Cerebrospinal Fluid as a Platform for Biomarker Identification in Traumatic Brain Injury

Thelin, Eric P.; Lindblad, Caroline

doi:10.1007/978-3-030-87302-8_78-1

Cited by 1 publication

(3 citation statements)

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“…One tentative technique that is feasible for early implementation is fluid biomarkers that are readily available to quantify across both CSF and cerebral microdialysis. Numerous techniques are available and were recently reviewed [ 108 ]. This would naturally implement neuroinflammation in clinical decision making.…”

Section: Discussionmentioning

confidence: 99%

“…[ 17 ]. Different protein quantification techniques hold promise for protein biomarker discovery in CSF following trauma [ 108 ]. In a uniquely large cohort of patients, Lindblad and colleagues assessed n = 177 proteins observationally following human severe TBI across both CSF and blood.…”

Section: Interleukin-1 Receptor Antagonist Treatment Shifts the Infla...mentioning

confidence: 99%

“…To summarize, robust clinical data demonstrate an injury-dependent altered neuroinflammatory response in the injured brain [ 17 , 58 , 108 ]. This response is CNS-specific and production of at least some core cytokines occurs in CNS compartments such as CSF and brain extracellular fluid [ 111 ].…”

Section: Interleukin-1 Receptor Antagonist Treatment Shifts the Infla...mentioning

confidence: 99%

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Interleukin-1 Receptor Antagonist as Therapy for Traumatic Brain Injury

Lindblad,

Rostami,

Helmy

2023

Neurotherapeutics

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Traumatic brain injury is a common type of acquired brain injury of varying severity carrying potentially deleterious consequences for the afflicted individuals, families, and society. Following the initial, traumatically induced insult, cellular injury processes ensue. These are believed to be amenable to treatment. Among such injuries, neuroinflammation has gained interest and has become a specific focus for both experimental and clinical researchers. Neuroinflammation is elicited almost immediately following trauma, and extend for a long time, possibly for years, after the primary injury. In the acute phase, the inflammatory response is characterized by innate mechanisms such as the activation of microglia which among else mediates cytokine production. Among the earliest cytokines to emerge are the interleukin- (IL-) 1 family members, comprising, for example, the agonist IL-1β and its competitive antagonist, IL-1 receptor antagonist (IL-1ra). Because of its early emergence following trauma and its increased concentrations also after human TBI, IL-1 has been hypothesized to be a tractable treatment target following TBI. Ample experimental data supports this, and demonstrates restored neurological behavior, diminished lesion zones, and an attenuated inflammatory response following IL-1 modulation either through IL-1 knock-out experiments, IL-1β inhibition, or IL-1ra treatment. Of these, IL-1ra treatment is likely the most physiological. In addition, recombinant human IL-1ra (anakinra) is already approved for utilization across a few rheumatologic disorders. As of today, one randomized clinical controlled trial has utilized IL-1ra inhibition as an intervention and demonstrated its safety. Further clinical trials powered for patient outcome are needed in order to demonstrate efficacy. In this review, we summarize IL-1 biology in relation to acute neuroinflammatory processes following TBI with a particular focus on current evidence for IL-1ra treatment both in the experimental and clinical context.

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Section: Discussionmentioning

confidence: 99%

Section: Interleukin-1 Receptor Antagonist Treatment Shifts the Infla...mentioning

confidence: 99%