cortex,” explains Charles Lynch. “If a person has an arm amputated, the representation of the amputated limb in the motor cortex will shrink, while the size of the compensatory representation of the intact limb will increase,” he adds.
The fact that the expansion of the salience network is present from early stages of brain development and several years before the first symptoms of depression suggests a strong genetic basis, although this finding does not rule out the possible contribution of stressors or experiences in early life. “This is something we hope to investigate next,” says Lynch. The Cornell researcher speculates that having experiences processed by the salience network too often, such as those that give us immediate pleasure or the direction of our attention toward relevant information, positive or negative, could contribute to depressive symptoms, such as a lack of desire or an exaggerated attention to negative aspects of life and things that scare us.
Although the size of the network did not vary with symptoms of depression, a more in-depth analysis of some patients, who were observed for a year and a half, in some cases with up to 62 MRIs, revealed that there were functional changes between the nodes of the network that could be related to loss of desire or anxiety. This, according to the authors, suggests that the salience network plays a crucial role in depression, not so much due to structural changes, but due to how its nodes communicate during different emotional states.
“There are multiple potential long-term clinical implications, but at the same time, it is important to be clear that we do not expect brain scans to be used to diagnose depression,” Lynch says. “There is still much work to be done, such as determining how specific this effect is for depression compared to other types of psychiatric illness,” he adds. “However,” he concludes, “in the short term, we believe it would be possible to incorporate information about how these functional brain networks are organized in individuals with depression to adjust for the effects of brain scans.” [en tratamientos personalizados] the way we deliver brain stimulation therapies, such as transcranial magnetic stimulation or deep brain stimulation.”
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