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Preliminary associations between brain derived neurotrophic factor, memory impairment, functional cognition, and depressive symptoms following severe TBI
  • Published Date:
    Aug 13 2015
  • Source:
    Neurorehabil Neural Repair. 30(5):419-430.


Public Access Version Available on: June 01, 2017 information icon
Please check back on the date listed above.
Details:
  • Pubmed ID:
    26276123
  • Pubmed Central ID:
    PMC4752939
  • Funding:
    R01 HD048162/HD/NICHD NIH HHS/United States
    R49 CE323155/CE/NCIPC CDC HHS/United States
  • Document Type:
  • Description:
    Background

    Traumatic brain injury (TBI) often leads to mood and cognitive complications, impacting functional recovery. Understanding neurobiological alterations common in post-TBI depression (PTD) and cognition may identify novel biomarkers for TBI complications. Brain-derived neurotrophic factor (BDNF) is a likely target based on evidence of reduced BDNF signaling in experimental TBI and depression models and its role in learning and memory.

    Objective

    Evaluate BDNF as a biomarker for PTD, cognitive impairment, and functional cognition in a prospective cohort with severe TBI.

    Methods

    Participants with TBI (n=113) were evaluated for PTD (Patient Health Questionnaire-9), cognitive impairment (cognitive composite score) and functional cognition (Functional Independence Measure–Cognition, FIM-Cog). BDNF levels were measured in cerebrospinal fluid (CSF) and serum 0–6 days post-injury and in serum at 6 and 12 months post-injury.

    Results

    Serum BDNF was reduced after TBI versus controls at all time-points. Acute serum BDNF positively correlated with Memory composites (6 months: r=0.43, p=0.019, n=30; 12 months: r=0.53, p=0.005, n=26) and FIM-Memory scores (6 months: r=0.35, p=0.019, n=45; 12 months: r=0.38, p=0.018, n=38). Acute serum BDNF negatively correlated with 12 month PHQ-9 scores (r=−0.38, p=0.044, n=29). At 12 months, chronic serum BDNF tended to be lower in participants with PTD (p=0.07) and correlated with PHQ-9 scores (r=−0.41, p=0.019, n=32).

    Conclusions

    Acute BDNF associations with memory recovery may implicate hippocampal damage/degeneration. Comparatively, BDNF associations with PTD status were not as strong as associations with PTD severity. Further investigation may delineate longitudinal BDNF patterns, and BDNF responsive treatments, reflecting mood and cognitive recovery following TBI.

  • Supporting Files:
    No Additional Files