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From restoration of neuroplasticity to the treatment of depression: clinical experience.
European Neuropsychopharmacology : the Journal of the European College of Neuropsychopharmacology 2004 December
The adult brain has more plasticity than previously believed. Neurogenesis, growth and branching of dendrites, and remodeling of synaptic contacts in different regions of the brain occur continuously. Numerous studies have reported a decrease in neuroplasticity in depressed patients and/or in animals subjected to stress and to different models of depression. This has led to the proposal of a new approach to the pathophysiology of depression: depression could be the result of the decrease in neuroplasticity in brain structures involved in the control of mood. This new approach to the pathophysiology of depression can lead to better understanding of, or the proposal of more solid hypotheses about, some issues such as the impact of genetics and environmental factors on the occurrence of depressive episodes, the increased risk of depression in patients with somatic diseases in which there are alterations of neuroplasticity, or the increased risk of depressive relapse in depressed patients in partial remission in whom we suspect that neuroplasticity is only partially restored. These observations have also led to the proposal of new hypotheses concerning the mode of action of antidepressant drugs. In this regard, tianeptine is of particular interest. Tianeptine's pharmacological and clinical properties have been extensively studied. Tianeptine has specific neurotrophic properties, and its antidepressant properties have been well demonstrated. Tianeptine provides early relief of anxious symptoms without sedation in depressed patients. The acceptability and safety profiles of tianeptine are appreciated by both physicians and patients; for instance, tianeptine does not induce sexual dysfunction, nausea, or weight gain. It is of interest to focus on what we already know about tianeptine's pharmacological and clinical properties, and to create mechanistic hypotheses about the similarities and differences observed in clinical practice between tianeptine and other antidepressants.
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