title: [The neurotrophic hypothesis of depression].
abstract: BACKGROUND
  The neurotrophic hypothesis of depression postulates that neuronal plasticity is a key factor in the development of depression and in the clinical response to antidepressants. Brain-derived neurotrophic factor (BDNF) is an important protein in this process.
  
  
  OBJECTIVE
  To provide a survey of the current scientific view regarding the neurotrophic hypothesis of depression.
  
  
  METHODS
  We studied the literature using PubMed.
  
  
  RESULTS
  The serum bdnf level was found to be consistently lower in depressed patients compared to healthy controls. In short open-label antidepressant treatment trials the bdnf levels were found to be higher post-treatment than pre-treatment. Longitudinal analysis of a large naturalistic cohort study revealed that it was more likely that bdnf serum levels were lower as a result of depression than that they represented an etiological factor for the illness.
  
  
  CONCLUSIONS
  These findings show that the neurotrophic hypothesis of depression is more complex than previously assumed. Animal studies have shown a correlation between stress, diminished bdnf expression in the brain and depressive-like behavior. Studies in humans, on the other hand, particularly those with a longitudinal design, suggest that the decrease in serum bdnf is a consequence of the depression rather than vice versa. This is in sharp contrast to the original assumptions of the neurotrophic hypothesis.
authors.forename: B A A
authors.initials: BA
authors.lastname: Bus
authors.forename: M L
authors.initials: ML
authors.lastname: Molendijk
mesh_terms: D000928:Antidepressive Agents / Q000627:therapeutic use; D019208:Brain-Derived Neurotrophic Factor / Q000097:blood*; D003865:Major Depressive Disorder / Q000097:blood* / Q000188:drug therapy; D006801:Humans
chemical_list: D000928:Antidepressive Agents; D019208:Brain-Derived Neurotrophic Factor