BDNF and NGF Signalling in Early Phases of Psychosis: Relationship With Inflammation and Response to Antipsychotics After 1 Year

Schizophr Bull. 2016 Jan;42(1):142-51. doi: 10.1093/schbul/sbv078. Epub 2015 Jun 30.

Abstract

Previous studies have indicated systemic deregulation of the proinflammatory or anti-inflammatory balance in individuals with first-episode psychosis (FEP) that persists 12 months later. To identify potential risk/protective factors and associations with symptom severity, we assessed possible changes in plasma levels of neurotrophins (brain-derived neurotrophic factor [BDNF] and nerve growth factor [NGF]) and their receptors in peripheral blood mononuclear cells (PBMCs). Expression of the 2 forms of BDNF receptors (active TrkB-FL and inactiveTrkB-T1) in PBMCs of FEP patients changed over time, TrkB-FL expression increasing by 1 year after diagnosis, while TrkB-T1 expression decreased. The TrkB-FL/TrkB-T1 ratio (hereafter FL/T1 ratio) increased during follow-up in the nonaffective psychosis group only, suggesting different underlying pathophysiological mechanisms in subgroups of FEP patients. Further, the expression of the main NGF receptor, TrkA, generally increased in patients at follow-up. After adjusting for potential confounders, baseline levels of inducible isoforms of nitric oxide synthase, cyclooxygenase, and nuclear transcription factor were significantly associated with the FL/T1 ratio, suggesting that more inflammation is associated with higher values of this ratio. Interestingly, the FL/T1 ratio might have a role as a predictor of functioning, a regression model of functioning at 1 year suggesting that the effect of the FL/T1 ratio at baseline on functioning at 1 year depended on whether patients were treated with antipsychotics. These findings may have translational relevance; specifically, it might be useful to assess the expression of TrkB receptor isoforms before initiating antipsychotic treatment in FEPs.

Keywords: BDNF; NGF; antipsychotic; first-episode psychosis; inflammation; schizophrenia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Affective Disorders, Psychotic / drug therapy*
  • Affective Disorders, Psychotic / immunology
  • Affective Disorders, Psychotic / metabolism
  • Antipsychotic Agents / therapeutic use*
  • Brain-Derived Neurotrophic Factor / metabolism*
  • Case-Control Studies
  • Cyclooxygenase 2 / immunology
  • Cyclooxygenase 2 / metabolism
  • Female
  • Humans
  • Inflammation
  • Leukocytes, Mononuclear / metabolism
  • Longitudinal Studies
  • Male
  • NF-kappa B / immunology
  • NF-kappa B / metabolism
  • Nerve Growth Factor / metabolism*
  • Nitric Oxide Synthase Type II / immunology
  • Nitric Oxide Synthase Type II / metabolism
  • Prognosis
  • Prostaglandin D2 / analogs & derivatives
  • Prostaglandin D2 / immunology
  • Prostaglandin D2 / metabolism
  • Protein Isoforms
  • Psychotic Disorders / drug therapy*
  • Psychotic Disorders / immunology
  • Psychotic Disorders / metabolism
  • Receptor, trkA / metabolism*
  • Receptor, trkB / metabolism*
  • Regression Analysis
  • Signal Transduction
  • Young Adult

Substances

  • 15-deoxyprostaglandin J2
  • Antipsychotic Agents
  • Brain-Derived Neurotrophic Factor
  • NF-kappa B
  • NGF protein, human
  • Protein Isoforms
  • BDNF protein, human
  • Nerve Growth Factor
  • NOS2 protein, human
  • Nitric Oxide Synthase Type II
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Receptor, trkA
  • Receptor, trkB
  • Prostaglandin D2