Traumatic Brain Injury

Galgano, Michael A.; Toshkezi, Gentian; Qiu, Xuecheng; Russell, Thomas M.; Chin, Lawrence S.; Zhao, Li-Ru

doi:10.1177/0963689717714102

Cited by 434 publications

(221 citation statements)

References 136 publications

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“…The importance of PACAP in the neuronal regeneration lies in the upregulation of endogenous PACAP and its receptors and the protective effect of exogenous PACAP after different central nervous system injury. The animal models not only can help us understand the pathophysiology of TBI, but allow us to develop interventions for preventing secondary injury, enhancing brain repair and improving recovery after TBI [74]. The results of the aforementioned animal experiments indicate that PACAP may also be a promising therapeutic agent in case of TBI due to its anti-inflammatory, anti-apoptotic and anti-oxidant effects (Figure 1).…”

Section: Resultsmentioning

confidence: 99%

The Neuroprotective and Biomarker Potential of PACAP in Human Traumatic Brain Injury

Tóth

Tamás

Reglődi

2020

IJMS

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Traumatic brain injury remains a growing public health concern and represents the greatest contributor to death and disability globally among all trauma-related injuries. There are limited clinical data regarding biomarkers in the diagnosis and outcome prediction of TBI. The lack of real effective treatment for recovery calls for research of TBI to be shifted into the area of prevention, treatment of secondary brain injury and neurorehabilitation. The neuropeptide pituitary adenylate cyclase activating polypeptide (PACAP) has been reported to act as a hormone, a neuromodulator, a neurotransmitter and a trophic factor, and has been implicated in a variety of developmental and regenerative processes. The importance of PACAP in neuronal regeneration lies in the upregulation of endogenous PACAP and its receptors and the protective effect of exogenous PACAP after different central nervous system injury. The aim of this minireview is to summarize both the therapeutic and biomarker potential of the neuropeptide PACAP, as a novel possible target molecule presently being investigated in several human conditions including TBI, and with encouraging results in animal models of TBI.

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Section: Resultsmentioning

confidence: 99%

The Neuroprotective and Biomarker Potential of PACAP in Human Traumatic Brain Injury

Tóth

Tamás

Reglődi

2020

IJMS

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“…Oxidative stress accompanies neurodegenerative disorders, causing neuronal dysfunctions and vascular damage [30,44]. The latest studies have shown that the level of oxidative stress is elevated in disorders of consciousness [7].…”

Section: Discussionmentioning

confidence: 99%

“…The latest study documented that MSC transplantation suppressed oxidative stress in Alzheimer's disease [26]. Studies on cell cultures and animal models show that MSC transplantation improved motor and receptive functions after cerebral stroke [27][28][29], TBI, spinal cord injury [30,31], and promoted nerve remodeling [32]. In rodents, injection of MSC after TBI leads to neuroprotection by maintaining blood-brain barrier integrity, promoting activated microglial apoptosis, and improving cognitive function [33][34][35].…”

mentioning

confidence: 99%

Influence of Bone Marrow-Derived Mesenchymal Stem Cell Therapy on Oxidative Stress Intensity in Minimally Conscious State Patients

Jezierska-Woźniak

Sinderewicz

Czelejewska

et al. 2020

JCM

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Neurological disorders, including minimally conscious state (MCS), may be associated with the presence of high concentrations of reactive oxygen species within the central nervous system. Regarding the documented role of mesenchymal stem cells (MSCs) in oxidative stress neutralization, the aim of this study is to evaluate the effect of bone marrow-derived MSC (BM-MSC) transplantation on selected markers of oxidative stress in MCS patients. Antioxidant capacity was measured in cerebrospinal fluid (CSF) and plasma collected from nine patients aged between 19 and 45 years, remaining in MCS for 3 to 14 months. Total antioxidant capacity, ascorbic acid and ascorbate concentrations, superoxide dismutase, catalase, and peroxidase activity were analyzed and the presence of tested antioxidants in the CSF and plasma was confirmed. Higher ascorbic acid (AA) content and catalase (CAT) activity were noted in CSF relative to plasma, whereas superoxide dismutase (SOD) activity and total antioxidant capacity were higher in plasma relative to CSF. Total antioxidant capacity measured in CSF was greater after BM-MSC transplantations. The content of ascorbates was lower and CAT activity was higher both in CSF and plasma after the administration of BM-MSC. The above results suggest that MSCs modulate oxidative stress intensity in MCS patients, mainly via ascorbates and CAT activity.

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“…Despite intense and sustained efforts deployed for the development of new therapeutic strategies, very few clinical treatment options have been successful [32]. NFκB-mediated neuroinflammation is the driving force behind the secondary wave of degeneration.…”

Section: Discussionmentioning

confidence: 99%

Crosstalk between Estrogen Withdrawal and NFκB Signaling following Penetrating Brain Injury

Cook

Hung

Duncan

2018

Neuroimmunomodulation

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Objectives: Characterized by neuroinflammation, traumatic brain injury (TBI) induces neuropathological changes and cognitive deficits. Estrogens are neuroprotective by increasing cell survival and this increase is mediated by a decrease in neuroinflammation. To further explore the relationship between estrogens, brain injury, and neuroinflammation, we examined the expression of the IKK/NFκB complex. The IKK/NFκB complex is a pleiotropic regulator of many cellular signaling pathways linked to inflammation, as well as three major cytokines (IL-1β, IL-6, and TNF-α). We hypothesized that NFκB expression would be upregulated following injury and that this increase would be exacerbated when circulating estrogens were decreased with fadrozole (aromatase inhibitor). Methods: Using adult zebra finches, we first determined the expression of major components of the NFκB complex (NFκB, IκB-α, and IκB-β) following injury using qPCR. Next, male and female finches were collected at 2 time points (2 or 24 h after injury) and brain tissue was analyzed to determine whether NFκB expression was differentially expressed in males and females at either time point. Finally, we examined how the expression of NFκB changed when estrogen levels were decreased immediately after injury. Results: Our study documented an increase in the expression of the major components of the NFκB complex (NFκB, IκB-α, and IκB-β) following injury. Decreasing estrogen levels resulted in a surprising decrease in the NFκB complex studied here. Discussion: These data further expand the model of how estrogens and other steroid hormones interact with the inflammatory pathways following injury and may prove beneficial when developing therapies for treatment of TBI.

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Traumatic Brain Injury

Cited by 434 publications

References 136 publications

The Neuroprotective and Biomarker Potential of PACAP in Human Traumatic Brain Injury

The Neuroprotective and Biomarker Potential of PACAP in Human Traumatic Brain Injury

Influence of Bone Marrow-Derived Mesenchymal Stem Cell Therapy on Oxidative Stress Intensity in Minimally Conscious State Patients

Crosstalk between Estrogen Withdrawal and NFκB Signaling following Penetrating Brain Injury

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