Review
Critical Care Medicine
Nikolett Szarka, Dora Szellar, Szabolcs Kiss, Nelli Farkas, Zsolt Szakacs, Andras Czigler, Zoltan Ungvari, Peter Hegyi, Andras Buki, Peter Toth
Summary: Through literature review and meta-analysis, it was found that GH replacement therapy after TBI can moderately improve cognitive function and quality of life, as well as alleviate the severity of depressive symptoms.
JOURNAL OF NEUROTRAUMA
(2021)
Article
Clinical Neurology
Lindsay Ferguson, Christopher C. Giza, Rebecka O. Serpa, Tiffany Greco, Michael Folkerts, Mayumi L. Prins
Summary: Adolescents and young adults have the highest incidence of mild traumatic brain injury (mTBI), with sports activities being a major contributor. Utilizing voluntary exercise in adolescent rats can change the baseline functioning of the brain, and delayed return to activity helps improve cognitive recovery in those with repeated mTBI.
FRONTIERS IN NEUROLOGY
(2021)
Article
Pharmacology & Pharmacy
Ibrahim Bulama, Suleiman Nasiru, Abubakar Bello, Abdullahi Yahaya Abbas, Jinjiri Ismail Nasiru, Yusuf Saidu, Musa Samaila Chiroma, Mohamad Aris Mohd Moklas, Che Norma Mat Taib, Ali Waziri, Bilbis Lawal Suleman
Summary: This study evaluated the antioxidative neuroprotective property and learning and memory-enhancing effects of dimethyl sulfoxide (DMSO) in a rat model after traumatic brain injury (TBI). The results showed that DMSO improved learning and memory, locomotor function, and decreased anxiety in rats with induced TBI. Additionally, DMSO decreased oxidative stress and S100B levels, while increasing the activity of antioxidant enzymes.
FRONTIERS IN PHARMACOLOGY
(2022)
Review
Endocrinology & Metabolism
Valentina Gasco, Valeria Cambria, Fabio Bioletto, Ezio Ghigo, Silvia Grottoli
Summary: Traumatic brain injury (TBI)-related hypopituitarism has been found to be more common than previously thought, affecting pituitary hormones such as growth hormone, gonadotropins, thyroid hormones, etc. The mechanisms of pituitary damage in TBI patients involve primary and secondary injuries, with long-standing growth hormone deficiency leading to neurocognitive and behavioral deficits. Further research is needed to better understand and characterize this clinical syndrome.
FRONTIERS IN ENDOCRINOLOGY
(2021)
Review
Neurosciences
Panxing Wu, Bao He, Xiaoliang Li, Hongwei Zhang
Summary: Traumatic brain injury (TBI) is a leading cause of mortality worldwide, with limited prevention and treatment options. MiR-124, abundantly expressed in the brain, plays a critical role in regulating apoptosis and proliferation, and is closely associated with the pathophysiology of TBI. It interacts with multiple biomolecules and signaling pathways and acts as a crucial regulatory factor in TBI. However, further research is needed to elucidate the specific mechanisms of miR-124 in TBI, and large-scale clinical studies are required to evaluate its therapeutic significance.
FRONTIERS IN CELLULAR NEUROSCIENCE
(2023)
Article
Medicine, General & Internal
Jun-Quan Chen, Shuang-Qi Gao, Lun Luo, Zong-Yuan Jiang, Chao-Feng Liang, Hai-Yong He, Ying Guo
Summary: This study investigates the role of redox states of HMGB1 in neurite outgrowth and regeneration, finding that nonoxid-HMGB1 promotes this process through upregulated expression of SH3RF2. The results suggest that nonoxid-HMGB1 may be a potential therapeutic candidate for the treatment of TBI.
FRONTIERS IN MEDICINE
(2022)
Article
Neurosciences
Yin Feng, Keguo Li, Elizabeth Roth, Dongman Chao, Christina M. Mecca, Quinn H. Hogan, Christopher Pawela, Wai-Meng Kwok, Amadou K. S. Camara, Bin Pan
Summary: The study utilized a rat model of rmTBI to investigate behavioral disruptions, electrophysiological changes in the mPFC, and mitochondrial dysfunction post-injury. The findings showed abnormal behaviors in rats after rmTBI, increased neuronal activity in the mPFC, and impaired inhibitory synaptic transmission due to mitochondrial dysfunction.
FRONTIERS IN CELLULAR NEUROSCIENCE
(2021)
Article
Biochemistry & Molecular Biology
Christian Macks, Daun Jeong, Sooneon Bae, Ken Webb, Jeoung Soo Lee
Summary: Dexamethasone-loaded hydrogels can reduce neuroinflammation, apoptosis, and lesion volume, as well as improve neuronal cell survival and motor function recovery in a rat mild-TBI model, making it a promising therapeutic intervention for TBI treatment.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Immunology
Wende Xu, Shenglei Yue, Peng Wang, Bin Wen, Xiaojue Zhang
Summary: Patients with TBI exhibit higher levels of inflammatory cytokines, which are associated with worsening memory and predict poor cognitive performance.
IMMUNITY INFLAMMATION AND DISEASE
(2022)
Article
Clinical Neurology
Lindsay Wilson, Lindsay Horton, Kevin Kunzmann, Barbara J. Sahakian, Virginia F. J. Newcombe, Emmanuel A. Stamatakis, Nicole von Steinbuechel, Katrin Cunitz, Amra Covic, Andrew Maas, Dominique Van Praag, David Menon
Summary: This study found significant differences in cognitive performance at different levels of disability, with processing speed playing a key role in daily life functioning. Surprisingly, cognitive performance at higher levels showed similarity in function, but there were decreases even in patients reporting complete recovery without significant symptoms.
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY
(2021)
Article
Cell Biology
Wan-Chao Yang, Hong-Ling Cao, Yue-Zhen Wang, Ting-Ting Li, Hong-Yu Hu, Qiang Wan, Wen-Zhi Li
Summary: Hyperglycemia worsens brain damage by affecting vascular endothelial function. Nitric oxide synthase plays a crucial role in diabetic rats with traumatic brain injury, including anti-inflammatory, anti-oxidative stress, and anti-apoptotic activities.
NEURAL REGENERATION RESEARCH
(2021)
Article
Neurosciences
Leilei Mao, Limin Sun, Jingyi Sun, Baoliang Sun, Yanqin Gao, Hong Shi
Summary: The study demonstrates that EP treatment can improve sensorimotor function following TBI, reduce white matter injury, and modulate microglia polarization toward the anti-inflammatory M2 phenotype during the acute phase of TBI recovery, improving the release of inflammatory-related factors.
CNS NEUROSCIENCE & THERAPEUTICS
(2021)
Article
Oncology
Lijuan Quan, Yue Zhao, Chengfeng Ouyang, Dexia Ying, Zhichao Xiong, Xunxin Li, Ziqin Liao, Jun Luo, Howe Liu
Summary: Objective: This study aimed to investigate the role of chemokine receptor ACKR2 in cognitive impairment in young rats with traumatic brain injury. Methods: Various techniques were employed to examine the effects of ACKR2 in young rats, including water maze test, electron microscope, staining, ELISA, RT-PCR, and Western blotting. Results: The study found that the expression of ACKR2 was decreased in TBI rats, resulting in decreased learning and memory abilities, increased inflammatory factors levels, and elevated expressions of Tau and NG2. Conclusion: Overexpression of ACKR2 combined with sensory integration improved the cognitive abilities of TBI rats, suggesting that ACKR2 may be an effective method for improving outcomes in young rats with traumatic brain injury.
AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH
(2023)
Article
Biochemistry & Molecular Biology
Margarita Heredia, Virginia Sanchez-Robledo, Ines Gomez, Jose Maria Criado, Antonio de la Fuente, Jesus Devesa, Pablo Devesa, Adelaida Sanchez Riolobos
Summary: The study found that GH treatment and rehabilitation significantly improved the motor deficit caused by the injury and promoted cell proliferation in the PC of the injured side of the brain. This increased cell proliferation may be related to the observed improvement and could be involved in compensatory mechanisms of the brain after injury.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Multidisciplinary Sciences
MaryLourdes Andreu, Nathalie Matti, Helen M. M. Bramlett, Yan Shi, Shyam Gajavelli, W. Dalton Dietrich
Summary: Traumatic brain injury (TBI) often leads to long-lasting neurological deficits. Recent studies have shown that transplantation of human neural stem cells (hNSCs) can provide neuroprotection after penetrating TBI (pTBI). This study aimed to investigate the association between hNSC-mediated neuroprotection and reduced microglial activation in the pericontusional cortical areas. The results demonstrated a dose-dependent reduction in inflammatory cell activation and increased intersections in the protected areas after hNSC transplantation.