ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020
Traumatic brain injury increases plasma astrocyte-derived exosome levels of neurotoxic complement proteins.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 70 citations in OpenAlex.
- Complement in Traumatic Brain Injury: Linking Acute Injury to Chronic Neurodegeneration.European journal of immunology · 2026Review
- Ceramide-rich extracellular vesicles as pathogenic biomarkers in traumatic brain injury.bioRxiv : the preprint server for biology · 2026Article
- RPS3-Enriched Extracellular Vesicles Mediate Liver-Spinal Cord Inter-Organ Communication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Molecular characterization ofOpen veterinary journal · 2026Article
- Exosome-Based Diagnostics and Cell-Free Therapeutics for Traumatic Brain Injury: From Mechanisms to Bedside.International journal of nanomedicine · 2026Review
- Extracellular vesicles: translational research and applications in neurology.Nature reviews. Neurology · 2025Review
- Nerve growth factor precursor alterations in neuron-derived extracellular vesicles from individuals with Down syndrome along the Alzheimer's disease continuum.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Investigating T-cell-derived extracellular vesicles as biomarkers of disease activity, axonal injury, and disability in multiple sclerosis.Clinical and experimental immunology · 2025Article
- Isolating Astrocyte-Derived Extracellular Vesicles From Urine.International journal of nanomedicine · 2025Article
- Elevation of astrocyte-derived extracellular vesicles over the first month post-stroke in humans.Scientific reports · 2024Article
- Nature vs. Manmade: Comparing Exosomes and Liposomes for Traumatic Brain Injury.The AAPS journal · 2023Review
- Biomarkers for parkinsonian disorders in CNS-originating EVs: promise and challenges.Acta neuropathologica · 2023Review
- Complement protein levels in serum astrocyte-derived exosomes are associated with cognitive impairment in obstructive sleep apnea.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2023Article
- Tackling Neuroinflammation After Traumatic Brain Injury: Complement Inhibition as a Therapy for Secondary Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Cell-Derived Exosomes as Therapeutic Strategies and Exosome-Derived microRNAs as Biomarkers for Traumatic Brain Injury.Journal of clinical medicine · 2022Review
- Extracellular vesicles as mediators and markers of acute organ injury: current concepts.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2022Review
- Improved post-stroke spontaneous recovery by astrocytic extracellular vesicles.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Metabolomics of Extracellular Vesicles: A Future Promise of Multiple Clinical Applications.International journal of nanomedicine · 2022Review
- Neuroinflammation of traumatic brain injury: Roles of extracellular vesicles.Frontiers in immunology · 2022Review
- Elevations in Tumor Necrosis Factor Alpha and Interleukin 6 From Neuronal-Derived Extracellular Vesicles in Repeated Low-Level Blast Exposed Personnel.Frontiers in neurology · 2022Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Possible involvement of complement (C) systems in the pathogenesis of traumatic brain injury (TBI) was investigated by quantifying Cproteins in plasma astrocyte-derived exosomes (ADEs) of subjects with sports-related TBI (sTBI) and TBI in military veterans (mtTBI) without cognitive impairment. All sTBI subjects (n = 24) had mild injuries, whereas eight of the mtTBI subjects had moderate, and 17 had mild injuries. Plasma levels of ADEs were decreased after acute sTBI and returned to normal within months. Cprotein levels in ADEs were from 12- to 35-fold higher than the corresponding levels in neuron-derived exosomes. CD81 exosome marker-normalized ADE levels of classical pathway C4b, alternative pathway factor D and Bb, lectin pathway mannose-binding lectin (MBL), and shared neurotoxic effectors C3b and C5b-9 terminal C complex were significantly higher and those of C regulatory proteins CR1 and CD59 were lower in the first week of acute sTBI (n = 12) than in controls (n = 12). Most C abnormalities were no longer detected in chronic sTBI at 3-12 months after acute sTBI, except for elevated levels of factor D, Bb, and MBL. In contrast, significant elevations of ADE levels of C4b, factor D, Bb, MBL, C3b and C5b-9 terminal C complex, and depressions of CR1 and CD59 relative to those of controls were observed after 1-4 years in early chronic mtTBI (n = 10) and persisted for decades except for normalization of Bb, MBL, and CD59 in late chronic mtTBI (n = 15). Complement inhibitors may be useful therapeutically in acute TBI and post-concussion syndrome.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.