The monoamine hypothesis has been the dominant pathophysiological model for half a century 2. Major depressive disorder (MDD) is the leading cause of disability worldwide 1, but the biological underpinnings of the disorder are still largely unknown. The finding adds new information on the pathophysiology of major depressive disorder. Our results suggest that previously reported cross-sectional molecular imaging findings of the serotonin transporter in depression most likely reflect the depressive state, rather than a permanent trait. Our main finding was that patients suffering from a depressive episode show an overall increase in cerebral serotonin transporter availability as symptoms are alleviated. No significant difference between patients at baseline and healthy controls were observed in the composite region ( p = 0.97) or the median raphe ( p = 0.95). MADAM binding in patients increased in the composite region after treatment ( p = 0.01), while no change was observed in the median raphe ( p = 0.51). Depression severity decreased following treatment ( p < 0.001). All image analyses and confirmatory statistical tests were preregistered. Differences before and after treatment, as well as between patients and controls, were assessed in a composite cerebral region and in the median raphe nuclei. Cerebellum was used as reference to calculate the binding potential. In all, 17 matched healthy control subjects were examined once. We examined 17 patients with major depressive disorder with positron emission tomography using MADAM, a radioligand that binds to the serotonin transporter, before and after treatment with internet-based cognitive behavioral therapy. a trait), or only at the time of the depressive episode (i.e. Whether or not this difference also is present before disease onset and after remission (i.e. Molecular imaging studies have shown low cerebral concentration of serotonin transporter in patients suffering from depression, compared to healthy control subjects.

Serotonin transporter