The intercellular communication within the central nervous system (CNS) is of great importance for in maintaining brain function, homeostasis, and CNS regulation. When the equilibrium of CNS is disrupted or injured, microglia are immediately activated and respond to CNS injury. Microglia-derived exosomes are capable of participating in intercellular communication within the CNS by transporting various bioactive substances, including nucleic acids, proteins, lipids, amino acids, and metabolites. Nevertheless, microglia activation is a double-edged sword. Activated microglia can coordinate the neural repair process and, conversely, can amplify tissue injury and impede CNS repair. This work reviewed the roles of exosomes derived from microglia stimulated by different environments (mainly lipopolysaccharide, interleukin-4, and other specific preconditioning) in CNS injury and their possible therapeutic potentials. This work focuses on the regulation of exosomes derived from microglia stimulated by different environments on nerve cells. Meanwhile, we summarized the molecular mechanisms by which the relevant exosomes exert regulatory effects. Exosomes, derived from microglia stimulated by different environments, regulate other nerve cells during the repair of CNS injury, having beneficial or detrimental effects on CNS repair. A comprehensive understanding of the molecular mechanisms underlying their role can provide a robust foundation for the clinical treatment of CNS injury.
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http://dx.doi.org/10.1016/j.neuroscience.2024.11.011 | DOI Listing |
J Child Neurol
January 2025
Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, MA, USA.
We examined the association between social determinants of health and the likelihood of sustaining a concussion among adolescents. Participants in this cross-sectional study were 7164 high school students who completed the 2021 Adolescent Behaviors and Experiences Survey (52.7% girls; mean age = 16.
View Article and Find Full Text PDFBiomed Pharmacother
January 2025
Maj Institute of Pharmacology, Polish Academy of Sciences, Department of Neurochemistry, 12 Smetna Str., Krakow 31-343, Poland. Electronic address:
Neuropathic pain is a disorder affecting the somatosensory nervous system. However, this condition is also characterized by significant neuroinflammation, primarily involving CNS-resident non-neuronal cells. A promising target for developing new analgesics is histamine H receptor (HR); thus, we aimed to determine the influence of a novel HR antagonist/inverse agonist, E-98 (1-(7-(4-chlorophenoxy)heptyl)-3-methylpiperidine), on pain symptoms and glia activation in model of neuropathic pain in male mice (chronic constriction injury to the sciatic nerve).
View Article and Find Full Text PDFEpilepsia
January 2025
Department of Neurosciences, Faculty of Medicine, Université de Montréal, Montreal, Quebec, Canada.
Objective: Tuberous sclerosis complex (TSC) is a monogenetic disorder associated with sustained mechanistic target of rapamycin (mTOR) activation, leading to heterogeneous clinical manifestations. Epilepsy and renal angiomyolipoma are the most important causes of morbidity in adult people with TSC (pwTSC). mTOR is a key player in inflammation, which in turn could influence TSC-related clinical manifestations.
View Article and Find Full Text PDFCNS Neurosci Ther
January 2025
Department of Anatomy, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Objectives: Endoplasmic reticulum (ER) stress-induced protein homeostasis perturbation is a core pathological element in the pathogenesis of neurodegenerative diseases. This study aims to clarify the unique role played by C/EBP homologous protein (CHOP) as a biomarker of the unfolded protein response (UPR) in the etiology of chronic pain and related cognitive impairments following chronic constrictive nerve injury (CCI).
Methods: The memory capability following CCI was assessed utilizing the Morris water maze (MWM) and fear conditioning test (FCT).
Fluids Barriers CNS
January 2025
Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital of Southern Medical University, Guangzhou, 510515, China.
Oxidative stress and neuronal apoptosis could be an important factor leading to post-hemorrhagic consequences after germinal matrix hemorrhage (GMH). Previously study have indicated that relaxin 2 receptor activation initiates anti-oxidative stress and anti-apoptosis in ischemia-reperfusion injury. However, whether relaxin 2 activation can attenuate oxidative stress and neuronal apoptosis after GMH remains unknown.
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