We have previously demonstrated the release of membranous structures by cells into their extracellular environment, which are termed exosomes, microvesicles or extracellular vesicles depending on specific characteristics, including size, composition and biogenesis pathway. With activation, injury, stress, transformation or infection, cells express proteins and RNAs associated with the cellular responses to these events. The exosomes released by these cells can exhibit an array of proteins, lipids and nucleic acids linked to these physiologic events. This review focuses on exosomes associated with traumatic brain injury, which may be both diagnostic and a causative factor in the progression of the injury. Based on current data, exosomes play essential roles as conveyers of intercellular communication and mediators of many of the pathological conditions associated with development, progression and therapeutic failures and cellular stress in a variety of pathologic conditions. These extracellular vesicles express components responsible for angiogenesis promotion, stromal remodelling, signal pathway activation through growth factor/receptor transfer, chemoresistance, immunologic activation and genetic exchange. These circulating exosomes not only represent a central mediator of the pro-inflammatory microenvironment linked with secondary brain injury, but their presence in the peripheral circulation may serve as a surrogate for biopsies, enabling real-time diagnosis and monitoring of neurodegenerative progression.
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http://dx.doi.org/10.1098/rstb.2013.0503 | DOI Listing |
BMC Neurosci
January 2025
Department of Emergency, Nantong Haimen District People's Hospital, No. 1201 Peking Road, Haimen District, Nantong, 226100, China.
Background: Intracerebral hemorrhage (ICH) is a common subtype of stroke, characterized by a high mortality rate and a tendency to cause neurological damage. This study aims to investigate the role and mechanisms of lncRNA HCP5 in ICH.
Methods: We simulated ICH in vivo by injecting collagenase into rats and established an in vitro model using hemoglobin-treated BV2 cells.
Nat Commun
January 2025
Institute of Developmental Biology and Neurobiology, Faculty of Biology, Johannes Gutenberg University Mainz, Mainz, Germany.
After a peripheral nerve injury, Schwann cells (SCs), the myelinating glia of the peripheral nervous system, convert into repair cells that foster axonal regrowth, and then remyelinate or re-ensheath regenerated axons, thereby ensuring functional recovery. The efficiency of this mechanism depends however on the time needed for axons to regrow. Here, we show that ablation of histone deacetylase 8 (HDAC8) in SCs accelerates the regrowth of sensory axons and sensory function recovery.
View Article and Find Full Text PDFJ Neurosci
January 2025
Wellcome Centre for Integrative Neuroimaging; Nuffield Department of Clinical Neuroscience, University of Oxford.
Damage to the primary visual cortex (V1) results in visual field deficits on the contralateral side of the world corresponding to the damaged region. Patients with such loss nonetheless show varying residual vision within this apparently blind region, with the neural mechanisms underlying this ability obscured by small study populations. We identified lesions on structural scans from 39 patients (12 female) with hemianopia and occipital lobe damage.
View Article and Find Full Text PDFExp Anim
January 2025
Department of Neurosciences, School of Medical Sciences, Universiti Sains Malaysia.
Status epilepticus is linked to cognitive decline due to damage to the hippocampus, a key structure involved in cognition. The hippocampus's high vulnerability to epilepsy-related damage is the main reason for this impairment. Convulsive seizures, such as those observed in status epilepticus, can cause various hippocampal pathologies, including inflammation, abnormal neurogenesis, and neuronal death.
View Article and Find Full Text PDFBrain Res Bull
January 2025
Key Laboratory of Biomechanics and Mechanobiology, Ministry of Education, Beijing Advanced Innovation Center for Biomedical Engineering, School of Biological Science and Medical Engineering, Beihang University - Yifu Science Hall, 37 Xueyuan Road, Haidian, Beijing, 100191, China. Electronic address:
Quantifying axons and myelin is essential for understanding spinal cord injury (SCI) mechanisms and developing targeted therapies. This study proposes and validates an automated method to measure axons and myelin, applied to compare contusion, dislocation, and distraction SCIs in a rat model. Spinal cords were processed and stained for neurofilament, tubulin, and myelin basic protein, with histology images segmented into dorsal, lateral, and ventral white matter regions.
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