Abstract

Mild traumatic brain injury (mTBI) is the most common neurological insult and leads to long-lasting cognitive impairments. The immune system modulates brain functions and plays a key role in cognitive deficits, however, the relationship between TBI-induced changes in inflammation-related cytokine levels and cognitive consequences is unclear. This was investigated in the present study in two cohorts of individuals within 1 week of mTBI (n = 52, n = 43) and 54 matched healthy control subjects. Patients with mTBI were also followed up at 1 and 3 months post-injury. Measures included cognitive assessments and a 9-plex panel of serum cytokines including interleukin (IL)-1β, IL-4, IL-6, IL-8, IL-10, IL-12, chemokine ligand 2 (CCL2), interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α). The contribution of cytokine levels to cognitive function was evaluated by multivariate linear regression analysis. The results showed that serum levels of IL-1β, IL-6, and CCL2 were acutely elevated in mTBI patients relative to controls; CCL2 level was remained high over 3 months whereas IL-1β and IL-6 levels were declined by 3 months post-injury. A high level of CCL2 was associated with greater severity of post-concussion symptoms (which survived in the multiple testing correction); elevated IL-1β was associated with worse working memory in acute phase (which failed in correction); and acute high CCL2 level predicted higher information processing speed at 3 months post-injury (which failed in correction). Thus, acute serum cytokine levels are useful for evaluating post-concussion symptoms and predicting cognitive outcome in participants with mTBI.

Highlights

  • Traumatic brain injury (TBI) is a public health burden and its incidence ranging from 106 to 790 per 1,00,000 people worldwide yearly [1]

  • There were no significant differences between Mild traumatic brain injury (mTBI) Cohorts 1 and 2 in terms of clinical characteristics (Supplementary Table S1)

  • There were no differences in age, gender, and education level between mTBI patients and controls subjects

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Summary

Introduction

Traumatic brain injury (TBI) is a public health burden and its incidence ranging from 106 to 790 per 1,00,000 people worldwide yearly [1]. About 70–90% of TBI are classified as mild TBI (mTBI) [2], which is associated with long-term cognitive impairment including deficits in attention, working memory and executive function. Clarifying the pathogenic changes underlying cognitive impairment following mTBI can lead to the development of more effective treatment. Inflammation played a crucial role in cognitive deficits [5,6,7]; for instance, an elevated level of interleukin (IL)−6 was found to be associated with impaired executive function following stroke [8]. A robust inflammatory response is induced in the injured brain and peripheral circulatory system following a traumatic impact [10], that can persist for many months [11]. MTBI-induced changes of inflammatory cytokines and its association with cognitive consequences have not been investigated

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