Preliminary Associations between Brain-Derived Neurotrophic Factor, Memory Impairment, Functional Cognition, and Depressive Symptoms Following Severe TBI

Michelle D. Failla, Shannon B. Juengst, Patricia M. Arenth, Amy K. Wagner

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Background. Traumatic brain injury (TBI) often leads to mood and cognitive complications, affecting 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. To 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 [PHQ-9]), cognitive impairment (cognitive composite score), and functional cognition (Functional Independence Measure-Cognition, FIM-Cog). BDNF levels were measured in cerebrospinal fluid and serum at 0 to 6 days postinjury and in serum at 6 and 12 months postinjury. 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 =.019, n = 30; 12 months: r = 0.53, P =.005, n = 26) and FIM-Memory scores (6 months: r = 0.35, P =.019, n = 45; 12 months: r = 0.38, P =.018, n = 38). Acute serum BDNF negatively correlated with 12-month PHQ-9 scores (r = '0.38; P =.044; n = 29). At 12 months, chronic serum BDNF tended to be lower in participants with PTD (P =.07) and correlated with PHQ-9 scores (r = '0.41; P =.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.

Original languageEnglish (US)
Pages (from-to)419-430
Number of pages12
JournalNeurorehabilitation and Neural Repair
Volume30
Issue number5
DOIs
StatePublished - Jan 1 2015

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Brain-Derived Neurotrophic Factor
Cognition
Depression
Serum
Traumatic Brain Injury
Health
Biomarkers
Cerebrospinal Fluid
Learning

Keywords

  • BDNF
  • biomarker
  • cognitive impairment
  • depression
  • rehabilomics
  • traumatic brain injury

ASJC Scopus subject areas

  • Rehabilitation
  • Neurology
  • Clinical Neurology

Cite this

Preliminary Associations between Brain-Derived Neurotrophic Factor, Memory Impairment, Functional Cognition, and Depressive Symptoms Following Severe TBI. / Failla, Michelle D.; Juengst, Shannon B.; Arenth, Patricia M.; Wagner, Amy K.

In: Neurorehabilitation and Neural Repair, Vol. 30, No. 5, 01.01.2015, p. 419-430.

Research output: Contribution to journalArticle

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abstract = "Background. Traumatic brain injury (TBI) often leads to mood and cognitive complications, affecting 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. To 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 [PHQ-9]), cognitive impairment (cognitive composite score), and functional cognition (Functional Independence Measure-Cognition, FIM-Cog). BDNF levels were measured in cerebrospinal fluid and serum at 0 to 6 days postinjury and in serum at 6 and 12 months postinjury. 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 =.019, n = 30; 12 months: r = 0.53, P =.005, n = 26) and FIM-Memory scores (6 months: r = 0.35, P =.019, n = 45; 12 months: r = 0.38, P =.018, n = 38). Acute serum BDNF negatively correlated with 12-month PHQ-9 scores (r = '0.38; P =.044; n = 29). At 12 months, chronic serum BDNF tended to be lower in participants with PTD (P =.07) and correlated with PHQ-9 scores (r = '0.41; P =.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.",
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N2 - Background. Traumatic brain injury (TBI) often leads to mood and cognitive complications, affecting 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. To 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 [PHQ-9]), cognitive impairment (cognitive composite score), and functional cognition (Functional Independence Measure-Cognition, FIM-Cog). BDNF levels were measured in cerebrospinal fluid and serum at 0 to 6 days postinjury and in serum at 6 and 12 months postinjury. 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 =.019, n = 30; 12 months: r = 0.53, P =.005, n = 26) and FIM-Memory scores (6 months: r = 0.35, P =.019, n = 45; 12 months: r = 0.38, P =.018, n = 38). Acute serum BDNF negatively correlated with 12-month PHQ-9 scores (r = '0.38; P =.044; n = 29). At 12 months, chronic serum BDNF tended to be lower in participants with PTD (P =.07) and correlated with PHQ-9 scores (r = '0.41; P =.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.

AB - Background. Traumatic brain injury (TBI) often leads to mood and cognitive complications, affecting 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. To 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 [PHQ-9]), cognitive impairment (cognitive composite score), and functional cognition (Functional Independence Measure-Cognition, FIM-Cog). BDNF levels were measured in cerebrospinal fluid and serum at 0 to 6 days postinjury and in serum at 6 and 12 months postinjury. 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 =.019, n = 30; 12 months: r = 0.53, P =.005, n = 26) and FIM-Memory scores (6 months: r = 0.35, P =.019, n = 45; 12 months: r = 0.38, P =.018, n = 38). Acute serum BDNF negatively correlated with 12-month PHQ-9 scores (r = '0.38; P =.044; n = 29). At 12 months, chronic serum BDNF tended to be lower in participants with PTD (P =.07) and correlated with PHQ-9 scores (r = '0.41; P =.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.

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KW - rehabilomics

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