Systemic inflammation in traumatic brain injury predicts poor cognitive function

Xu, Wende; Yue, Shenglei; Wang, Peng; Wen, Bin; Zhang, Xiaojue

doi:10.1002/iid3.577

Cited by 12 publications

(6 citation statements)

References 32 publications

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“…PNDs are an ordinary postoperative complication among old patients. e release of systemic acute inflammation and proinflammatory cytokines after the operation are critical factors [1,18]. Peripheral operation and remote organ injury induce neuroinflammation [19], which is a critical factor in cognitive impairment, especially in the hippocampus [20,21].…”

Section: Discussionmentioning

confidence: 99%

Impact of Dexamethasone Preconditioning on Prevention of Development of Cognitive Impairment following Acute Inflammation

Cheng

Song

Liu

et al. 2022

Contrast Media & Molecular Imaging

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To assess the preventive role of dexamethasone (Dex) in the development of neuroinflammation and concomitant neurocognitive disorders following acute inflammation. C57BL6 mice were fallen into the sham group, ischemia-reperfusion (I/R) group, and I/R + Dex group randomly. In the end, behavioral alterations were assessed with the Morris water maze (MWM) test, passive avoidance test (PAT), and open field test (OFT). The serum levels of IL-1β and TNF-α were detected by ELISA. Immunofluorescence was adopted to observe the NF-kB expression in the hippocampus. In addition, TLR4, NF-kB, CD68, and CD206 were examined by Western blot. The cognitive ability of mice can be impaired by tourniquet-induced acute inflammation, and these changes were prevented by Dex. Compared to the I/R group, Dex pretreatment could decrease levels of IL-1β and TNF-α proteins in serum. Besides, Dex preconditioning significantly decreased the utterance of NF-kB immunoreactive cells and TLR4, NF-kB, and CD68 overexpression in the hippocampus. Dex partly through inhibiting microglia transformation to the M1 polarization state and inactivating the TLR4/NF-kB pathway attenuates the cognitive disorders in mice.

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Section: Discussionmentioning

confidence: 99%

Impact of Dexamethasone Preconditioning on Prevention of Development of Cognitive Impairment following Acute Inflammation

Cheng

Song

Liu

et al. 2022

Contrast Media & Molecular Imaging

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“…It is estimated that in the United States there are 3.17 million people suffering with long term disability resulting from TBI, representing an annual economic impact in excess of Pharmaceuticals 2022, 15, 660 2 of 18 $56 billion [6]. TBI presents as a biphasic pathology in which the effects of the initial traumatic insult results in persistent inflammation and the chronic activation of the innate immune system [7][8][9][10]. Primary injury involves the release of damage associated molecular patterns (DAMPS) from injured tissue resulting in the activation of the innate immune response and formation of the inflammasome [11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Inflammatory Biomarkers of Traumatic Brain Injury

et al. 2022

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Traumatic brain injury (TBI) has a complex pathology in which the initial injury releases damage associated proteins that exacerbate the neuroinflammatory response during the chronic secondary injury period. One of the major pathological players in the inflammatory response after TBI is the inflammasome. Increased levels of inflammasome proteins during the acute phase after TBI are associated with worse functional outcomes. Previous studies reveal that the level of inflammasome proteins in biological fluids may be used as promising new biomarkers for the determination of TBI functional outcomes. In this study, we provide further evidence that inflammatory cytokines and inflammasome proteins in serum may be used to determine injury severity and predict pathological outcomes. In this study, we analyzed blood serum from TBI patients and respective controls utilizing Simple Plex inflammasome and V-PLEX inflammatory cytokine assays. We performed statistical analyses to determine which proteins were significantly elevated in TBI individuals. The receiver operating characteristics (ROC) were determined to obtain the area under the curve (AUC) to establish the potential fit as a biomarker. Potential biomarkers were then compared to documented patient Glasgow coma scale scores via a correlation matrix and a multivariate linear regression to determine how respective biomarkers are related to the injury severity and pathological outcome. Inflammasome proteins and inflammatory cytokines were elevated after TBI, and the apoptosis-associated speck like protein containing a caspase recruitment domain (ASC), interleukin (IL)-18, tumor necrosis factor (TNF)-α, IL-4 and IL-6 were the most reliable biomarkers. Additionally, levels of these proteins were correlated with known clinical indicators of pathological outcome, such as the Glasgow coma scale (GCS). Our results show that inflammatory cytokines and inflammasome proteins are promising biomarkers for determining pathological outcomes after TBI. Additionally, levels of biomarkers could potentially be utilized to determine a patient’s injury severity and subsequent pathological outcome. These findings show that inflammation-associated proteins in the blood are reliable biomarkers of injury severity that can also be used to assess the functional outcomes of TBI patients.

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“…Extensive inflammatory cytokine release is observed following TBI, functioning as an innate mechanism to promote self-healing and stabilize the parenchymal microenvironment of the CNS [ 74 , 75 ]. However, chronic inflammation can prolong clinical recovery and predispose patients to additional deficits [ 36 , 76 ].…”

Section: Discussionmentioning

confidence: 99%

Traumatic Brain Injury, Sleep, and Melatonin—Intrinsic Changes with Therapeutic Potential

et al. 2023

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Traumatic brain injury (TBI) is one of the most prevalent causes of morbidity in the United States and is associated with numerous chronic sequelae long after the point of injury. One of the most common long-term complaints in patients with TBI is sleep dysfunction. It is reported that alterations in melatonin follow TBI and may be linked with various sleep and circadian disorders directly (via cellular signaling) or indirectly (via free radicals and inflammatory signaling). Work over the past two decades has contributed to our understanding of the role of melatonin as a sleep regulator and neuroprotective anti-inflammatory agent. Although there is increasing interest in the treatment of insomnia following TBI, a lack of standardization and rigor in melatonin research has left behind a trail of non-generalizable data and ambiguous treatment recommendations. This narrative review describes the underlying biochemical properties of melatonin as they are relevant to TBI. We also discuss potential benefits and a path forward regarding the therapeutic management of TBI with melatonin treatment, including its role as a neuroprotectant, a somnogen, and a modulator of the circadian rhythm.

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Systemic inflammation in traumatic brain injury predicts poor cognitive function

Cited by 12 publications

References 32 publications

Impact of Dexamethasone Preconditioning on Prevention of Development of Cognitive Impairment following Acute Inflammation

Impact of Dexamethasone Preconditioning on Prevention of Development of Cognitive Impairment following Acute Inflammation

Inflammatory Biomarkers of Traumatic Brain Injury

Traumatic Brain Injury, Sleep, and Melatonin—Intrinsic Changes with Therapeutic Potential

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