Traumatic brain injury (TBI) is characterized by neuroinflammation and structural damage leading to symptoms and altered brain function. Biomarkers are useful in understanding neuroinflammation and correlations with TBI sequalae. The purpose of this paper is to identify and discuss biomarkers of neuroinflammation used to study TBI and its sequalae. A systematic review was conducted using PubMed, CINAHL, Embase, and Web of Science. A total of 350 articles met criteria; 70 used biomarkers. PRISMA criteria were used for Quality Assessment. Articles included reviews ( = 17), case-control ( = 25), cross-sectional ( = 25) studies, and randomized controlled trials ( = 3). Twenty-seven biomarkers were identified, including inflammasomes, cytokines, neuropeptides, complement complexes, miRNA and exosomes, and glial cell-specific proteins. Biomarkers aid in predicting morbidity and mortality and advance our understanding of neuroinflammation in TBI. This systematic review advances our understanding of the neuroinflammatory response to better enable nurses and clinicians to provide informed care of TBI patients.
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http://dx.doi.org/10.1177/10547738221107081 | DOI Listing |
J Neuroophthalmol
December 2024
Experimental and Clinical Research Center (FCO, HGZ, SM, CB, ESA, CC, FP, AUB), Max Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany; NeuroCure Clinical Research Center (FCO, HGZ, SM, CB, ESA, CC, FP, AUB), Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany; Department of Neurology (AJG), University of California San Francisco, San Francisco, California; Neurology (RM, ACC), Multiple Sclerosis, Myelin Disorders and Neuroinflammation Pierre Wertheimer Neurological Hospital, Hospices Civils de Lyon, France; Centre d'Esclerosi Múltiple de Catalunya (Cemcat) (ACC), Department of Neurology/Neuroimmunology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain; Experimental Neurophysiology Unit (LL, MP, M. Radaelli), Institute of Experimental Neurology (INSPE) Scientific Institute, Hospital San Raffaele and University Vita-Salute San Raffaele, Milan, Italy; Hospital Clinic of Barcelona-Institut d'Investigacions (PV, BS-D, EHM-L), Biomèdiques August Pi Sunyer, (IDIBAPS), Barcelona, Spain; CIEM MS Research Center (MAL-P, MAF), University of Minas Gerais, Medical School, Belo Horizonte, Brazil; Department of Neurology (OA, M. Ringelstein, PA), Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany; Department of Neurology (M. Ringelstein), Centre for Neurology and Neuropsychiatry, LVR Klinikum, Heinrich Heine University Düsseldorf, Düsseldorf, Germany; Department of Medicine (MRY), Harbor-University of California at Los Angeles (UCLA) Medical Center, and Lundquist Institute for Biomedical Innovation, Torrance, California; Department of Medicine (MRY), David Geffen School of Medicine at UCLA, Los Angeles, California; Departments of Ophthalmology and Visual Sciences (TJS), Kellogg Eye Center, University of Michigan Medical School, Ann Arbor, Michigan; Division of Metabolism, Endocrine and Diabetes (TJS, LC), Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan; Department of Neurology (FP), Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany; and Department of Neurology (AUB), University of California, Irvine, California.
Metab Brain Dis
January 2025
Department of Neurology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, OR, 97239, USA.
Neuroinflammation and mitochondrial dysfunction are early events in Alzheimer's disease (AD) and contribute to neurodegeneration and cognitive impairment. Evidence suggests that the inflammatory axis mediated by macrophage migration inhibitory factor (MIF) binding to its receptor, CD74, plays an important role in many central nervous system (CNS) disorders such as AD. Our group has developed DRhQ, a novel CD74 binding construct which competitively inhibits MIF binding, blocks macrophage activation and migration into the CNS, enhances anti-inflammatory microglia cell numbers and reduces pro-inflammatory gene expression.
View Article and Find Full Text PDFJ Neuroimmune Pharmacol
January 2025
Department of Cardiothoracic Surgery, Children's Hospital of Nanjing Medical University, Nanjing, 210008, China.
Parkinson's disease (PD) is a complex progressive neurodegenerative disorder and the pathogenesis and treatment methods are unknown. This aim is to investigate the effects of long non coding RNA NEAT1 (LncRNA NEAT1) on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson's disease (PD). Immunoprecipitation and western blot were used to search for the effects of LncRNA NEAT1 on PD.
View Article and Find Full Text PDFEMBO J
January 2025
Division of Neurology, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.
Polyglucosans are glycogen molecules with overlong chains, which are hyperphosphorylated in the neurodegenerative Lafora disease (LD). Brain polyglucosan bodies (PBs) cause fatal neurodegenerative diseases including Lafora disease and adult polyglucosan body disease (ABPD), for which treatments, biomarkers, and good understanding of their pathogenesis are currently missing. Mutations in the genes for the phosphatase laforin or the E3 ubiquitin ligase malin can cause LD.
View Article and Find Full Text PDFNeuronal pentraxin 2 (NP2) plays a significant role in synaptic plasticity, neuronal survival, and excitatory synapse regulation. Emerging research suggests that NP2 is implicated in the pathogenesis of various neurological disorders, including neurodegenerative diseases, neuropsychiatric disorders, and neuropathies. This literature review extensively analyzes NP2's role in these conditions, thereby highlighting its contributions to synaptic dysfunction, neuroinflammation, and neurotoxic protein aggregation.
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