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A group of researchers at the Salk Institute discovered differences in neuronal growth patterns in patients resistant to selective serotonin reuptake inhibitors (SSRIs), a clbad of antidepressants used to treat major depressive disorders, also called major depression.
Despite its effectiveness, about thirty percent of patients with clinical depression do not respond well to SSRIs. Although the cause of depression is not known, it can be correlated with the serotoninergic circuit in the brain. SSRIs increase the serotonin neurotransmitter at the level of synapsis, thus relieving the symptoms of depression.
"With each new study, we are getting closer to a more complete understanding of the complex neural circuits underlying neuropsychiatric diseases, including major depression," said Rusty Gage, the lead author of the study. ;study.
"This document, along with another one we recently published, not only provides information on this common treatment, but also suggests that other drugs, such as serotonergic antagonists, might be additional options for some patients."
As part of this study, researchers examined 800 patients with major depression and selected the most extreme cases of SSRI response, patients with significant improvement and those who did not receive therapeutic effects. The researchers took skin samples and reprogrammed the cells into induced pluripotent stem cells (iPSCs) to create serotoninergic neurons.
In addition, the researchers studied the serotonergic targets in the patient's serotonergic neurons, the protein that carries it, and the enzyme that breaks it down. Between the groups, they found a difference in the response of the neurons depending on the shape.
"The neurons of the non-responders SSRIs had neuronal projections longer than those of the responders. Gene badysis revealed that non-responders SSRIs also had low levels of key genes (protocadherins PCDHA6 and PCDHA8) involved in the formation of neural circuits, "the study revealed.
"When these genes were rendered non-functional in serotonergic neurons (mimicking the low levels of previously observed genes), neurons developed the same exceptionally long projections in non-responders SSRIs."
"These abnormal features could lead to excessive neuronal communication in certain areas of the brain and inadequate in other parts, impairing communication within the serotoninergic circuit and explaining why SSRIs do not always work to treat CT."
"These findings contribute to a new way of looking at, understanding and treating depression."
The results were published in Molecular Psychiatry.
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