Background: Mood disorders, consisting of unipolar and bipolar depression, are complex diseases
characterized by depressed mood and anhedonia. These core symptoms are accompanied in a varying manner by
anxiety, several neurovegetative symptoms and cognitive impairment. Mood disorders are characterized by decreases
in neurogenesis, alteration in synaptic structure and synaptic transmission, all of them regulated by
BDNF, a neurotrophin that performs multiple functions in the adult central nervous system. Many evidences
show that BDNF is critically decreased in mood disorders and plays an essential role in most anti-depressant
treatments. In turn, the transcription factor NF-kB has recently emerged as an important player in the pathophysiology
of depression, with roles in neurogenesis, synaptic transmission and plasticity.
Methodology: We review the bidirectional interactions between BDNF and NF-kB signaling pathways.
Results and Conclusions: We discuss a potential beneficial effect of a positive feedback loop between BDNF and
NF-kB activated pathways in antidepressant action. This could be transduced into the identification of downstream
NF-kB gene targets able to potentiate antidepressant mechanisms, thus guiding the development of novel
and faster acting antidepressant drugs.