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Research paper

The role of neuroplasticity in the etiology and treatment of depressive disorders

By
Ina Konstantinović ,
Ina Konstantinović

Klinički centar Niš , Niš , Serbia

Milena Trandafilović Orcid logo
Milena Trandafilović

University of Nis , Niš , Serbia

Abstract

Introduction/Aim. Depression is a mood disorder that prevents the patients from performing everyday activities, due to the constant presence of negative feelings. Depression is a worldwide medical disorder which is highly prevalent and has therefore become a huge financial burden for the health system. Biological, psychological, and social factors are most commonly described in the pathophysiology of depressive disorders, although the mechanisms behind depression are still not fully understood. Neuroplasticity is the ability of the nervous system to reorganize its structure and function in response to different stimuli. The aim of this paper was to summarize the available literature on neuroplasticity and its role in the pathophysiology and treatment of depressive disorders. Literature review. Depression is often accompanied by chronic illnesses and is more prevalent in women than men. The most commonly used treatment options for depressive disorders are antidepressants, electroconvulsive therapy, and psychosocial therapy. Neuroplasticity has led to the development of a new clinical discipline called neurorehabilitation, and recent studies have shown a possible link between neuroplasticity and depression. It has been observed that different mechanisms behind neuroplasticity affect the structure of the limbic and paralimbic structures, especially the hippocampus, prefrontal cortex, and amygdala. Conclusion. Limbic and paralimbic structures also undergo structural changes in depressed patients treated with electroconvulsive therapy and medications, which could lead to a better understanding of depressive disorders and how they should be treated.

References

1.
Normann C, Frase S, Haug V, von Wolff G, Clark K, Münzer P, et al. Antidepressants Rescue Stress-Induced Disruption of Synaptic Plasticity via Serotonin Transporter–Independent Inhibition of L-Type Calcium Channels. Biological Psychiatry. 2018;84(1):55–64.

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