Recent advances in traumatic brain injury

Khellaf, Abdelhakim; Khan, Danyal Z.; Helmy, Adel

doi:10.1007/s00415-019-09541-4

Cited by 296 publications

(205 citation statements)

References 73 publications

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“…The secondary brain injury is due to the neuroimmune and inflammatory response to TBI [2]. TBI may disrupt normal functions of the brain and other organs [3]. The severity of a TBI pathogenesis may range from "mild" with a slight change in mental status or consciousness to "severe" with unconsciousness or amnesia after the brain injury.…”

Section: Introductionmentioning

confidence: 99%

“…The severity of a TBI pathogenesis may range from "mild" with a slight change in mental status or consciousness to "severe" with unconsciousness or amnesia after the brain injury. The acute and chronic effects of brain injuries vary significantly from person to person or in animal models of TBI [3,4]. Therefore, no two TBIs are the same with reference to the neuroimmune response and disease severity.…”

Section: Introductionmentioning

confidence: 99%

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Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury

Kempuraj

Ahmed

Selvakumar

et al. 2020

Mediators of Inflammation

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Traumatic brain injury (TBI) is one of the major health problems worldwide that causes death or permanent disability through primary and secondary damages in the brain. TBI causes primary brain damage and activates glial cells and immune and inflammatory cells, including mast cells in the brain associated with neuroinflammatory responses that cause secondary brain damage. Though the survival rate and the neurological deficiencies have shown significant improvement in many TBI patients with newer therapeutic options, the underlying pathophysiology of TBI-mediated neuroinflammation, neurodegeneration, and cognitive dysfunctions is understudied. In this study, we analyzed mast cells and neuroinflammation in weight drop-induced TBI. We analyzed mast cell activation by toluidine blue staining, serum chemokine C-C motif ligand 2 (CCL2) level by enzyme-linked immunosorbent assay (ELISA), and proteinase-activated receptor-2 (PAR-2), a mast cell and inflammation-associated protein, vascular endothelial growth factor receptor 2 (VEGFR2), and blood-brain barrier tight junction-associated claudin 5 and Zonula occludens-1 (ZO-1) protein expression in the brains of TBI mice. Mast cell activation and its numbers increased in the brains of 24 h and 72 h TBI when compared with sham control brains without TBI. Mouse brains after TBI show increased CCL2, PAR-2, and VEGFR2 expression and derangement of claudin 5 and ZO-1 expression as compared with sham control brains. TBI can cause mast cell activation, neuroinflammation, and derangement of tight junction proteins associated with increased BBB permeability. We suggest that inhibition of mast cell activation can suppress neuroimmune responses and glial cell activation-associated neuroinflammation and neurodegeneration in TBI.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury

Kempuraj

Ahmed

Selvakumar

et al. 2020

Mediators of Inflammation

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“…Today in the world one of the leading causes of death and disability among the working-age population of the earth is traumatic brain injury (TBI). Especially the situation has changed in the last 10-15 years [1,2], the number of man-made disasters, natural disasters, acts of terrorism and military conflicts on earth has sharply increased, which is accompanied by a high degree of trauma, in the structure of which the damage to the skull and brain is more than 1/3 of all injuries [2][3][4]. In different countries, traumatism in the structure of mortality follows cardiovascular and oncological diseases, but the economic and medico-social damage caused to society brings TBI to the first place.…”

Section: Problem Descriptionmentioning

confidence: 99%

Analysis of the Role of Central Cholinoreactivity in Experimental Traumatic Brain Injury

Khudoley¹

2020

ScienceRise

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The aim of the research. To study effects of activation and inhibition of the central cholinergic systems (CCS) in traumatic brain injury (TBI). Studied problem. To investigate the influence of the reactivity of the central cholinergic systems on the course of the acute period of traumatic brain injury, in an acute experiment on laboratory animals in vivo. The main scientific results. It was found that in the acute period of TBI (the first three days), both activation and blockade of CCS led to a decrease in mortality, which was statistically confirmed only for their activation. The control group was characterized by the progression of neurological deficit, which was realized due to motor disorders and reflex sphere. Upon activation of the CCS, the degree of neurological deficit was significantly less than in other groups, but, nevertheless, it increased from 48 hours after the injury, as regards behavioral and consciousness disorders. Inhibition of cholinergic systems led to a sharp increase in neurological deficit in all areas immediately after injury, to a greater extent due to reflex disorders. This, together with a high mortality rate, indicated a negative effect of the pharmacological shutdown of CCS in TBI. The area of practical use of the research results. The obtained results will allow a deeper study of the influence of the central cholinergic systems on the course and descent of TBI. To develop effective methods of pharmacological correction in the treatment of patients in the acute period of TBI. Innovative technological product: pathogenetically substantiated medical treatment of the acute period of traumatic brain injury, development of new methods of pharmacological neuroprotection for persons with a priori high risk of injury, development of effective options for reducing mortality and disability from TBI. Scope of the innovative technological product. The important role of CCS in the realization of the response of the central nervous system to TBI was established, and the possibility of using pharmacological stimulation of the central nervous system with cholinomimetics of the central type of action was justified.

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“…For years, despite decreasing incidence of severe types, traumatic brain injury (TBI) is still the disease that causes the morbidity and mortality around world 1 , 2 . Canonically, researchers mainly pour energy and captivity into exploring the neural recovery methods, such as medicine or cell treatment to enhance the neurogenesis 3 , whereas little achievements were acquired 4 .…”

Section: Introductionmentioning

confidence: 99%

Niche Cells Crosstalk In Neuroinflammation After Traumatic Brain Injury

Jia¹,

Wang²,

Ye³

et al. 2021

Int. J. Biol. Sci.

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Traumatic brain injury (TBI) is recognized as the disease with high morbidity and disability around world in spite of the work ongoing in neural protection. Due to heterogeneity among the patients, it's still hard to acquire satisfying achievements in clinic. Neuroinflammation, which exists since primary injury occurs, with elusive duality, appear to be of significance from recovery of injury to neurogenesis. In recent years, studied have revealed that communication in neurogenic niche is more than “cell to cell” communication, and study on NSCs represent it as central role in the progress of neural regeneration. Hence, the neuroinflammation-affecting crosstalk after TBI, and clarifying definitive role of NSCs in the course of regeneration is a promising subject for researchers, for its great potential in overcoming the frustrating status quo in clinic, promoting welfare of TBI patient.

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Recent advances in traumatic brain injury

Cited by 296 publications

References 73 publications

Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury

Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury

Analysis of the Role of Central Cholinoreactivity in Experimental Traumatic Brain Injury

Niche Cells Crosstalk In Neuroinflammation After Traumatic Brain Injury

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