Background: Mitochondrial dysfunctions are implicated in the pathophysiology of mood disorders. We measured and examined the following selected mitochondrial parameters: citrate synthase (CS) activity, electron transport system (ETS) complex (complexes I, II, and IV) activities, and mitochondrial respiration in blood platelets. Patients and methods: The analyses were performed for 24 patients suffering from a depressive episode of bipolar affective disorder (BD), compared to 68 patients with MDD and 104 healthy controls. BD and unipolar depression were clinically evaluated using well-established diagnostic scales and questionnaires. Results: The CS, complex II, and complex IV activities were decreased in the depressive episode of BD patients; complex I and complex I/CS ratio were significantly increased compared to healthy controls. We observed significantly decreased complex II and CS activities in patients suffering from MDD compared to controls. Decreased respiration after complex I inhibition and increased residual respiration were found in depressive BD patients compared to controls. Physiological respiration and capacity of the ETS were decreased, and respiration after complex I inhibition was increased in MDD patients, compared to controls. Increased complex I activity can be a compensatory mechanism for decreased CS and complex II and IV activities.
Conclusion: We can conclude that complex I and its abnormal activity contribute to the defects in cellular energy metabolism during a depressive episode of BD. The observed parameters could be used in a panel of biomarkers that could selectively distinguish BD depression from MDD and can be easily examined from blood elements.

Background: According to recent data, dissociation may play an important role in borderline personality disorder (BPD), nevertheless specific influences of psychotropic medication on dissociative symptoms in BPD and their therapeutic indications are largely unknown. The purpose of this study was to assess relationships of dissociative symptoms in BPD patients with levels of psychotropic medication and compare these results with a subgroup of patients with schizophrenia. Materials and methods: In this study, we investigated 52 BPD patients and compared the results with a control group of 36 schizophrenia patients. In all participants, we assessed actual day doses of antipsychotic medication in chlorpromazine equivalents and antidepressant medication in fluoxetine equivalents. Dissociative symptoms were measured by Dissociative Experiences Scale (DES), and other psychopathological symptoms were measured using Health of the Nation Outcome Scales. Results: Results indicate that dissociative symptoms measured by DES were significantly correlated with antipsychotic medication (Spearman R=0.45, P<0.01) in chlorpromazine equivalents and antidepressant medication in fluoxetine equivalents (0.36, P<0.01). These relationships between medication and dissociative symptoms were not found in the control group of schizophrenia patients. Conclusion: The results suggest that levels of antipsychotic medication and antidepressant medication are significantly associated with dissociative symptoms in BPD but not in schizophrenia.

Mitochondria, the cellular powerhouses with bacterial evolutionary origins, play a pivotal role in maintaining neuronal function and cognitive health. Several viruses have developed sophisticated mechanisms to target and disrupt mitochondrial function which contribute to cognitive decline and neurodegeneration. The interplay between viruses and mitochondria might be traced to their co-evolutionary history with bacteria and may reflect ancient interactions that have shaped modern mitochondrial biology.