Abstract
Biological markers of depression, predictors of the response to the drug administration and molecular targets of new antidepressants are searched on the basis of recently known hypotheses of affective disorders. We come out mostly from stimuli of neurotrophic hypothesis and mitochondrial hypothesis.
According to these hypotheses, the leading role in the pathophysiology of mood disorders and therapeutic effects of antidepressants has mitochondria. Mitochondrial dysfunctions and thereby impaired neuronal metabolism can lead to disturbances in neuronal function, plasticity and brain circuitry.
Impaired functions of mitochondria contribute to a wide range of diseases; the role of mitochondria in the pathophysiology of schizophrenia, bipolar disorder, and major depressive disorder is supported by studies investigating genomic differences, changes of energy metabolism and mitochondrial changes included.