Models of traumatic brain injury-highlights and drawbacks

Zhao, Qinghui; Zhang, Jianhua; Li, Huige; Li, Hongru; Xie, Fei

doi:10.3389/fneur.2023.1151660

Cited by 20 publications

(9 citation statements)

References 87 publications

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“…A variety of methodologies for administering traumatic injury to the brain have been employed in the study of the mechanisms and therapeutics of TBI and regeneration [ 116 , 139 , 140 , 141 ]. These can be considered diffuse or focal injury models.…”

Section: Models and Organisms Used For The Study Of Neurotrauma And R...mentioning

confidence: 99%

“…Cortical stab injury, either through the skull or following craniotomy, is performed with a controlled injury delivered by typically a scalpel [ 141 ]. Lateral fluid percussion injury is delivered by a pendulum device that “percusses” a volume of sterile fluid onto the cortical surface, which somewhat diffuses the injury across a wider area than CCI [ 116 , 139 , 140 , 141 ]. Penetrating ballistic-like brain injury utilises the inflation of a balloon catheter inflated after cannulation of the brain to a subcortical depth.…”

Section: Models and Organisms Used For The Study Of Neurotrauma And R...mentioning

confidence: 99%

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Neurotrauma—From Injury to Repair: Clinical Perspectives, Cellular Mechanisms and Promoting Regeneration of the Injured Brain and Spinal Cord

Stevens,

Belli,

Ahmed

2024

Biomedicines

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Traumatic injury to the brain and spinal cord (neurotrauma) is a common event across populations and often causes profound and irreversible disability. Pathophysiological responses to trauma exacerbate the damage of an index injury, propagating the loss of function that the central nervous system (CNS) cannot repair after the initial event is resolved. The way in which function is lost after injury is the consequence of a complex array of mechanisms that continue in the chronic phase post-injury to prevent effective neural repair. This review summarises the events after traumatic brain injury (TBI) and spinal cord injury (SCI), comprising a description of current clinical management strategies, a summary of known cellular and molecular mechanisms of secondary damage and their role in the prevention of repair. A discussion of current and emerging approaches to promote neuroregeneration after CNS injury is presented. The barriers to promoting repair after neurotrauma are across pathways and cell types and occur on a molecular and system level. This presents a challenge to traditional molecular pharmacological approaches to targeting single molecular pathways. It is suggested that novel approaches targeting multiple mechanisms or using combinatorial therapies may yield the sought-after recovery for future patients.

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Section: Models and Organisms Used For The Study Of Neurotrauma And R...mentioning

confidence: 99%

Section: Models and Organisms Used For The Study Of Neurotrauma And R...mentioning

confidence: 99%

Neurotrauma—From Injury to Repair: Clinical Perspectives, Cellular Mechanisms and Promoting Regeneration of the Injured Brain and Spinal Cord

Stevens,

Belli,

Ahmed

2024

Biomedicines

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“…The hippocampus is highly involved in memory formation, which is often disrupted after TBI (25,26). However, many previous approaches use more generalized TBI models, such as mechanical-force weight drop, fluid percussion, and blast-induced injury (27). Needle-induced cavitation (NIC) is a technique allowing for highly localized brain injury (5,28).…”

Section: Precision Model For Studying Traumatic Brain Injurymentioning

confidence: 99%

Acute and Chronic Neural and Glial Response to Mild Traumatic Brain Injury in the Hippocampus

Dougan,

Roberts,

Crosby

et al. 2024

Preprint

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Traumatic brain injury (TBI) is an established risk factor for developing neurodegenerative disease. However, how TBI leads from acute injury to chronic neurodegeneration is limited to post-mortem models. There is a lack of connections between in vitro and in vivo TBI models that can relate injury forces to both macroscale tissue damage and brain function at the cellular level. Needle-induced cavitation (NIC) is a technique that can produce small cavitation bubbles in soft tissues, which allows us to relate small strains and strain rates in living tissue to ensuing acute and chronic cell death, tissue damage, and tissue remodeling. Here, we applied NIC to mouse brain slices to create a new model of TBI with high spatial and temporal resolution. We specifically targeted the hippocampus, which is a brain region critical for learning and memory and an area in which injury causes cognitive pathologies in humans and rodent models. By combining NIC with patch-clamp electrophysiology, we demonstrate that NIC in the Cornu Ammonis (CA)3 region of the hippocampus dynamically alters synaptic release onto CA1 pyramidal neurons in a cannabinoid 1 receptor (CB1R)-dependent manner. Further, we show that NIC induces an increase in extracellular matrix proteins associated with neural repair that is mitigated by CB1R antagonism. Together, these data lay the groundwork for advanced approaches in understanding how TBI impacts neural function at the cellular level, and the development of treatments that promote neural repair in response to brain injury.

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“…Integrating various in vitro and in vivo models could increase the chances of obtaining reliable and promising results, minimizing the risk of false positive neuroprotective effects from drugs and treatments. However, in vitro TBI models also have limitations, including the potential for cell damage during sampling [134].…”

Section: Challenges and Future Prospectsmentioning

confidence: 99%

Innovative Insights into Traumatic Brain Injuries: Biomarkers and New Pharmacological Targets

Silvestro,

Raffaele,

Quartarone

et al. 2024

IJMS

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A traumatic brain injury (TBI) is a major health issue affecting many people across the world, causing significant morbidity and mortality. TBIs often have long-lasting effects, disrupting daily life and functionality. They cause two types of damage to the brain: primary and secondary. Secondary damage is particularly critical as it involves complex processes unfolding after the initial injury. These processes can lead to cell damage and death in the brain. Understanding how these processes damage the brain is crucial for finding new treatments. This review examines a wide range of literature from 2021 to 2023, focusing on biomarkers and molecular mechanisms in TBIs to pinpoint therapeutic advancements. Baseline levels of biomarkers, including neurofilament light chain (NF-L), ubiquitin carboxy-terminal hydrolase-L1 (UCH-L1), Tau, and glial fibrillary acidic protein (GFAP) in TBI, have demonstrated prognostic value for cognitive outcomes, laying the groundwork for personalized treatment strategies. In terms of pharmacological progress, the most promising approaches currently target neuroinflammation, oxidative stress, and apoptotic mechanisms. Agents that can modulate these pathways offer the potential to reduce a TBI’s impact and aid in neurological rehabilitation. Future research is poised to refine these therapeutic approaches, potentially revolutionizing TBI treatment.

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Models of traumatic brain injury-highlights and drawbacks

Cited by 20 publications

References 87 publications

Neurotrauma—From Injury to Repair: Clinical Perspectives, Cellular Mechanisms and Promoting Regeneration of the Injured Brain and Spinal Cord

Neurotrauma—From Injury to Repair: Clinical Perspectives, Cellular Mechanisms and Promoting Regeneration of the Injured Brain and Spinal Cord

Acute and Chronic Neural and Glial Response to Mild Traumatic Brain Injury in the Hippocampus

Innovative Insights into Traumatic Brain Injuries: Biomarkers and New Pharmacological Targets

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