Effect of Oxcarbazepine on Serum Brain Derived Neurotrophic Factor (BDNF) in Bipolar Disorder

Bipolar disorder (BD) is a chronic psychiatric illness of partially unknown pathophysiology. BD likely involves, at a molecular and cellular level, dysfunctions of critical neurotrophic, cellular plasticity and resilience pathways and neuroprotective processes. Abnormalities of neurotrophins (NTs) and other trophic factors orchestrate important alterations which could be implicated in the etiology of BD. As consistently reported in post-mortem studies, these modifications are generally associated with the disruption of distinct subregions and functions of the brain, one of which is the deregulation of neurotrophins. NTs are capable of signaling neurons, glial cells and other cellular systems to enable survival, differentiation and growth. BDNF is one of the most studied and abundant NTs in the brain, which plays an important role in a variety of neural processes during the development of both animals and humans. Initially, BDNF is important for neurogenesis, neuronal survival, and normal maturation of neural development pathways. In the adult, BDNF is not only important for synaptic plasticity and dendritic growth, but also for long-term memory consolidation. Several studies have proved that BDNF is significantly reduced in manic, hypomanic or depressive stages of BD, whereas euthymic patients exhibit BDNF levels similar to healthy controls. Rafael T. de Sousa et al have observed a significant increase in serum BDNF levels after 28 days of lithium monotherapy in patients with BD and suggested neuroprotective role of lithium due to its direct regulatory effect on BDNF. Oxcarbazepine is a commonly used mood stabilizer which has demonstrated comparable efficacy to divalproate sodium and better tolerability profile but till date there is no study on its effect on BDNF. The aim of the present study is to evaluate the change in serum BDNF level with oxcarbazepine monotherapy in bipolar disorder and to explore the possibility of its neuroprotective effect.