CoChat
Sign Up
Cited by 22Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchNeuroinflammation and Neurodegeneration Mechanisms

Traumatic Brain Injury and Inflammation: Emerging Role of Innate and Adaptive Immunity

Open access
Dardiotis, Efthimios, Karanikas, Vaios, Paterakis, Konstantinos, Fountas, Kostas, M., Georgios·2012·Brain Injury - Pathogenesis, Monitoring, Recovery and Management
DOI 10.5772/27840
Open this paper in CoChat — free accountOpen PDF

Abstract

Traumatic brain injury (TBI) has long been recognized as a leading cause of mortality and permanent neurological disability worldwide and has been described as a silent epidemic of modern societies.It is most common amongst young individuals, in their productive years of life, thereby causing a significant social and financial burden for them, their families and the public health system (Maas et al., 2008).The pathophysiology of TBI is complex and multifactorial with several pathways involved in the damage of the brain.TBI has been classified into primary and secondary injury.The primary injury is the result of the external mechanical force at the moment of trauma leading to skull fractures, brain contusions, lacerations, diffuse axonal injuries, vascular tearing and intracranial hemorrhages (Maas et al., 2008).The initial impact damages directly the neuronal tissue via excitatory amino acids release and massive ionic influx referred to as traumatic depolarization (Katayama et al., 1995).Secondary neuronal damage is induced immediately after primary injury and is mediated through several pathophysiologic mechanisms including raised intracranial pressure, disruption of blood brain barrier, brain edema, decreased cerebral blood flow, altered tissue perfusion, cerebral hypoxia, ischemia and reperfusion injury (Graham et al., 2000).Furthermore, a cascade of molecular, neurochemical, cellular and immune processes contribute to secondary damage such as disruption of calcium homeostasis, oxidative stress, excitatory mediators release, cytoskeletal and mitochondrial dysfunction, Ab-peptide deposition, inflammatory cell infiltration and neuronal cell apoptosis and death (Greve & Zink, 2009).Gene expression studies have demonstrated that several genes are implicated in the pathophysiology of secondary brain damage (Lei et al., 2009).Secondary cascade of events were found to dramatically aggregate primary neuronal damage and given that primary injury is unavoidable and irreversible, secondary processes are the targets of current therapeutic strategies and trials on neuroprotective agents (Jain, 2008).

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.5772/27840

Cites

6 of 6 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Excessive or chronic neuroinflammation is linked to progressive changes, including atrophy, neuronal loss, and axonal degeneration.

    “Excessive or chronic neuroinflammation is linked to progressive changes, including atrophy, neuronal loss, and axonal degeneration (84, 103–105).”

    From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [103]

    The Innate immunity section (page not provided) links excessive or prolonged microglial activation to impaired neuronal survival and progressive degeneration after traumatic brain injury. The Introduction also describes neuronal apoptosis and death, but the cited passages do not specifically link chronic neuroinflammation to atrophy or axonal degeneration. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 112

  1. References Aihara, N., et al. (1995). Altered immunoexpression of microglia and macrophages after mild head injury. J Neurotrauma, 12, 1, pp. 53-63.
  2. Allan, S. M. and Rothwell, N. J. (2001). Cytokines and acute neurodegeneration. Nat Rev Neurosci, 2, 10, pp. 734-44.
  3. Aloisi, F. (2001). Immune function of microglia. Glia, 36, 2, pp. 165-79.
  4. Ankeny, D. P., et al. (2006). Spinal cord injury triggers systemic autoimmunity: evidence for chronic B lymphocyte activation and lupus-like autoantibody synthesis. J Neurochem, 99, 4, pp. 1073-87.
  5. Appel, E., et al. (1997). Regulation of GDNF expression in cultured astrocytes by inflammatory stimuli. Neuroreport, 8, 15, pp. 3309-12.
  6. Arand, M., et al. (2001). Early inflammatory mediator response following isolated traumatic brain injury and other major trauma in humans. Langenbecks Arch Surg, 386, 4, pp. 241-8.
  7. Arend, W. P. (1991). Interleukin 1 receptor antagonist. A new member of the interleukin 1 family. J Clin Invest, 88, 5, pp. 1445-51.
  8. Baskaya, M. K., et al. (1997). The biphasic opening of the blood-brain barrier in the cortex and hippocampus after traumatic brain injury in rats. Neurosci Lett, 226, 1, pp. 33-6.
  9. Becher, B., et al. (2000). Brain-immune connection: immuno-regulatory properties of CNS- resident cells. Glia, 29, 4, pp. 293-304.
  10. Beck, K. D., et al. (2010). Quantitative analysis of cellular inflammation after traumatic spinal cord injury: evidence for a multiphasic inflammatory response in the acute to chronic environment. Brain, 133, Pt 2, pp. 433-47.
  11. Bell, M. D., et al. (1996). Overriding the brain's intrinsic resistance to leukocyte recruitment with intraparenchymal injections of recombinant chemokines. Neuroscience, 74, 1, pp. 283-92.
  12. Bellinger, F. P., et al. (1993). Interleukin 1 beta inhibits synaptic strength and long-term potentiation in the rat CA1 hippocampus. Brain Res, 628, 1-2, pp. 227-34.
  13. Beschorner, R., et al. (2000). Differential regulation of the monocytic calcium-binding peptides macrophage-inhibiting factor related protein-8 (MRP8/S100A8) and allograft inflammatory factor-1 (AIF-1) following human traumatic brain injury. Acta Neuropathol, 100, 6, pp. 627-34.
  14. Block, M. L., et al. (2007). Microglia-mediated neurotoxicity: uncovering the molecular mechanisms. Nat Rev Neurosci, 8, 1, pp. 57-69.
  15. Carlos, T. M., et al. (1997). Expression of endothelial adhesion molecules and recruitment of neutrophils after traumatic brain injury in rats. J Leukoc Biol, 61, 3, pp. 279-85.
  16. Chiaretti, A., et al. (2008). Interleukin-6 and nerve growth factor upregulation correlates with improved outcome in children with severe traumatic brain injury. J Neurotrauma, 25, 3, pp. 225-34.
  17. Chiaretti, A., et al. (2005). Interleukin 1beta and interleukin 6 relationship with paediatric head trauma severity and outcome. Childs Nerv Syst, 21, 3, pp. 185-93; discussion 194.
  18. Cho, B. P., et al. (2006). Pathological dynamics of activated microglia following medial forebrain bundle transection. Glia, 53, 1, pp. 92-102.
  19. Csuka, E., et al. (1999). IL-10 levels in cerebrospinal fluid and serum of patients with severe traumatic brain injury: relationship to IL-6, TNF-alpha, TGF-beta1 and blood-brain barrier function. J Neuroimmunol, 101, 2, pp. 211-21.
  20. Czigner, A., et al. (2007). Kinetics of the cellular immune response following closed head injury. Acta Neurochir (Wien), 149, 3, pp. 281-9.
  21. Davalos, D., et al. (2005). ATP mediates rapid microglial response to local brain injury in vivo. Nat Neurosci, 8, 6, pp. 752-8.
  22. DeKosky, S. T., et al. (1994). Upregulation of nerve growth factor following cortical trauma. Exp Neurol, 130, 2, pp. 173-7.
  23. Dinarello, C. A. (1991). Interleukin-1 and interleukin-1 antagonism. Blood, 77, 8, pp. 1627-52.
  24. Dinkel, K., et al. (2004). Neurotoxic effects of polymorphonuclear granulocytes on hippocampal primary cultures. Proc Natl Acad Sci U S A, 101, 1, pp. 331-6.
  25. Engel, S., et al. (2000). Dynamics of microglial activation after human traumatic brain injury are revealed by delayed expression of macrophage-related proteins MRP8 and MRP14. Acta Neuropathol, 100, 3, pp. 313-22.
  26. Fagan, A. M. and Gage, F. H. (1990). Cholinergic sprouting in the hippocampus: a proposed role for IL-1. Exp Neurol, 110, 1, pp. 105-20.
  27. Fan, L., et al. (1995). Experimental brain injury induces expression of interleukin-1 beta mRNA in the rat brain. Brain Res Mol Brain Res, 30, 1, pp. 125-30.
  28. Farber, K. and Kettenmann, H. (2005). Physiology of microglial cells. Brain Res Brain Res Rev, 48, 2, pp. 133-43.
  29. Fee, D., et al. (2003). Activated/effector CD4+ T cells exacerbate acute damage in the central nervous system following traumatic injury. J Neuroimmunol, 136, 1-2, pp. 54-66.
  30. Fleming, J. C., et al. (2006). The cellular inflammatory response in human spinal cords after injury. Brain, 129, Pt 12, pp. 3249-69.
  31. Ford, A. L., et al. (1996). Microglia induce CD4 T lymphocyte final effector function and death. J Exp Med, 184, 5, pp. 1737-45.
  32. Gabellec, M. M., et al. (1999). Expression of interleukin-1 genes and interleukin-1 receptors in the mouse brain after hippocampal injury. Neurosci Res, 33, 4, pp. 251-60.
  33. Gao, H. M. and Hong, J. S. (2008). Why neurodegenerative diseases are progressive: uncontrolled inflammation drives disease progression. Trends Immunol, 29, 8, pp. 357-65.
  34. Gebicke-Haerter, P. J., et al. (1996). Molecular mechanisms of microglial activation. A. Implications for regeneration and neurodegenerative diseases. Neurochem Int, 29, 1, pp. 1-12.
  35. Gentleman, S. M., et al. (2004). Long-term intracerebral inflammatory response after traumatic brain injury. Forensic Sci Int, 146, 2-3, pp. 97-104.
  36. Goodman, J. C., et al. (1990). Elevation of t u m o r . J Neuroimmunol, 30, 2-3, pp. 213-7.
  37. Graham, D. I., et al. (2000). Recent advances in neurotrauma. J Neuropathol Exp Neurol, 59, 8, pp. 641-51.
  38. Greve, M. W. and Zink, B. J. (2009). Pathophysiology of traumatic brain injury. Mt Sinai J Med, 76, 2, pp. 97-104.
  39. Hanisch, U. K. and Kettenmann, H. (2007). Microglia: active sensor and versatile effector cells in the normal and pathologic brain. Nat Neurosci, 10, 11, pp. 1387-94.
  40. Hauben, E., et al. (2000). Passive or active immunization with myelin basic protein promotes recovery from spinal cord contusion. J Neurosci, 20, 17, pp. 6421-30.
  41. Herx, L. M., et al. (2000). Central nervous system-initiated inflammation and neurotrophism in trauma: IL-1 beta is required for the production of ciliary neurotrophic factor. J Immunol, 165, 4, pp. 2232-9.
  42. Hickey, W. F. (1999). Leukocyte traffic in the central nervous system: the participants and their roles. Semin Immunol, 11, 2, pp. 125-37.
  43. Holmin, S. and Mathiesen, T. (1999). Long-term intracerebral inflammatory response after experimental focal brain injury in rat. Neuroreport, 10, 9, pp. 1889-91.
  44. Holmin, S., et al. (1997). Delayed cytokine expression in rat brain following experimental contusion. J Neurosurg, 86, 3, pp. 493-504.
  45. Hopkins, S. J. and Rothwell, N. J. (1995). Cytokines and the nervous system. I: Expression and recognition. Trends Neurosci, 18, 2, pp. 83-8.
  46. Hoshino, S., et al. (1998). Emergence of immunoreactivities for phosphorylated tau and amyloid-beta protein in chronic stage of fluid percussion injury in rat brain. Neuroreport, 9, 8, pp. 1879-83.
  47. Ide, C. F., et al. (1996). Cellular and molecular correlates to plasticity during recovery from injury in the developing mammalian brain. Prog Brain Res, 108, pp. 365-77.
  48. Jain, K. K. (2008). Neuroprotection in traumatic brain injury. Drug Discov Today, 13, 23-24, pp. 1082-9.
  49. Karman, J., et al. (2004). Initiation of immune responses in brain is promoted by local dendritic cells. J Immunol, 173, 4, pp. 2353-61.
  50. Katayama, Y., et al. (1995). Role of excitatory amino acid-mediated ionic fluxes in traumatic brain injury. Brain Pathol, 5, 4, pp. 427-35.
  51. Kempermann, G. and Neumann, H. (2003). Neuroscience. Microglia: the enemy within? Science, 302, 5651, pp. 1689-90.
  52. Kettenmann, H., et al. (2011). Physiology of microglia. Physiol Rev, 91, 2, pp. 461-553.
  53. Kigerl, K. A., et al. (2006). Comparative analysis of lesion development and intraspinal inflammation in four strains of mice following spinal contusion injury. J Comp Neurol, 494, 4, pp. 578-94.
  54. Kil, K., et al. (1999). T cell responses to myelin basic protein in patients with spinal cord injury and multiple sclerosis. J Neuroimmunol, 98, 2, pp. 201-7.
  55. Knoblach, S. M. and Faden, A. I. (2002). Administration of either anti-intercellular adhesion molecule-1 or a nonspecific control antibody improves recovery after traumatic brain injury in the rat. J Neurotrauma, 19, 9, pp. 1039-50.
  56. Knoblach, S. M., et al. (1999). Early neuronal expression of tumor necrosis factor-alpha after experimental brain injury contributes to neurological impairment. J Neuroimmunol, 95, 1-2, pp. 115-25.
  57. Kossmann, T., et al. (1997). Interleukin-8 released into the cerebrospinal fluid after brain injury is associated with blood-brain barrier dysfunction and nerve growth factor production. J Cereb Blood Flow Metab, 17, 3, pp. 280-9.
  58. Lei, P., et al. (2009). Microarray based analysis of microRNA expression in rat cerebral cortex after traumatic brain injury. Brain Res, 1284, pp. 191-201.
  59. Lenzlinger, P. M., et al. (2001). Markers for cell-mediated immune response are elevated in cerebrospinal fluid and serum after severe traumatic brain injury in humans. J Neurotrauma, 18, 5, pp. 479-89.
  60. Ling, C., et al. (2003). In situ processing and distribution of intracerebrally injected OVA in the CNS. J Neuroimmunol, 141, 1-2, pp. 90-8.
  61. Liu, G. J., et al. (2009). Glutamate induces directed chemotaxis of microglia. Eur J Neurosci, 29, 6, pp. 1108-18.
  62. Loane, D. J. and Byrnes, K. R. (2010). Role of microglia in neurotrauma. Neurotherapeutics, 7, 4, pp. 366-77.
  63. Maas, A. I., et al. (2006). Efficacy and safety of dexanabinol in severe traumatic brain injury: results of a phase III randomised, placebo-controlled, clinical trial. Lancet Neurol, 5, 1, pp. 38-45.
  64. Maas, A. I., et al. (2008). Moderate and severe traumatic brain injury in adults. Lancet Neurol, 7, 8, pp. 728-41.
  65. Mantovani, A., et al. (2004). The chemokine system in diverse forms of macrophage activation and polarization. Trends Immunol, 25, 12, pp. 677-86.
  66. McCluskey, L. P. and Lampson, L. A. (2000). Local neurochemicals and site-specific immune regulation in the CNS. J Neuropathol Exp Neurol, 59, 3, pp. 177-87.
  67. McKeating, E. G., et al. (1998). Leukocyte adhesion molecule profiles and outcome after traumatic brain injury. Acta Neurochir Suppl, 71, pp. 200-2.
  68. Minambres, E., et al. (2003). Correlation between transcranial interleukin-6 gradient and outcome in patients with acute brain injury. Crit Care Med, 31, 3, pp. 933-8.
  69. Moalem, G., et al. (1999). Autoimmune T cells protect neurons from secondary degeneration after central nervous system axotomy. Nat Med, 5, 1, pp. 49-55.
  70. Morganti-Kossmann, M. C., et al. (2001). Role of cerebral inflammation after traumatic brain injury: a revisited concept. Shock, 16, 3, pp. 165-77.
  71. Morganti-Kossmann, M. C., et al. (2002). Inflammatory response in acute traumatic brain injury: a double-edged sword. Curr Opin Crit Care, 8, 2, pp. 101-5.
  72. Nakamura, Y. (2002). Regulating factors for microglial activation. Biol Pharm Bull, 25, 8, pp. 945-53.
  73. Neumann, H., et al. (1996). Neuronal control of MHC class II inducibility in rat astrocytes and microglia. Eur J Neurosci, 8, 12, pp. 2582-90.
  74. Nguyen, H. X., et al. (2007). Polymorphonuclear leukocytes promote neurotoxicity through release of matrix metalloproteinases, reactive oxygen species, and TNF-alpha. J Neurochem, 102, 3, pp. 900-12.
  75. Nimmerjahn, A., et al. (2005). Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo. Science, 308, 5726, pp. 1314-8.
  76. Penkowa, M., et al. (2003). Astrocyte-targeted expression of interleukin-6 protects the central nervous system during neuroglial degeneration induced by 6-aminonicotinamide. J Neurosci Res, 73, 4, pp. 481-96.
  77. Penkowa, M., et al. (2000). Impaired inflammatory response and increased oxidative stress and neurodegeneration after brain injury in interleukin-6-deficient mice. Glia, 32, 3, pp. 271-85.
  78. Pleines, U. E., et al. (1998). Soluble ICAM-1 in CSF coincides with the extent of cerebral damage in patients with severe traumatic brain injury. J Neurotrauma, 15, 6, pp. 399- 409.
  79. Popovich, P. G. and Longbrake, E. E. (2008). Can the immune system be harnessed to repair the CNS? Nat Rev Neurosci, 9, 6, pp. 481-93.
  80. Popovich, P. G., et al. (1996). Concept of autoimmunity following spinal cord injury: possible roles for T lymphocytes in the traumatized central nervous system. J Neurosci Res, 45, 4, pp. 349-63.
  81. Postler, E., et al. (1997). Expression of the S-100 proteins MRP-8 and -14 in ischemic brain lesions. Glia, 19, 1, pp. 27-34.
  82. Raivich, G. (2005). Like cops on the beat: the active role of resting microglia. Trends Neurosci, 28, 11, pp. 571-3.
  83. Rhodes, J. (2011). Peripheral immune cells in the pathology of traumatic brain injury? Curr Opin Crit Care, 17, 2, pp. 122-30.
  84. Riva-Depaty, I., et al. (1994). Contribution of peripheral macrophages and microglia to the cellular reaction after mechanical or neurotoxin-induced lesions of the rat brain. Exp Neurol, 128, 1, pp. 77-87.
  85. Romano, M., et al. (1997). Role of IL-6 and its soluble receptor in induction of chemokines and leukocyte recruitment. Immunity, 6, 3, pp. 315-25.
  86. Rothwell, N. J. and Hopkins, S. J. (1995). Cytokines and the nervous system II: Actions and mechanisms of action. Trends Neurosci, 18, 3, pp. 130-6.
  87. Rothwell, N. J. and Luheshi, G. N. (2000). Interleukin 1 in the brain: biology, pathology and therapeutic target. Trends Neurosci, 23, 12, pp. 618-25.
  88. Sanderson, K. L., et al. (1999). Interleukin-1 receptor antagonist attenuates regional neuronal cell death and cognitive dysfunction after experimental brain injury. J Cereb Blood Flow Metab, 19, 10, pp. 1118-25.
  89. Scherbel, U., et al. (1999). Differential acute and chronic responses of tumor necrosis factor- deficient mice to experimental brain injury. Proc Natl Acad Sci U S A, 96, 15, pp. 8721-6.
  90. Schwartz, M., et al. (2009). Boosting T-cell immunity as a therapeutic approach for neurodegenerative conditions: the role of innate immunity. Neuroscience, 158, 3, pp. 1133-42.
  91. Schwartz, M., et al. (2003). Protective autoimmunity against the enemy within: fighting glutamate toxicity. Trends Neurosci, 26, 6, pp. 297-302.
  92. Schwartz, M. and Shechter, R. (2010). Systemic inflammatory cells fight off neurodegenerative disease. Nat Rev Neurol, 6, 7, pp. 405-10.
  93. Semple, B. D., et al. (2010a). Deficiency of the chemokine receptor CXCR2 attenuates neutrophil infiltration and cortical damage following closed head injury. Neurobiol Dis, 40, 2, pp. 394-403.
  94. Serpe, C. J., et al. (2003). CD4+ T, but not CD8+ or B, lymphocytes mediate facial motoneuron survival after facial nerve transection. Brain Behav Immun, 17, 5, pp. 393-402.
  95. Shiozaki, T., et al. (2005). Cerebrospinal fluid concentrations of anti-inflammatory mediators in early-phase severe traumatic brain injury. Shock, 23, 5, pp. 406-10.
  96. Shlosberg, D., et al. (2010). Blood-brain barrier breakdown as a therapeutic target in traumatic brain injury. Nat Rev Neurol, 6, 7, pp. 393-403.
  97. Shohami, E., et al. (1997). Cytokine production in the brain following closed head injury: dexanabinol (HU-211) is a novel TNF-alpha inhibitor and an effective neuroprotectant. J Neuroimmunol, 72, 2, pp. 169-77.
  98. Shohami, E., et al. (1994). Closed head injury triggers early production of TNF alpha and IL- 6 by brain tissue. J Cereb Blood Flow Metab, 14, 4, pp. 615-9.
  99. Singhal, A., et al. (2002). Association between cerebrospinal fluid interleukin-6 concentrations and outcome after severe human traumatic brain injury. J Neurotrauma, 19, 8, pp. 929-37.
  100. Smith, D. H., et al. (1997). Progressive atrophy and neuron death for one year following brain trauma in the rat. J Neurotrauma, 14, 10, pp. 715-27.
  101. Spranger, M., et al. (1990). Regulation of Nerve Growth Factor (NGF) Synthesis in the Rat Central Nervous System: Comparison between the Effects of Interleukin-1 and Various Growth Factors in Astrocyte Cultures and in vivo. Eur J Neurosci, 2, 1, pp. 69-76.
  102. Streit, W. J., et al. (1999). Reactive microgliosis. Prog Neurobiol, 57, 6, pp. 563-81.
  103. Tehranian, R., et al. (2002). Improved recovery and delayed cytokine induction after closed head injury in mice with central overexpression of the secreted isoform of the interleukin-1 receptor antagonist. J Neurotrauma, 19, 8, pp. 939-51.
  104. Toulmond, S. and Rothwell, N. J. (1995). Interleukin-1 receptor antagonist inhibits neuronal damage caused by fluid percussion injury in the rat. Brain Res, 671, 2, pp. 261-6.
  105. Tyurin, V. A., et al. (2000). Oxidative stress following traumatic brain injury in rats: quantitation of biomarkers and detection of free radical intermediates. J Neurochem, 75, 5, pp. 2178-89.
  106. Wang, C. X. and Shuaib, A. (2002). Involvement of inflammatory cytokines in central nervous system injury. Prog Neurobiol, 67, 2, pp. 161-72.
  107. Weaver, K. D., et al. (2000). Effect of leukocyte-endothelial adhesion antagonism on neutrophil migration and neurologic outcome after cortical trauma. J Trauma, 48, 6, pp. 1081-90.
  108. Whalen, M. J., et al. (1999). Effect of traumatic brain injury in mice deficient in intercellular adhesion molecule-1: assessment of histopathologic and functional outcome. J Neurotrauma, 16, 4, pp. 299-309.
  109. Whalen, M. J., et al. (1999). Neutrophils do not mediate blood-brain barrier permeability early after controlled cortical impact in rats. J Neurotrauma, 16, 7, pp. 583-94.
  110. Whalen, M. J., et al. (2000). Interleukin-8 is increased in cerebrospinal fluid of children with severe head injury. Crit Care Med, 28, 4, pp. 929-34.
  111. Winter, C. D., et al. (2002). A microdialysis method for the recovery of IL-1beta, IL-6 and nerve growth factor from human brain in vivo. J Neurosci Methods, 119, 1, pp. 45-50.
  112. Wolf, S. A., et al. (2002). Neuroprotection by T-cells depends on their subtype and activation state. J Neuroimmunol, 133, 1-2, pp. 72-80.

Cited by

Sorted by citations

Authors
Dardiotis, E., Karanikas, V., Paterakis, K., Fountas, K., & M., G.
Affiliations
University of Thessaly (GR)
ORCID
Venue
Brain Injury - Pathogenesis, Monitoring, Recovery and Management
Publisher
InTech
Published
2012-03-23
DOI
10.5772/27840
OpenAlex
W1566553376
Cited by
22
References
6
Citations by year
2026: 1 · 2024: 2 · 2022: 1 · 2021: 1 · 2019: 1 · 2018: 1 · 2017: 3 · 2016: 6 · 2015: 2 · 2014: 2 · 2013: 1 · 2012: 1
FWCI
5.03
Type
book chapter
Language
en
Open access
Licence
cc-by
Locations
  • InTech eBooks (publishedVersion, cc-by)
  • BiblioBoard Library Catalog (Open Research Library) (submittedVersion, cc-by)
  • Contact-less Assessment of In-vivo Body Signals Using Microwave Doppler Radar (InTech) (submittedVersion, cc-by)
Topics
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
traumatic brain injury, neuroinflammation, innate immunity, adaptive immunity, secondary brain injury, primary brain injury, excitotoxicity, oxidative stress, ischemia-reperfusion injury, blood-brain barrier disruption, neuroprotection, inflammatory cell infiltration

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review