Abstract
Neuroplasticity is a fundamental mechanism of neuronal adaptation to external and internal stimuli. Neuronal plasticity is disrupted in mood disorders and as a result of chronic stress.
According to new biochemical hypotheses leading role in pathophysiology of mood disorders and therapeutic effects of antidepressants could be awarded to disturbed monoamine neurotransmission, dysfunction in energy metabolism of neurons, and changes in concentration of transcription factor CREB, brain-derived neurotrophic factor (BDNF) or other components involved in neuroplasticity and apoptosis. Role of mitochondrial dysfunctions is implicated due to high energy demand of processes related to the recovery of the neuroplasticity.
The aim of present study is to discover the relation between these biochemical parameters and clinical evaluation during depressive episode.