During the past decade there has been an increasing recognition of the incidence of mild traumatic brain injury (mTBI) and a better understanding of the subtle neurological and cognitive deficits that may result from it. A substantial, albeit suboptimal, effort has been made to define diagnostic criteria for mTBI and improve diagnostic accuracy. Thus, biomarkers that can accurately and objectively detect brain injury after mTBI and, ideally, aid in clinical management are needed. In this review, we discuss the current research on serum biomarkers for mTBI including their rationale and diagnostic performances. Sensitive and specific biomarkers reflecting brain injury can provide important information regarding TBI pathophysiology and serve as candidate markers for predicting abnormal computed tomography findings and/or the development of residual deficits in patients who sustain an mTBI. We also outline the roles of biomarkers in settings of specific interest including pediatric TBI, sports concussions and military injuries, and provide perspectives on the validation of such markers for use in the clinic. Finally, emerging proteomics-based strategies for identifying novel markers will be discussed.
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http://dx.doi.org/10.1002/med.21295 | DOI Listing |
Stem Cell Rev Rep
January 2025
Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China.
Background: The hypobaric hypoxic atmosphere can cause adverse reactions or sickness. The purpose of this study was to explore the preventive effect and mechanism of human umbilical cord mesenchymal stem cells (hUC-MSCs) on acute pathological injury in mice exposed to high-altitude.
Methods: We pretreated C57BL/6 mice with hUC-MSCs via the tail vein injection, and then the mice were subjected to hypobaric hypoxic conditions for five days.
Nat Commun
January 2025
Unit on the Development of Neurodegeneration, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
Traumatic brain injury (TBI) is a risk factor for neurodegeneration, however little is known about how this kind of injury alters neuron subtypes. In this study, we follow neuronal populations over time after a single mild TBI (mTBI) to assess long ranging consequences of injury at the level of single, transcriptionally defined neuronal classes. We find that the stress-responsive Activating Transcription Factor 3 (ATF3) defines a population of cortical neurons after mTBI.
View Article and Find Full Text PDFeNeuro
January 2025
Department of Biology, University of Ottawa, Ottawa, ON K1N 6N5, Canada.
Axons in the mammalian brain show significant diversity in myelination motifs, displaying spatial heterogeneity in sheathing along individual axons and across brain regions. However, its impact on neural signaling and susceptibility to injury remains poorly understood. To address this, we leveraged cable theory and developed model axons replicating the myelin sheath distributions observed experimentally in different regions of the mouse central nervous system.
View Article and Find Full Text PDFJ Biophotonics
January 2025
Britton Chance Center for Biomedical Photonics-MoE Key Laboratory for Biomedical Photonics, Huazhong University of Science and Technology, Wuhan, China.
Diabetes mellitus (DM), a chronic metabolic disorder that adversely affects the blood-brain barrier (BBB) and microglial function in the central nervous system (CNS), contributing to neuronal damage and neurodegenerative diseases. However, the underlying molecular mechanisms linking diabetes to BBB dysfunction and microglial dysregulation remain poorly understood. Here, we assessed the impacts of diabetes on BBB and microglial reactivity and investigated its mechanisms.
View Article and Find Full Text PDFFree Radic Biol Med
January 2025
Laboratory of Stem Cells and Tissue Regeneration, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, South Korea. Electronic address:
Human embryonic stem cells (hESCs) and their extracellular vesicles (EVs) hold significant potential for tissue repair and regeneration. Neural stem cells (NSCs) in the adult brain often acquire senescent phenotypes after ischemic injuries, releasing neurodegenerative senescence-associated secretory phenotype factors. In this study, we investigated the senotherapeutic effects of hESC-EVs on NSCs and confirmed their neuroprotective effects in neurons via rejuvenation of NSC secretions.
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