Lipid profiling of brain tissue and blood after traumatic brain injury

Nessel, Isabell; Michael‐Titus, Adina T.

doi:10.1016/j.semcdb.2020.08.004

Cited by 26 publications

(21 citation statements)

References 117 publications

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“…In both our single and repeat injury models, PC, PE, and PS decreased in abundance over the first 24 h post-injury. Several species-specific trends unique to the injury model were observed for glycerophospholipids, with human studies supporting these trends [53]. Decreases in phospholipid species via the activation of phospholipases likely contributed to the increased formation of free fatty acids such as arachidonic acid and stearic acid, which increased at all post-injury timepoints in our repeat injury model.…”

Section: Discussionsupporting

confidence: 55%

Lipidome Alterations following Mild Traumatic Brain Injury in the Rat

et al. 2022

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Traumatic brain injury (TBI) poses a major health challenge, with tens of millions of new cases reported globally every year. Brain damage resulting from TBI can vary significantly due to factors including injury severity, injury mechanism and exposure to repeated injury events. Therefore, there is need for robust blood biomarkers. Serum from Sprague Dawley rats was collected at several timepoints within 24 h of mild single or repeat closed head impacts. Serum samples were analyzed via ultra-high-performance liquid chromatography-mass spectrometry (UHPLC-MS) in positive and negative ion modes. Known lipid species were identified through matching to in-house tandem MS databases. Lipid biomarkers have a unique potential to serve as objective molecular measures of injury response as they may be liberated to circulation more readily than larger protein markers. Machine learning and feature selection approaches were used to construct lipid panels capable of distinguishing serum from injured and uninjured rats. The best multivariate lipid panels had over 90% cross-validated sensitivity, selectivity, and accuracy. These mapped onto sphingolipid signaling, autophagy, necroptosis and glycerophospholipid metabolism pathways, with Benjamini adjusted p-values less than 0.05. The novel lipid biomarker candidates identified provide insight into the metabolic pathways altered within 24 h of mild TBI.

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Section: Discussionsupporting

confidence: 55%

Lipidome Alterations following Mild Traumatic Brain Injury in the Rat

et al. 2022

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“…There is growing evidence from experimental and clinical studies that TBI may induce unique alterations in brain lipid species which can be detected in the blood [9,10]. These studies support the concept that changes to lipids and their metabolites in the blood may reflect disruptions to the structural integrity of lipid-rich cell membranes in the brain.…”

Section: Introductionmentioning

confidence: 64%

“…These studies support the concept that changes to lipids and their metabolites in the blood may reflect disruptions to the structural integrity of lipid-rich cell membranes in the brain. Depending on their structure and function, lipids can be classified into two categories: (1) lipids that lack fatty acids (e.g., cholesterol and vitamins) and ( 2) fatty acid-containing lipids [9]. The latter class includes storage lipids (e.g., mono-, di-, and triacylglycerols) and membrane lipids such as glycerophospholipids (e.g., phosphatidylcholine, PC; phosphatidylethanolamine, PE; phosphatidylserine, PS; and phosphatidylinositol, PI) and sphingolipids (e.g., ceramide, sphingomyelin (SM) and glycosphingolipids).…”

Section: Introductionmentioning

confidence: 99%

Plasma Lipid Profiles Change with Increasing Numbers of Mild Traumatic Brain Injuries in Rats

et al. 2022

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Mild traumatic brain injury (mTBI) causes structural, cellular and biochemical alterations which are difficult to detect in the brain and may persist chronically following single or repeated injury. Lipids are abundant in the brain and readily cross the blood-brain barrier, suggesting that lipidomic analysis of blood samples may provide valuable insight into the neuropathological state. This study used liquid chromatography-mass spectrometry (LC-MS) to examine plasma lipid concentrations at 11 days following sham (no injury), one (1×) or two (2×) mTBI in rats. Eighteen lipid species were identified that distinguished between sham, 1× and 2× mTBI. Three distinct patterns were found: (1) lipids that were altered significantly in concentration after either 1× or 2× F mTBI: cholesterol ester CE (14:0) (increased), phosphoserine PS (14:0/18:2) and hexosylceramide HCER (d18:0/26:0) (decreased), phosphoinositol PI(16:0/18:2) (increased with 1×, decreased with 2× mTBI); (2) lipids that were altered in response to 1× mTBI only: free fatty acid FFA (18:3 and 20:3) (increased); (3) lipids that were altered in response to 2× mTBI only: HCER (22:0), phosphoethanolamine PE (P-18:1/20:4 and P-18:0/20:1) (increased), lysophosphatidylethanolamine LPE (20:1), phosphocholine PC (20:0/22:4), PI (18:1/18:2 and 20:0/18:2) (decreased). These findings suggest that increasing numbers of mTBI induce a range of changes dependent upon the lipid species, which likely reflect a balance of damage and reparative responses.

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“…Especially in patients with severe trauma, such as polytrauma with involvement of the central nervous system, the maintenance of metabolism represents a pivotal aspect of therapy [ 192 ]. Following TBI, insulin resistance, hyperglycaemia, ketones and distinct alterations in lipid profiles were commonly observed [ 160 , 196 , 207 , 208 , 209 ], while disturbed metabolic parameters were associated with a decreased neurological outcome in TBI [ 210 ]. As hyperglycaemia was shown in particular to negatively affect regeneration following TSCI and TBI in humans and in vivo [ 211 , 212 , 213 , 214 ], clinical trials were run to investigate the application of insulin to reduce the vital state of hyperglycaemia.…”

Section: Interaction Of Tsci and Tbimentioning

confidence: 99%

Future Perspectives in Spinal Cord Repair: Brain as Saviour? TSCI with Concurrent TBI: Pathophysiological Interaction and Impact on MSC Treatment

Köhli

Otto

Jahn

et al. 2021

Cells

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Traumatic spinal cord injury (TSCI), commonly caused by high energy trauma in young active patients, is frequently accompanied by traumatic brain injury (TBI). Although combined trauma results in inferior clinical outcomes and a higher mortality rate, the understanding of the pathophysiological interaction of co-occurring TSCI and TBI remains limited. This review provides a detailed overview of the local and systemic alterations due to TSCI and TBI, which severely affect the autonomic and sensory nervous system, immune response, the blood–brain and spinal cord barrier, local perfusion, endocrine homeostasis, posttraumatic metabolism, and circadian rhythm. Because currently developed mesenchymal stem cell (MSC)-based therapeutic strategies for TSCI provide only mild benefit, this review raises awareness of the impact of TSCI–TBI interaction on TSCI pathophysiology and MSC treatment. Therefore, we propose that unravelling the underlying pathophysiology of TSCI with concomitant TBI will reveal promising pharmacological targets and therapeutic strategies for regenerative therapies, further improving MSC therapy.

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Lipid profiling of brain tissue and blood after traumatic brain injury

Cited by 26 publications

References 117 publications

Lipidome Alterations following Mild Traumatic Brain Injury in the Rat

Lipidome Alterations following Mild Traumatic Brain Injury in the Rat

Plasma Lipid Profiles Change with Increasing Numbers of Mild Traumatic Brain Injuries in Rats

Future Perspectives in Spinal Cord Repair: Brain as Saviour? TSCI with Concurrent TBI: Pathophysiological Interaction and Impact on MSC Treatment

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