BDNF/NF-κB signaling in the neurobiology of depression

Ariel Caviedes, Carlos Lafourcade, Claudio Soto, Ursula Wyneken

Research output: Contribution to journalScientific reviewpeer-review

65 Scopus citations

Abstract

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.
Original languageAmerican English
Pages (from-to)3154-3163
Number of pages10
JournalCurrent Pharmaceutical Design
Volume23
Issue number21
DOIs
StatePublished - 1 Jan 2017

Keywords

  • Anhedonia
  • BDNF
  • Mood disorders
  • Neurogenesis
  • NF-κB
  • Plasticity

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