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Journal articles on the topic 'CNS damage'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Kontos, Hermes A. "Oxygen radicals in CNS damage." Chemico-Biological Interactions 72, no. 3 (1989): 229–55. http://dx.doi.org/10.1016/0009-2797(89)90001-x.

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2

Lee, Jae-Min, You Jung Choi, Myung Chul Yoo, and Seung Geun Yeo. "Central Facial Nervous System Biomolecules Involved in Peripheral Facial Nerve Injury Responses and Potential Therapeutic Strategies." Antioxidants 12, no. 5 (2023): 1036. http://dx.doi.org/10.3390/antiox12051036.

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Peripheral facial nerve injury leads to changes in the expression of various neuroactive substances that affect nerve cell damage, survival, growth, and regeneration. In the case of peripheral facial nerve damage, the injury directly affects the peripheral nerves and induces changes in the central nervous system (CNS) through various factors, but the substances involved in these changes in the CNS are not well understood. The objective of this review is to investigate the biomolecules involved in peripheral facial nerve damage so as to gain insight into the mechanisms and limitations of target

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Mikołajewska, Emilia, and Dariusz Mikołajewski. "Neuroplasticity in rehabilitation after central nervous system damages – computational models." Advances in Rehabilitation 26, no. 1 (2012): 51–58. http://dx.doi.org/10.2478/rehab-2013-0029.

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AbstractIncreasing survival rates in severe illnesses and traumatic injuries can lead to an increase in the number of disabled people with central nervous system (CNS) damages. Motor training after CNS damage is an important part of neurorehabilitation. It can partially reverse the loss of cortical representation after lesion thanks to neuroplasticity. Patients may regain some motor functions in the months following damage due both to spontaneous recovery and physical therapy interventions targeted at further improvement of function. The neural correlates of motor training after CNS damage hav

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Guidi, Patrizia, Margherita Bernardeschi, Mara Palumbo, et al. "Suitability of a Cellulose-Based Nanomaterial for the Remediation of Heavy Metal Contaminated Freshwaters: A Case-Study Showing the Recovery of Cadmium Induced DNA Integrity Loss, Cell Proliferation Increase, Nuclear Morphology and Chromosomal Alterations on Dreissena polymorpha." Nanomaterials 10, no. 9 (2020): 1837. http://dx.doi.org/10.3390/nano10091837.

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The contamination of freshwaters by heavy metals represents a great problem, posing a threat for human and environmental health. Cadmium is classified as carcinogen to humans and its mechanism of carcinogenicity includes genotoxic events. In this study a recently developed eco-friendly cellulose-based nanosponge (CNS) was investigated as a candidate in freshwater nano-remediation process. For this purpose, CdCl2 (0.05 mg L−1) contaminated artificial freshwater (AFW) was treated with CNS (1.25 g L−1 for 2 h), and cellular responses were analyzed before and after CNS treatment in Dreissena polym

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Magaryshkina, O. V., and N. A. Abdulaeva. "Ophthalmological manifestations of CNS damage in neurosyphilis." Modern technologies in ophtalmology, no. 4 (December 7, 2020): 188–89. http://dx.doi.org/10.25276/2312-4911-2020-4-188-189.

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6

Millichap, J. Gordon. "Fetal CNS Damage with Maternal Prenatal Trauma." Pediatric Neurology Briefs 10, no. 12 (1996): 92. http://dx.doi.org/10.15844/pedneurbriefs-10-12-6.

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7

Kapadia, Minesh, and Boris Sakic. "Autoimmune and inflammatory mechanisms of CNS damage." Progress in Neurobiology 95, no. 3 (2011): 301–33. http://dx.doi.org/10.1016/j.pneurobio.2011.08.008.

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8

Hong, Sung Jun, Minsung Bock, Songzi Zhang, Seong Bae An, and Inbo Han. "Therapeutic Transplantation of Human Central Nervous System Organoids for Neural Reconstruction." International Journal of Molecular Sciences 25, no. 15 (2024): 8540. http://dx.doi.org/10.3390/ijms25158540.

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Damage to the central nervous system (CNS) often leads to irreversible neurological deficits, and there are currently few effective treatments available. However, recent advancements in regenerative medicine have identified CNS organoids as promising therapeutic options for addressing CNS injuries. These organoids, composed of various neurons and supporting cells, have shown potential for direct repair at injury sites. CNS organoids resemble the structure and function of actual brain tissue, which allows them to adapt and function well within the physiological environment when transplanted int

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9

Pavlinova, E. B., A. A. Gubich, O. A. Savchenko, D. G. Novikov, K. S. Tagakov, and N. A. Kirichenko. "FUTURE USE OF ANTIOXIDANT DEFENSE SYSTEM COMPONENTS AS MARKERS OF ORGANIC DAMAGE TO THE CENTRAL NERVOUS SYSTEM IN THE NEONATAL PERIOD IN PREMATURE NEWBORNS." Pediatria. Journal named after G.N. Speransky 101, no. 1 (2022): 39–46. http://dx.doi.org/10.24110/0031-403x-2022-101-1-39-46.

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Objective of the study: to assess the significance of superoxide dismutase (SOD) and glutathione as markers of severe CNS damage in premature infants. Materials and methods of research: a onestage comparative study with a control group – a part of an observational prospective longitudinal non-randomized multicenter study. The main group – 60 premature infants with gestational age (GA) less than 36 weeks inclusive (32 boys (53%) and 28 girls (47%), the control group – 25 fullterm newborns (15 boys (60%) and 10 girls (40%). In the process of dynamic observation, the main group was divided into s

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Рамазанова, Сельми Фаиковна, А. В. Аракелян, А. А. Семенова та ін. "Диффузная В-крупноклеточная лимфома с высоким риском поражения центральной нервной системы (обзор литературы, вопросы профилактики, лечение, прогноз)". Clinical Oncohematology 18, № 1 (2025): 51–64. https://doi.org/10.21320/2500-2139-2025-18-1-51-64.

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AIM. To assess the feasibility of preventing the CNS damage in intermediate/high risk patients with newly diagnosed diffuse large B-cell lymphoma (DLBCL) in accordance with CNS-IPI criteria. MATERIALS & METHODS. The trial was based on the clinical data from 60 patients with newly diagnosed DLBCL treated at the NN Blokhin National Medical Cancer Research Center from 2018 to 2024. The patients were 29–80 years of age (median 59 years); there were 34 women and 26 men. In accordance with the immunohistochemical algorithm of C.P. Hans, GCB subtype of DLBCL was identified in 18 (30 %) patients,

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11

Robert, Tom. "Immune Privilege in the Central Nervous System: Implications for Neuroinflammatory Diseases." RESEARCH INVENTION JOURNAL OF BIOLOGICAL AND APPLIED SCIENCES 4, no. 2 (2024): 13–17. https://doi.org/10.59298/rijbas/2024/421317.

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The central nervous system (CNS) has long been considered an immune-privileged site, where immune responses are tightly regulated to protect neural tissue from inflammation-induced damage. Immune privilege in the CNS is maintained through various mechanisms, including the blood-brain barrier (BBB), the absence of conventional lymphatic drainage, the specialized function of CNS-resident immune cells, and the expression of immunosuppressive molecules like TGF-β and IL-10. These protective systems are essential for preserving CNS homeostasis, as uncontrolled immune activity in the CNS can lead to

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12

Alessi, Iside, Anna Maria Caroleo, Luca de Palma, et al. "Short and Long-Term Toxicity in Pediatric Cancer Treatment: Central Nervous System Damage." Cancers 14, no. 6 (2022): 1540. http://dx.doi.org/10.3390/cancers14061540.

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Neurotoxicity caused by traditional chemotherapy and radiotherapy is well known and widely described. New therapies, such as biologic therapy and immunotherapy, are associated with better outcomes in pediatric patients but are also associated with central and peripheral nervous system side effects. Nevertheless, central nervous system (CNS) toxicity is a significant source of morbidity in the treatment of cancer patients. Some CNS complications appear during treatment while others present months or even years later. Radiation, traditional cytotoxic chemotherapy, and novel biologic and targeted

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13

Lukens, John R., Calli E. Bellinger, Elizabeth L. Frost, Mariah E. Shaw, Ashley C. Bolte, and Catherine R. Lammert. "Key roles for the innate immune response to genotoxic stress in neurological disease." Journal of Immunology 202, no. 1_Supplement (2019): 187.7. http://dx.doi.org/10.4049/jimmunol.202.supp.187.7.

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Abstract Mounting evidence indicates that DNA damage accumulation in the brain centrally contributes to a number of neurodevelopmental, psychiatric, and neurodegenerative disorders. Yet, little is currently known about the specific molecular pathways that the brain relies on to safeguard itself from DNA insults or how altered regulation of these pathways leads to neurological disease. In recent years, a number of new innate immune signaling pathways that respond to genotoxic stress have been identified. While many of these genomic sensors are highly expressed in the central nervous system (CNS

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Hasan, Husam Fadhil, Mojtaba Qati Dahdoh, and Hayder Mohsin Ali. "GENETIC FEATURES OF STREPTOCOCCUS PNEUMONIAE AND ITS ROLE IN CAUSING MENINGITIS." European Journal of Medical Genetics and Clinical Biology 2, no. 1 (2024): 1–26. https://doi.org/10.61796/jmgcb.v2i1.1070.

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Objective: To understand the mechanism by which Streptococcus pneumoniae (S. pneumoniae) causes meningitis and the resulting central nervous system (CNS) injury, focusing on bacterial features and the host immune response. Methods: A comprehensive review of existing literature on the role of CNS barriers, nasopharyngeal colonization, and the genetic features of S. pneumoniae was conducted. The antibacterial and inflammatory responses of the human CNS defense system were analyzed alongside bacterial traits that promote meningitis. Results: The study highlights how S. pneumoniae crosses CNS barr

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15

Marchi, Nicola, Peter Rasmussen, Miranda Kapural, et al. "Peripheral markers of brain damage and blood-brain barrier dysfunction." Restorative Neurology and Neuroscience 21, no. 3-4 (2003): 109–21. https://doi.org/10.3233/rnn-2003-00231.

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Purpose: Occurrence of brain damage is frequently associated with abnormal blood-brain barrier (BBB) function. Two brain-specific proteins, S100β and neuron-specific enolase (NSE) are released systemically in a variety of neurological diseases, but S100β levels sometimes rise in the absence of neuronal damage, suggesting that S100β is a marker of BBB rather than neuronal damage. Methods: We measured both proteins in the serum of patients undergoing iatrogenic BBB disruption with intrarterial mannitol, followed by chemotherapy. Results: Serum S100β increased significantly after mannitol infusio

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16

Anchesi, Ivan, Giovanni Schepici, and Emanuela Mazzon. "LncRNAs and CircRNAs as Strategies against Pathological Conditions Caused by a Hypoxic/Anoxic State." Biomolecules 13, no. 11 (2023): 1622. http://dx.doi.org/10.3390/biom13111622.

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Brain damage can be induced by oxygen deprivation. It is known that hypoxic or anoxic conditions can lead to changes in the expression levels of non-coding RNAs (ncRNAs), which, in turn, can be related to Central Nervous System (CNS) injuries. Therefore, it could be useful to investigate the involvement of non-coding RNAs (ncRNAs), as well as the underlying mechanisms which are able to modulate them in brain damage induced by hypoxic or anoxic conditions. In this review, we focused on recent research that associates these conditions with long non-coding RNAs (lncRNAs) and circular RNAs (circRN

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Sarich, Sarah C., Virinchipuram S. Sreevidya, Ava J. Udvadia, Kurt R. Svoboda, and Jennifer H. Gutzman. "The transcription factor Jun is necessary for optic nerve regeneration in larval zebrafish." PLOS ONE 20, no. 3 (2025): e0313534. https://doi.org/10.1371/journal.pone.0313534.

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Damage to the axons of the adult mammalian central nervous system (CNS) from traumatic injury or neurodegenerative diseases often results in permanent loss of function due to failure of axons to regenerate. Zebrafish, however, can express regeneration-associated genes to revert CNS neurons to a growth-competent state and regenerate damaged axons to functionality. An established model for CNS axon regeneration is optic nerve injury in zebrafish, where it was previously shown that thousands of genes are temporally expressed during the regeneration time course. It is likely that hubs of key trans

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18

Huang, Lixiang, and Gan Wang. "The Effects of Different Factors on the Behavior of Neural Stem Cells." Stem Cells International 2017 (2017): 1–16. http://dx.doi.org/10.1155/2017/9497325.

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The repair of central nervous system (CNS) injury has been a worldwide problem in the biomedical field. How to reduce the damage to the CNS and promote the reconstruction of the damaged nervous system structure and function recovery has always been the concern of nerve tissue engineering. Multiple differentiation potentials of neural stem cell (NSC) determine the application value for the repair of the CNS injury. Thus, how to regulate the behavior of NSCs becomes the key to treating the CNS injury. So far, a large number of researchers have devoted themselves to searching for a better way to

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19

Illes, Peter. "P2X7 Receptors Amplify CNS Damage in Neurodegenerative Diseases." International Journal of Molecular Sciences 21, no. 17 (2020): 5996. http://dx.doi.org/10.3390/ijms21175996.

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ATP is a (co)transmitter and signaling molecule in the CNS. It acts at a multitude of ligand-gated cationic channels termed P2X to induce rapid depolarization of the cell membrane. Within this receptor-channel family, the P2X7 receptor (R) allows the transmembrane fluxes of Na+, Ca2+, and K+, but also allows the slow permeation of larger organic molecules. This is supposed to cause necrosis by excessive Ca2+ influx, as well as depletion of intracellular ions and metabolites. Cell death may also occur by apoptosis due to the activation of the caspase enzymatic cascade. Because P2X7Rs are locali

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20

Malone, John I. "Diabetic Central Neuropathy: CNS Damage Related to Hyperglycemia." Diabetes 65, no. 2 (2016): 355–57. http://dx.doi.org/10.2337/dbi15-0034.

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21

Dommerholt, J., T. Issa, and J. D. Nutt. "DBS and diathermy interaction induces severe CNS damage." Neurology 57, no. 12 (2001): 2324–25. http://dx.doi.org/10.1212/wnl.57.12.2324-a.

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22

Nutt, J. G., V. C. Anderson, J. H. Peacock, J. P. Hammerstad, and K. J. Burchiel. "DBS and diathermy interaction induces severe CNS damage." Neurology 56, no. 10 (2001): 1384–86. http://dx.doi.org/10.1212/wnl.56.10.1384.

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23

Locatelli, Giuseppe, Arianna Baggiolini, Bettina Schreiner, Burkhard Becher, and Thorsten Buch. "Plastic response of mature oligodendrocytes following CNS damage." Journal of Neuroimmunology 275, no. 1-2 (2014): 186. http://dx.doi.org/10.1016/j.jneuroim.2014.08.500.

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24

Hopewell, J. W. "Models of CNS radiation damage during space flight." Advances in Space Research 14, no. 10 (1994): 433–42. http://dx.doi.org/10.1016/0273-1177(94)90497-9.

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25

Blanco, Margarita, Graciela Romano, Maria R. Barrera, and Adriana Carra. "Evoked potentials: Evaluation of infants with CNS damage." Pediatric Neurology 8, no. 5 (1992): 403. http://dx.doi.org/10.1016/0887-8994(92)90322-p.

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26

Clase, Amanda C., and Bruce W. Banfield. "Corticosteroids Are Unable To Protect against Pseudorabies Virus-Induced Tissue Damage in the Developing Brain." Journal of Virology 77, no. 8 (2003): 4979–84. http://dx.doi.org/10.1128/jvi.77.8.4979-4984.2003.

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ABSTRACT After intraocular injection of the virulent pseudorabies virus (PRV) strain Becker into late-stage chicken embryos, the virus spreads and replicates in the brain, where severe edema and hemorrhaging follow. By contrast, the attenuated Bartha strain does not cause severe brain pathology despite viral replication and spread throughout the brain (B. W. Banfield, G. S. Yap, A. C. Knapp, and L. W. Enquist, J. Virol. 72:4580-4588, 1998). These observations prompted us to explore the mechanism by which the virulent Becker strain mediates pathology in the chicken embryo central nervous system

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Masini, Lucia, Massimo Apicella, Carmen De Luca, et al. "Fetal Central Nervous System and Infectious Diseases." Donald School Journal of Ultrasound in Obstetrics and Gynecology 11, no. 4 (2017): 314–27. http://dx.doi.org/10.5005/jp-journals-10009-1539.

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ABSTRACT Maternal infectious diseases are frequent complications of pregnancy and can cause negative outcomes. Perinatal infections can cause serious damage to fetal central nervous system (CNS), but incidence of symptomatic congenital infections at birth is low. Complete and multidisciplinary (obstetric, infectologist, microbiologist, neonatologist/pediatrician, psychologist) evaluation of the pregnant women is crucial to define fetal prognosis. The ultrasound (US) surveillance has an irreplaceable role in identifying serious fetal damage and complications. Complete evaluation of the fetus in

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Petrashenko, Viktoria A., Andrii M. Loboda, Olexandr I. Smiyan, et al. "LABORATORY CRITERIA OF PERINATAL DAMAGE OF CENTRAL NERVOUS SYSTEM AT PREMATURE NEWBORNS." Wiadomości Lekarskie 72, no. 8 (2019): 1512–16. http://dx.doi.org/10.36740/wlek201908118.

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Introduction: Fetal and neonatal hypoxia takes a special place among the damaging factors of central nervous system (CNS). All forms of oxygen deficiency are accompanied by the development of bioenergetic hypoxia, which leads to tension of metabolic processes of the organism. Metabolic effect of hypoxia includes stark reduce of mitochondrial activity due to a significant inhibition enzymes of the Krebs cycle: succinate dehydrogenase (SDH) and lactate dehydrogenase (LDH). In newborn babies is not always possible to objectively assess the condition of the CNS defeat, because very often the sever

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Millán Solano, Mara Verónica, Citlaltepetl Salinas Lara, Carlos Sánchez-Garibay, et al. "Effect of Systemic Inflammation in the CNS: A Silent History of Neuronal Damage." International Journal of Molecular Sciences 24, no. 15 (2023): 11902. http://dx.doi.org/10.3390/ijms241511902.

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Central nervous system (CNS) infections including meningitis and encephalitis, resulting from the blood-borne spread of specific microorganisms, provoke nervous tissue damage due to the inflammatory process. Moreover, different pathologies such as sepsis can generate systemic inflammation. Bacterial lipopolysaccharide (LPS) induces the release of inflammatory mediators and damage molecules, which are then released into the bloodstream and can interact with structures such as the CNS, thus modifying the blood–brain barrier’s (BBB´s) and blood–cerebrospinal fluid barrier´s (BCSFB´s) function and

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Granziera, Cristina, Jens Wuerfel, Frederik Barkhof, et al. "Quantitative magnetic resonance imaging towards clinical application in multiple sclerosis." Brain 144, no. 5 (2021): 1296–311. http://dx.doi.org/10.1093/brain/awab029.

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Abstract Quantitative MRI provides biophysical measures of the microstructural integrity of the CNS, which can be compared across CNS regions, patients, and centres. In patients with multiple sclerosis, quantitative MRI techniques such as relaxometry, myelin imaging, magnetization transfer, diffusion MRI, quantitative susceptibility mapping, and perfusion MRI, complement conventional MRI techniques by providing insight into disease mechanisms. These include: (i) presence and extent of diffuse damage in CNS tissue outside lesions (normal-appearing tissue); (ii) heterogeneity of damage and repai

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Hajduková, Lenka, Ondřej Sobek, Darina Prchalová, et al. "Biomarkers of Brain Damage: S100B and NSE Concentrations in Cerebrospinal Fluid—A Normative Study." BioMed Research International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/379071.

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NSE and S100B belong among the so-called structural proteins of the central nervous system (CNS). Lately, this group of structural proteins has been profusely used as specific biomarkers of CNS tissue damage. So far, the majority of the research papers have focused predominantly on the concentrations of these proteins in blood in relation to CNS damage of various origins. Considering the close anatomic and functional relationship between the brain or spinal cord and cerebrospinal fluid (CSF), in case of a CNS injury, a rapid and pronounced increase of the concentrations of structural proteins

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Moon, Eunjung, Jeong Eun Han, Sejin Jeon, Jong Hoon Ryu, Ji Woong Choi, and Jerold Chun. "Exogenous S1P Exposure Potentiates Ischemic Stroke Damage That Is Reduced Possibly by Inhibiting S1P Receptor Signaling." Mediators of Inflammation 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/492659.

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Initial and recurrent stroke produces central nervous system (CNS) damage, involving neuroinflammation. Receptor-mediated S1P signaling can influence neuroinflammation and has been implicated in cerebral ischemia through effects on the immune system. However, S1P-mediated events also occur within the brain itself where its roles during stroke have been less well studied. Here we investigated the involvement of S1P signaling in initial and recurrent stroke by using a transient middle cerebral artery occlusion/reperfusion (M/R) model combined with analyses of S1P signaling. Gene expression for S

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Wang, Xinyu. "Review of clinical nerve repair strategies for neurorestoration of central nervous system tumor damage." Journal of Neurorestoratology 8, no. 3 (2020): 172–81. http://dx.doi.org/10.26599/jnr.2020.9040018.

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Central nervous system (CNS) tumors are common. In recent years, with the continuous development and popularization of neurosurgery and the advancement of diagnostic and therapeutic instruments, the diagnosis and treatment of diseases have made great progress, but the prognosis of patients depends on multiple clinical factors. In this study, we selected various literatures in the PubMed and Google Scholar search engines using the keywords "nerve repair strategies" , "central nervous system tumor" as well as searched scientifically reviewed historical perspectives and recent advancements and ac

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Liberatori, Giulia, Giacomo Grassi, Patrizia Guidi, et al. "Effect-Based Approach to Assess Nanostructured Cellulose Sponge Removal Efficacy of Zinc Ions from Seawater to Prevent Ecological Risks." Nanomaterials 10, no. 7 (2020): 1283. http://dx.doi.org/10.3390/nano10071283.

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To encourage the applicability of nano-adsorbent materials for heavy metal ion removal from seawater and limit any potential side effects for marine organisms, an ecotoxicological evaluation based on a biological effect-based approach is presented. ZnCl2 (10 mg L−1) contaminated artificial seawater (ASW) was treated with newly developed eco-friendly cellulose-based nanosponges (CNS) (1.25 g L−1 for 2 h), and the cellular and tissue responses of marine mussel Mytilus galloprovincialis were measured before and after CNS treatment. A control group (ASW only) and a negative control group (CNS in A

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Xu, Jintao, Lori M. Neal, Anutosh Ganguly, et al. "Chemokine receptor CXCR3 is required for lethal brain pathology but not pathogen clearance during cryptococcal meningoencephalitis." Science Advances 6, no. 25 (2020): eaba2502. http://dx.doi.org/10.1126/sciadv.aba2502.

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Cryptococcal meningoencephalitis (CM) is the major cause of infection-related neurological death, typically seen in immunocompromised patients. However, T cell–driven inflammatory response has been increasingly implicated in lethal central nervous system (CNS) immunopathology in human patients and murine models. Here, we report marked up-regulation of the chemokine receptor CXCR3 axis in human patients and mice with CM. CXCR3 deletion in mice improves survival, diminishes neurological deficits, and limits neuronal damage without suppressing fungal clearance. CD4+ T cell accumulation and TH1 sk

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Chauhan, Vinita, and Ian Marriott. "Prophylactic and therapeutic targeting of the neurokinin-1 receptor limits neuroinflammation in a murine model of streptococcal meningitis (161.7)." Journal of Immunology 186, no. 1_Supplement (2011): 161.7. http://dx.doi.org/10.4049/jimmunol.186.supp.161.7.

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Abstract Bacterial meningitis is a rapid, severe and highly damaging infection of the central nervous system (CNS) that is accompanied with high degree of inflammation. We have previously determined an important role for the neuropeptide substance P (SP) in the initiation and progression of bacterially-induced CNS inflammation. In the present study, we provide evidence that SP augments inflammatory glial responses to the important Gram-positive CNS pathogen Streptococcus pneumoniae, and show that endogenous SP/NK-1 receptor interactions play a critical role in the development of neuroinflammat

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37

Bykov, Yu. "TYPE 1 DIABETES MELLITUS IN PEDIATRIC PRACTICE AND DAMAGE TO THE CENTRAL NERVOUS SYSTEM." Tavricheskiy Mediko-Biologicheskiy Vestnik 23, no. 4 (2022): 91–97. http://dx.doi.org/10.29039/2070-8092-2020-23-4-91-97.

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Diabetes mellitus (DM) is one of severe and progressive endocrine system diseases that occur in childhood. Type 1 DM, the form most commonly seen in children and adolescents, develops as an autoimmune process that gradually inflicts damage and causes death of pancreatic β cells. During its course MD gives rise to a number of severe complications, the most significant of which is the dysfunction and damage of the central nervous system (CNS). The leading causes of CNS damage in DM can be subdivided into vascular, metabolic, neurodegenerative and inflammatory. The main clinical presentation of D

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Xia, Liu, Li Ci, Shi Chunying, Sun Shuwei, and Fang Yiqun. "Advancements in Elucidating the Mechanisms of Central Nervous System Damage Induced by Infrasound Exposure." American Journal of Life Sciences 13, no. 1 (2025): 7–13. https://doi.org/10.11648/j.ajls.20251301.12.

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Infrasound, defined as sound waves with frequencies below 20 Hz, is gaining attention for its potential effects on human health, particularly the central nervous system (CNS). It can impact the CNS through direct and indirect mechanisms, such as damaging neuronal membranes, interfering with neurotransmitter release, altering intracellular signaling, and compromising the blood-brain barrier. These effects may cause neuronal dysfunction, neurotransmitter imbalances, increased oxidative stress, and inflammation, affecting mood, cognition, and memory. This review summarizes the current understandi

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Jacob, Stanley W., and Jack C. de la Torre. "Pharmacology of dimethyl sulfoxide in cardiac and CNS damage." Pharmacological Reports 61, no. 2 (2009): 225–35. http://dx.doi.org/10.1016/s1734-1140(09)70026-x.

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Ahmed, Waqas, Adeel Khan, Wish Hal Sundar, et al. "Neurological diseases caused by coronavirus infection of the respiratory airways." Brain Science Advances 6, no. 4 (2020): 324–43. http://dx.doi.org/10.26599/bsa.2020.9050022.

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Infections of the central nervous system (CNS) infections are critical problems for public health. They are caused by several different organisms, including the respiratory coronaviruses (CoVs). CoVs usually infect the upper respiratory tract causing the common cold. However, in infants, and in elderly and immunocompromised persons, they can also affect the lower respiratory tract causing pneumonia and various syndromes of respiratory distress. CoVs also have neuroinvasive capabilities because they can spread from the respiratory tract to the CNS. Once infection begins in the CNS cells, it can

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Wilkinson, Daniel S., Cosette Champion, Pakawat Chongsathidkiet, Haichen Wang, Daniel Laskowitz, and Peter Fecci. "Bone marrow T cell sequestration as a novel mode of CNS immune privilege." Journal of Immunology 204, no. 1_Supplement (2020): 78.14. http://dx.doi.org/10.4049/jimmunol.204.supp.78.14.

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Abstract The central nervous system (CNS), although a site of relative immune “privilege,” is continuously monitored by immune cells. The CNS must possess means for limiting excess inflammation that can otherwise cause irreparable damage or death. Recently, we characterized a unique mode of cancer-induced immunosuppression whereby T cells become sequestered in high numbers in the bone marrow (BM) of humans and mice with intracranial tumors. Sequestration of T cells is mediated in part by the loss of sphingosine-1-phosphate receptor 1 (S1P1) from the T cell surface. Interestingly, this phenomen

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Përgjegji, Mateo, Klei Bame, Ketrina Ceka, Jera Cenalia , Sibora Bërdica , and Teona Bushati. "Oligodendrocyte Injury in Multiple Sclerosis." Albanian Journal of Trauma and Emergency Surgery 9, no. 1 (2025): 1682–90. https://doi.org/10.32391/ajtes.v9i1.443.

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Introduction: Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system (CNS), marked by inflammation, demyelination, and significant oligodendrocyte injury. This disease arises from a complex interplay of genetic predispositions and environmental triggers that drive immune-mediated damage to oligodendrocytes and myelin proteins. This research paper explores the multifaceted aspects of oligodendrocyte injury in MS, ranging from underlying pathophysiological mechanisms to potential therapeutic interventions and translational implications for clinical practice. Oligo

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Kravchenko, L. V., M. A. Levkovich, S. B. Berezhanskaya, et al. "Clinical and immunological criteria for prediction of thechronic course of cytomegalovirus infection on the background of hypoxic-ischemic damage of the central nervous system in children in the first year of life." HIV Infection and Immunosuppressive Disorders 14, no. 3 (2022): 35–42. http://dx.doi.org/10.22328/2077-9828-2022-14-3-35-42.

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Objective. To develop prognostic criteria for the chronic course of cytomegalovirus infection by studying disorders of the regulation of the immune response in children of the first year of life against the background of hypoxic-ischemic CNS damage.Materials and methods. 108 newborns with cytomegalovirus infection occurring against the background of perinatal hypoxicischemic lesions of the central unequal system were examined. All observed patients at 1 and 3 months of life conducted an immunological examination, including the determination of T and B-lymphocytes. Determination of the populati

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Zhelev, V. A., A. S. Pogudina, E. V. Mikhalev, et al. "Features of the recovery period of hypoxic lesion to the central nervous system in children of the first year of life with congenital heart disease." Siberian Journal of Clinical and Experimental Medicine 35, no. 3 (2020): 53–58. http://dx.doi.org/10.29001/2073-8552-2020-35-3-53-58.

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Aim. To study the features of recovery period of hypoxic lesion to the central nervous system (CNS) in children of the first year of life in the presence of congenital heart disease (CHD).Material and Methods. The study involved 80 children born full-term and premature with gestational status of 35–37 weeks with hypoxic damage to the CNS. The main observation group comprised 50 children with CHD (interventricular and atrial septal defects, open ductus arteriosus). All children underwent a comprehensive health assessment, standard echocardiography, and neurosonography at ages of five to seven d

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Woodson, Caitlin M., Shannon K. Carney, and Kylene Kehn-Hall. "Neuropathogenesis of Encephalitic Alphaviruses in Non-Human Primate and Mouse Models of Infection." Pathogens 14, no. 2 (2025): 193. https://doi.org/10.3390/pathogens14020193.

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Encephalitic alphaviruses, including eastern, Venezuelan, and western equine encephalitis virus (EEEV, VEEV, and WEEV, respectively) are New World alphaviruses primarily transmitted by mosquitos that cause debilitating and lethal central nervous system (CNS) disease in both humans and horses. Despite over one hundred years of research on these viruses, the underpinnings of the molecular mechanisms driving virally induced damage to the CNS remain unresolved. Moreover, virally induced encephalitis following exposure to these viruses causes catastrophic damage to the CNS, and survivors of infecti

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Lee, Eun-Jae. "Oculomotor manifestations in inflammatory central nervous system demyelinating diseases: a narrative review." Research in Vestibular Science 24, no. 1 (2025): 27–36. https://doi.org/10.21790/rvs.2024.022.

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Inflammatory central nervous system (CNS) demyelinating diseases are a group of disorders in which inflammation within the CNS damages the myelin sheath, a protective and conductive layer surrounding nerve fiber in the brain and spinal cord, leading to various neurological symptoms. Common conditions include multiple sclerosis and neuromyelitis optica spectrum disorders, both characterized by relapses and progressive deterioration over time. Given their frequent involvement of the brainstem and cerebellum, these diseases often manifest with oculomotor findings, such as ocular misalignment and

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Manapova, R. M., Alaudin M. Aliskandiev, and M. I. Izrailov. "RISK FACTORS FOR GASTRODUODENAL PATHOLOGY IN CHILDREN WITH PERINATAL DAMAGE TO THE CENTRAL NERVOUS SYSTEM." Russian Pediatric Journal 21, no. 6 (2019): 345–49. http://dx.doi.org/10.18821/1560-9561-2018-21-6-345-349.

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It is generally accepted the risk factors for the development of the gastrointestinal tract (GIT) diseases to have a hereditary predisposition, unfavorable environmental conditions, eating disorders, emotional stress, excessive body weight, and inactivity. Also in a number of studies, it was convincingly shown the perinatal central nervous system (CNS) damage to be a risk factor for the development of GIT diseases; in the history of children with perinatal CNS lesions, chronic gastrointestinal diseases develop 3-4 times more often than in children without it in the history. Perinatal CNS damag

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Nedelea, Gabriel, Mădălina Iuliana Muşat, Smaranda Ioana Mitran, Mihai Călin Ciorbagiu, and Bogdan Cătălin. "Acute liver damage generates age independent microglia morphology changes in mice." Romanian Journal of Morphology and Embryology 65, no. 4 (2025): 679–85. https://doi.org/10.47162/rjme.65.4.15.

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Non-alcoholic fatty liver disease (NAFLD) has emerged as a silent global epidemic, frequently contributing to systemic inflammation. As the primary immune cells of the central nervous system (CNS), microglia undergo morphological changes that serve as critical indicators of CNS health. In this study, we aimed to quantify alterations in microglial morphology within the cortex of young and aged mice with liver damage. Our results demonstrated that hepatic dysfunction leads to a significant increase in total branch length in both young (285.79±68.23 μm) and aged animals (268.67±69.06 μm), compare

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Jiang, Qian, Run-Ping Li, Ying Tang, Ye-Qing Wang, Chong Liu та Mei-Li Guo. "Bakkenolide-IIIa Protects Against Cerebral Damage Via Inhibiting NF-κB Activation". CNS Neuroscience & Therapeutics 21, № 12 (2015): 943–52. http://dx.doi.org/10.1111/cns.12470.

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D'Amico, A., F. Briganti, F. Caranci, et al. "Studio RM dei danni da chemio e radioterapia sul sistema nervoso centrale in età pediatrica." Rivista di Neuroradiologia 16, no. 3 (2003): 439–44. http://dx.doi.org/10.1177/197140090301600318.

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Chemotherapy and radiotherapy are essential in the treatment of certain childhood CNS tumours. Unfortunately, their well-known neurotoxic potential may cause CNS injury, especially in childhood. This study describes literature reports on the possible neurotoxic damage caused by chemotherapy and radiotherapy and our own experience in the MR follow-up of 58 patients.

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