Review
Pharmacology & Pharmacy
Qinghui Zhao, Huige Li, Hongru Li, Jianhua Zhang
Summary: Traumatic brain injury (TBI) has become a significant cause of death and disability worldwide. Neuroinflammatory responses induced after TBI play a crucial role in persistent neuronal damage, but they also contribute to debris removal and tissue repair. The concept of pleiotropic neuroprotection explores multi-target interventions to inhibit post-TBI neuroinflammation, aiming to improve treatment efficacy. This review discusses advancements in developing pleiotropic neuroprotective pharmaceuticals for TBI management, providing insights for early clinical interventions.
FRONTIERS IN PHARMACOLOGY
(2023)
Article
Neurosciences
Jing Wang, Yujiao Lu, Christopher Carr, Krishnan M. Dhandapani, Darrell W. Brann
Summary: This study found that long-term (months) after traumatic brain injury (TBI), there is a significant presence of proinflammatory senescent cells in the brain. The administration of senolytic drugs can improve long-term functional outcomes by reducing inflammation and neurodegeneration.
FRONTIERS IN NEUROSCIENCE
(2023)
Review
Clinical Neurology
Mackenzie M. Aychman, David L. Goldman, Joshua S. Kaplan
Summary: Cannabidiol (CBD) has potential therapeutic effects against the secondary injury cascade from traumatic brain injury (TBI) by initiating anti-inflammatory, antioxidative, and antiepileptic properties. The lack of effective broad treatment strategies for TBI highlights the importance of CBD's mechanistic support in countering the damaging mechanisms and providing neuroprotective benefits. Future clinical research and ongoing clinical trials are necessary to further examine CBD's efficacy in TBI treatment protocols.
FRONTIERS IN NEUROLOGY
(2023)
Article
Multidisciplinary Sciences
Yongfeng Dai, Jinghua Dong, Yu Wu, Minzhen Zhu, Wenchao Xiong, Huanyu Li, Yulu Zhao, Bruce D. Hammock, Xinhong Zhu
Summary: Traumatic brain injury (TBI) is a global problem with no effective treatment. The liver is found to play an important role in TBI, as demonstrated by decreased hepatic soluble epoxide hydrolase (sEH) activity following TBI. Hepatic Ephx2 downregulation improves TBI-induced neurological deficits, while overexpression of hepatic sEH exacerbates TBI-associated impairments. Hepatic sEH ablation promotes generation of neuroprotective factors and alters plasma levels of EET, which mediate the neuroprotective effect observed after hepatic sEH ablation. Targeting hepatic EET signaling may be a promising therapeutic strategy for TBI.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2023)
Article
Neurosciences
Jingshu Tang, Yuying Kang, Longjian Huang, Xinhong Feng, Lei Wu, Ying Peng
Summary: The study revealed that Hemocoagulase Agkistrodon (HCA) has neuroprotective effects in experimental traumatic brain injury (TBI), improving neurological deficits, reducing brain edema and hemorrhage, lowering proinflammatory cytokines while increasing anti-inflammatory cytokine levels, and diminishing BBB disruption by regulating tight junction proteins. These findings suggest the therapeutic potential of HCA in acute TBI to mitigate neuropathological damage.
BRAIN RESEARCH BULLETIN
(2021)
Article
Neurosciences
Yu-Syuan Wang, Tsai-Wei Hung, Eun-Kyung Bae, Kuo-Jen Wu, Wei Hsieh, Seong-Jin Yu
Summary: Naltrexone has shown neuroprotective effects in cell culture and a mouse model of traumatic brain injury by reducing neurodegeneration and inflammation. The drug also improved motor deficits and modulated the expression of specific proteins related to brain injury.
CNS NEUROSCIENCE & THERAPEUTICS
(2021)
Article
Clinical Neurology
Can Sezer, Selim Zirh, Murat Gokten, Aykut Sezer, Ridvan Acikalin, Emre Bilgin, Elham Bahador Zirh
Summary: This study investigated the neuroprotective effect of milrinone after traumatic brain injury in rats. The results showed that milrinone treatment significantly improved neurological and neurobehavioral functions and reduced inflammation, oxidative stress, and apoptosis.
WORLD NEUROSURGERY
(2023)
Review
Biochemistry & Molecular Biology
Codrin-Constantin Burlacu, Maria-Adriana Neag, Andrei-Otto Mitre, Alexandru-Constantin Sirbu, Andrei-Vlad Badulescu, Anca-Dana Buzoianu
Summary: By modulating miRNAs, DEX has neuroprotective effects and can be used in the treatment of various brain disorders, including cerebral ischemia, traumatic brain injury, neurodegenerative diseases, and postoperative cognitive dysfunction.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Clinical Neurology
Todd A. Verdoorn, Tom J. Parry, Graziano Pinna, Jonathan Lifshitz
Summary: Traumatic brain injury (TBI) leads to various pathological effects on multiple biochemical and physiological systems in and outside the brain. The recovery of patients is hindered by early brain edema, inflammation, cell death, and neurovascular disruption. Drug treatments targeting these deficits are being developed, and it is likely that effective therapy would require interruption of the TBI-induced pathological processes by either a combination of drugs or a single pleiotropic drug. The complex neurosteroid system offers potential options for the research and development of pleiotropic drug treatments for TBI.
Review
Clinical Neurology
Daniel T. Laskowitz, David W. Van Wyck
Summary: The lack of targeted therapies for traumatic brain injury (TBI) is due to difficulties in animal modeling and clinical trial design. A reverse translational approach that focuses on translating endogenous mechanisms known to influence outcomes after TBI to develop druggable targets is proposed.
Review
Anatomy & Morphology
Yating Ling, Murugan Ramalingam, Xiaorui Lv, Yu Zeng, Yun Qiu, Yu Si, Jose Luis Pedraz, Hae-Won Kim, Jiabo Hu
Summary: Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide, and its treatment has seen limited progress in recent years due to the challenges of drug delivery to the brain. However, nanomedicine using nanomaterials as drug carriers is emerging as a promising strategy for the treatment of TBI. This review article provides insights into the pathophysiology of TBI, current treatment options, and emerging nanomedicine strategies, offering a comprehensive overview of the state-of-the-art in treating TBI.
Article
Immunology
Zhongyu Wang, Zhaoyang Wang, Anqi Wang, Juan Li, Junmin Wang, Jingjing Yuan, Xin Wei, Fei Xing, Wei Zhang, Na Xing
Summary: This study aimed to investigate the mechanism of Sevo in TBI by downregulating HES1 via the FGF2/EZH2 axis. Results showed that Sevo reduced brain edema, improved neurological scores, and decreased neuronal apoptosis and autophagy in TBI rats. Upregulation of FGF2 by Sevo preconditioning increased EZH2 expression, leading to downregulation of HES1 in TBI rats.
JOURNAL OF NEUROINFLAMMATION
(2022)
Article
Biochemistry & Molecular Biology
Changmeng Cui, Changshui Wang, Feng Jin, Mengqi Yang, Lingsheng Kong, Wenxiu Han, Pei Jiang
Summary: The study revealed that calcitriol can alleviate oxidative damage induced by TBI by promoting autophagy and activating Nrf2 signaling. Furthermore, treatment with chloroquine (CQ) and genetic knockout of Nrf2 both eliminated the protective effects of calcitriol against TBI-induced neurological deficits and neuronal apoptosis.
MOLECULAR MEDICINE
(2021)
Article
Neurosciences
Viktoriya V. Antonova, Denis N. Silachev, Ivan A. Ryzhkov, Konstantin N. Lapin, Sergey N. Kalabushev, Irina Ostrova, Lydia A. Varnakova, Oleg A. Grebenchikov
Summary: This study evaluated the therapeutic effects of a three-hour inhalation of argon after an open traumatic brain injury (TBI) in rats. The results showed that this treatment did not have a neuroprotective effect.
Review
Nutrition & Dietetics
Matthew Boyko, Benjamin F. Gruenbaum, Anna Oleshko, Igor Merzlikin, Alexander Zlotnik
Summary: Traumatic brain injury (TBI) has long-term impacts on cognitive and mental functioning and significantly decreases quality of life. The blood-brain barrier (BBB) plays a crucial role in regulating glutamate levels in the brain. Studies have shown that reducing excess glutamate can help treat post-TBI depression, anxiety, and aggression. This article evaluates the role of dietary glutamate in the development of depression after TBI.
