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Neuroinflammation and Hypothalamo-Pituitary Dysfunction: Focus of Traumatic Brain Injury

Mele, Chiara, Pingue, Valeria, Caputo, Marina, Zavattaro, Marco, Pagano, Loredana, Prodam, Flavia, Nardone, Antonio, Aimaretti, Gianluca, Marzullo, Paolo·2021·International Journal of Molecular Sciences

Abstract

The incidence of traumatic brain injury (TBI) has increased over the last years with an important impact on public health. Many preclinical and clinical studies identified multiple and heterogeneous TBI-related pathophysiological mechanisms that are responsible for functional, cognitive, and behavioral alterations. Recent evidence has suggested that post-TBI neuroinflammation is responsible for several long-term clinical consequences, including hypopituitarism. This review aims to summarize current evidence on TBI-induced neuroinflammation and its potential role in determining hypothalamic-pituitary dysfunctions.

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Research works printed but not linked: 142

  1. Maas, 2008, Moderate and severe traumatic brain injury in adults, Lancet Neurol., 7, 728, 10.1016/S1474-4422(08)70164-9 · DOI · Paper page
  2. Dinet, 2019, Brain-Immune Interactions and Neuroinflammation after Traumatic Brain Injury, Front. Neurosci., 13, 1178, 10.3389/fnins.2019.01178 · DOI
  3. Kaur, 2018, Recent Advances in Pathophysiology of Traumatic Brain Injury, Curr. Neuropharmacol., 16, 1224, 10.2174/1570159X15666170613083606 · DOI · Paper page
  4. Hinzman, 2016, Excitotoxicity and Metabolic Crisis Are Associated with Spreading Depolarizations in Severe Traumatic Brain Injury Patients, J. Neurotrauma, 33, 1775, 10.1089/neu.2015.4226 · DOI
  5. Russo, 2016, Inflammatory neuroprotection following traumatic brain injury, Science, 353, 783, 10.1126/science.aaf6260 · DOI · Paper page
  6. Pearn, 2017, Pathophysiology Associated with Traumatic Brain Injury: Current Treatments and Potential Novel Therapeutics, Cell Mol. Neurobiol., 37, 571, 10.1007/s10571-016-0400-1 · DOI · Paper page
  7. Chandran, 2018, A combination antioxidant therapy to inhibit NOX2 and activate Nrf2 decreases secondary brain damage and improves functional recovery after traumatic brain injury, J. Cereb. Blood Flow Metab., 38, 1818, 10.1177/0271678X17738701 · DOI
  8. Shi, 2019, Dissemination of brain inflammation in traumatic brain injury, Cell Mol. Immunol., 16, 523, 10.1038/s41423-019-0213-5 · DOI
  9. Olson, 2004, Microglia initiate central nervous system innate and adaptive immune responses through multiple TLRs, J. Immunol., 173, 3916, 10.4049/jimmunol.173.6.3916 · DOI · Paper page
  10. Hailer, 2008, Immunosuppression after traumatic or ischemic CNS damage: It is neuroprotective and illuminates the role of microglial cells, Prog. Neurobiol., 84, 211, 10.1016/j.pneurobio.2007.12.001 · DOI
  11. Plesnila, 2016, The immune system in traumatic brain injury, Curr. Opin. Pharmacol., 26, 110, 10.1016/j.coph.2015.10.008 · DOI
  12. Needham, 2019, The immunological response to traumatic brain injury, J. Neuroimmunol., 332, 112, 10.1016/j.jneuroim.2019.04.005 · DOI
  13. Pop, 2011, A neurovascular perspective for long-term changes after brain trauma, Transl. Stroke Res., 2, 533, 10.1007/s12975-011-0126-9 · DOI
  14. Nguyen, 2016, The International Incidence of Traumatic Brain Injury: A Systematic Review and Meta-Analysis, Can. J. Neurol. Sci., 43, 774, 10.1017/cjn.2016.290 · DOI · Paper page
  15. Peeters, 2015, Epidemiology of traumatic brain injury in Europe, Acta Neurochir., 157, 1683, 10.1007/s00701-015-2512-7 · DOI · Paper page
  16. Gennarelli, 1994, Comparison of mortality, morbidity, and severity of 59,713 head injured patients with 114,447 patients with extracranial injuries, J. Trauma, 37, 962, 10.1097/00005373-199412000-00016 · DOI
  17. Baum, 2016, Predictors of Outcomes in Traumatic Brain Injury, World Neurosurg., 90, 525, 10.1016/j.wneu.2015.12.012 · DOI
  18. Jain, S., and Iverson, L.M. (2021, January 14). Glasgow Coma Scale, Available online: https://www.ncbi.nlm.nih.gov/books/NBK513298/.
  19. Pavlovic, 2019, Traumatic brain injury: Neuropathological, neurocognitive and neurobehavioral sequelae, Pituitary, 22, 270, 10.1007/s11102-019-00957-9 · DOI · Paper page
  20. Melmed, S., and Jameson, J.L. (2005). Disorders of the anterior pituitary and hypothalamus. Harrison’s Principles of Internal Medicine, McGraw-Hill. [16th ed.].
  21. Bondanelli, 2004, Occurrence of pituitary dysfunction following traumatic brain injury, J. Neurotrauma, 21, 685, 10.1089/0897715041269713 · DOI · Paper page
  22. Park, 2010, Anterior pituitary dysfunction in moderate-to-severe chronic traumatic brain injury patients and the influence on functional outcome, Brain Inj., 24, 1330, 10.3109/02699052.2010.506863 · DOI · Paper page
  23. Caputo, 2019, Clinical picture and the treatment of TBI-induced hypopituitarism, Pituitary, 22, 261, 10.1007/s11102-019-00956-w · DOI · Paper page
  24. Zheng, 2014, Dynamic pituitary hormones change after traumatic brain injury, Neurol. India, 62, 280, 10.4103/0028-3886.136922 · DOI · Paper page
  25. Popovic, 2005, Hypopituitarism following traumatic brain injury, Front. Horm. Res., 33, 33
  26. Schneider, 2005, Anterior pituitary hormone abnormalities following traumatic brain injury, J. Neurotrauma, 22, 937, 10.1089/neu.2005.22.937 · DOI
  27. Heather, 2011, Traumatic brain injury: Is the pituitary out of harm’s way?, J. Pediatr., 159, 686, 10.1016/j.jpeds.2011.05.054 · DOI
  28. Tanriverdi, 2008, Antipituitary antibodies after traumatic brain injury: Is head trauma-induced pituitary dysfunction associated with autoimmunity?, Eur. J. Endocrinol., 159, 7, 10.1530/EJE-08-0050 · DOI · Paper page
  29. Tanriverdi, 2008, Apolipoprotein E3/E3 genotype decreases the risk of pituitary dysfunction after traumatic brain injury due to various causes: Preliminary data, J. Neurotrauma, 25, 1071, 10.1089/neu.2007.0456 · DOI · Paper page
  30. Karaca, 2016, GH and Pituitary Hormone Alterations After Traumatic Brain Injury, Prog. Mol. Biol. Transl. Sci., 138, 167, 10.1016/bs.pmbts.2015.10.010 · DOI
  31. Tanriverdi, 2010, Persistent neuroinflammation may be involved in the pathogenesis of traumatic brain injury (TBI)-induced hypopituitarism: Potential genetic and autoimmune factors, J. Neurotrauma, 27, 301, 10.1089/neu.2009.1102 · DOI
  32. 2020, Traumatic brain injuries induced pituitary dysfunction: A call for algorithms, Endocr. Connect., 9, R112, 10.1530/EC-20-0117 · DOI · Paper page
  33. Carson, 2006, CNS immune privilege: Hiding in plain sight, Immunol. Rev., 213, 48, 10.1111/j.1600-065X.2006.00441.x · DOI · Paper page
  34. Puntambekar, 2018, Cellular players that shape evolving pathology and neurodegeneration following traumatic brain injury, Brain. Behav. Immun., 71, 9, 10.1016/j.bbi.2018.03.033 · DOI
  35. Lehto, 2020, Long-lasting blood-brain barrier dysfunction and neuroinflammation after traumatic brain injury, Neurobiol. Dis., 145, 105080, 10.1016/j.nbd.2020.105080 · DOI
  36. McKee, 2016, Emerging Roles for the Immune System in Traumatic Brain Injury, Front. Immunol., 7, 556, 10.3389/fimmu.2016.00556 · DOI · Paper page
  37. Shetty, 2014, Blood brain barrier dysfunction and delayed neurological deficits in mild traumatic brain injury induced by blast shock waves, Front. Cell Neurosci., 8, 232
  38. Bhowmick, 2019, Impairment of pericyte-endothelium crosstalk leads to blood-brain barrier dysfunction following traumatic brain injury, Exp. Neurol., 317, 260, 10.1016/j.expneurol.2019.03.014 · DOI
  39. Corrigan, 2016, Neurogenic inflammation after traumatic brain injury and its potentiation of classical inflammation, J. Neuroinflammation, 13, 264, 10.1186/s12974-016-0738-9 · DOI · Paper page
  40. Michinaga, 2018, Delayed Administration of BQ788, an ETB Antagonist, after Experimental Traumatic Brain Injury Promotes Recovery of Blood-Brain Barrier Function and a Reduction of Cerebral Edema in Mice, J. Neurotrauma, 35, 1481, 10.1089/neu.2017.5421 · DOI
  41. Sheikh, 2009, Lysophosphatidylcholine induces glial cell activation: Role of rho kinase, Glia, 57, 898, 10.1002/glia.20815 · DOI
  42. Martinon, 2002, The inflammosome: A molecular platform triggering activation of inflammatory caspases and processing proIL-beta. Mol, Cell, 10, 417
  43. Satgunaseelan, 2007, Modulation of immune response by head injury, Injury, 38, 1392, 10.1016/j.injury.2007.10.005 · DOI · Paper page
  44. Loane, 2016, Microglia in the TBI brain: The good, the bad, and the dysregulated, Exp. Neurol., 275, 316, 10.1016/j.expneurol.2015.08.018 · DOI · Paper page
  45. Wang, 2013, Microglia/macrophage polarization dynamics in white matter after traumatic brain injury, J. Cereb. Blood Flow Metab., 33, 1864, 10.1038/jcbfm.2013.146 · DOI · Paper page
  46. Chaput, 2015, Novel Molecular Insights into Classical and Alternative Activation States of Microglia as Revealed by Stable Isotope Labeling by Amino Acids in Cell Culture (SILAC)-based Proteomics, Mol. Cell Proteomics, 14, 3173, 10.1074/mcp.M115.053926 · DOI
  47. Homsi, 2010, Blockade of acute microglial activation by minocycline promotes neuroprotection and reduces locomotor hyperactivity after closed head injury in mice: A twelve-week follow-up study, J. Neurotrauma, 27, 911, 10.1089/neu.2009.1223 · DOI
  48. Burda, 2016, Astrocyte roles in traumatic brain injury, Exp. Neurol., 275, 305, 10.1016/j.expneurol.2015.03.020 · DOI · Paper page
  49. Zagadailov, 2010, YKL-40 expression in traumatic brain injury: An initial analysis, J. Neurotrauma, 27, 1215, 10.1089/neu.2010.1310 · DOI
  50. Lucas, 2006, The role of inflammation in CNS injury and disease, Br. J. Pharmacol., 147, S232, 10.1038/sj.bjp.0706400 · DOI · Paper page
  51. Thal, 2014, The blood-brain barrier as a target in traumatic brain injury treatment, Arch. Med. Res., 45, 698, 10.1016/j.arcmed.2014.11.006 · DOI
  52. Hans, 1999, TGF-beta is elevated in the CSF of patients with severe traumatic brain injuries and parallels blood-brain barrier function, J. Neurotrauma, 16, 617, 10.1089/neu.1999.16.617 · DOI
  53. Clausen, 2009, Neutralization of interleukin-1beta modifies the inflammatory response and improves histological and cognitive outcome following traumatic brain injury in mice, Eur. J. Neurosci., 30, 385, 10.1111/j.1460-9568.2009.06820.x · DOI
  54. Clausen, 2011, Neutralization of interleukin-1β reduces cerebral edema and tissue loss and improves late cognitive outcome following traumatic brain injury in mice, Eur. J. Neurosci., 34, 110, 10.1111/j.1460-9568.2011.07723.x · DOI
  55. Tehranian, 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, 939, 10.1089/089771502320317096 · DOI
  56. Chio, 2010, Therapeutic evaluation of etanercept in a model of traumatic brain injury, J. Neurochem., 115, 921, 10.1111/j.1471-4159.2010.06969.x · DOI
  57. Clark, 1994, Neutrophil accumulation after traumatic brain injury in rats: Comparison of weight drop and controlled cortical impact models, J. Neurotrauma, 11, 499, 10.1089/neu.1994.11.499 · DOI · Paper page
  58. Nourshargh, 2014, Leukocyte migration into inflamed tissues, Immunity, 41, 694, 10.1016/j.immuni.2014.10.008 · DOI · Paper page
  59. Holmin, 1995, Biphasic edema development after experimental brain contusion in rat, Neurosci. Lett., 194, 97, 10.1016/0304-3940(95)11737-H · DOI
  60. Fletcher, 2010, T cells in multiple sclerosis and experimental autoimmune encephalomyelitis, Clin. Exp. Immunol., 162, 1, 10.1111/j.1365-2249.2010.04143.x · DOI · Paper page
  61. Yoles, 2001, Protective autoimmunity is a physiological response to CNS trauma, J. Neurosci., 21, 3740, 10.1523/JNEUROSCI.21-11-03740.2001 · DOI · Paper page
  62. Hauben, 2000, Autoimmune T cells as potential neuroprotective therapy for spinal cord injury, Lancet, 355, 286, 10.1016/S0140-6736(99)05140-5 · DOI
  63. Walsh, 2015, MHCII-independent CD4+ T cells protect injured CNS neurons via IL-4, J. Clin. Invest., 125, 2547, 10.1172/JCI82458 · DOI
  64. Hammarberg, 2000, Neuroprotection by encephalomyelitis: Rescue of mechanically injured neurons and neurotrophin production by CNS-infiltrating T and natural killer cells, J. Neurosci., 20, 5283, 10.1523/JNEUROSCI.20-14-05283.2000 · DOI · Paper page
  65. Simon, 2018, Neuroinflammation in the evolution of secondary injury, repair, and chronic neurodegeneration after traumatic brain injury, Nat. Rev. Neurol., 13, 171, 10.1038/nrneurol.2017.13 · DOI · Paper page
  66. Weckbach, 2012, Challenging the role of adaptive immunity in neurotrauma: Rag1(-/-) mice lacking mature B and T cells do not show neuroprotection after closed head injury, J. Neurotrauma, 29, 1233, 10.1089/neu.2011.2169 · DOI
  67. Mentz, 2016, Interfering with the Chronic Immune Response Rescues Chronic Degeneration After Traumatic Brain Injury, J. Neurosci., 36, 9962, 10.1523/JNEUROSCI.1898-15.2016 · DOI
  68. Shitaka, 2011, Repetitive closed-skull traumatic brain injury in mice causes persistent multifocal axonal injury and microglial reactivity, J. Neuropathol. Exp. Neurol., 70, 551, 10.1097/NEN.0b013e31821f891f · DOI · Paper page
  69. Das, 2012, New perspectives on central and peripheral immune responses to acute traumatic brain injury, J. Neuroinflammation, 9, 236, 10.1186/1742-2094-9-236 · DOI · Paper page
  70. Lu, 2009, Systemic inflammatory response following acute traumatic brain injury, Front. Biosci., 14, 3795, 10.2741/3489 · DOI
  71. Jacome, 2018, Systemic Inflammatory Response Syndrome (SIRS) Score Independently Predicts Poor Outcome in Isolated Traumatic Brain Injury, Neurocrit. Care, 28, 110, 10.1007/s12028-017-0410-y · DOI
  72. Barrientos, 2015, Neuroinflammation in the normal aging hippocampus, Neuroscience, 309, 84, 10.1016/j.neuroscience.2015.03.007 · DOI · Paper page
  73. Hong, 2010, Inflammation as a psychophysiological biomarker in chronic psychosocial stress, Neurosci. Biobehav. Rev., 35, 115, 10.1016/j.neubiorev.2009.12.012 · DOI · Paper page
  74. Guerra, 2010, The design of barriers in the hypothalamus allows the median eminence and the arcuate nucleus to enjoy private milieus: The former opens to the portal blood and the latter to the cerebrospinal fluid, Peptides, 31, 757, 10.1016/j.peptides.2010.01.003 · DOI · Paper page
  75. Akmayev, 1977, Morphological aspects of the hypothalamic-hypophyseal system. VII. The tanycytes: Their relation to the hypophyseal adrenocorticotrophic function. An ultrastructural study, Cell Tissue Res., 180, 263
  76. Vallet, 1991, Colocalization of delta sleep inducing peptide and luteinizing hormone releasing hormone in neurosecretory vesicles in rat median eminence, Neuroendocrinology, 53, 103, 10.1159/000125705 · DOI
  77. Prevot, 2010, Gonadotrophin-releasing hormone nerve terminals, tanycytes and neurohaemal junction remodelling in the adult median eminence: Functional consequences for reproduction and dynamic role of vascular endothelial cells, J. Neuroendocrinol., 22, 639, 10.1111/j.1365-2826.2010.02033.x · DOI
  78. Devanney, 2020, Microglia and macrophage metabolism in CNS injury and disease: The role of immunometabolism in neurodegeneration and neurotrauma, Exp. Neurol., 329, 113310, 10.1016/j.expneurol.2020.113310 · DOI · Paper page
  79. Pham, 2020, The NLRP3 inflammasome in traumatic brain injury: Potential as a biomarker and therapeutic target, J. Neuroinflammation, 17, 104, 10.1186/s12974-020-01778-5 · DOI
  80. Irrera, N., Russo, M., Pallio, G., Bitto, A., Mannino, F., Minutoli, L., Altavilla, D., and Squadrito, F. (2020). The Role of NLRP3 Inflammasome in the Pathogenesis of Traumatic Brain Injury. Int. J. Mol. Sci., 21. · DOI
  81. Marcillo, 2009, Neuroprotective effects of bone morphogenetic protein 7 (BMP7) treatment after spinal cord injury, Neurosci. Lett., 465, 226, 10.1016/j.neulet.2009.09.013 · DOI
  82. Mortezaee, 2018, Inflammasome: Its role in traumatic brain and spinal cord injury, J. Cell Physiol., 233, 5160, 10.1002/jcp.26287 · DOI
  83. Lin, 2016, Heme oxygenase-1 promotes neuron survival through down-regulation of neuronal NLRP1 expression after spinal cord injury, J. Neuroinflammation, 13, 52, 10.1186/s12974-016-0521-y · DOI
  84. Liu, 2013, Expression of the NLRP3 inflammasome in cerebral cortex after traumatic brain injury in a rat model, Neurochem. Res., 38, 2072, 10.1007/s11064-013-1115-z · DOI · Paper page
  85. Lin, 2017, Omega-3 fatty acids regulate NLRP3 inflammasome activation and prevent behavior deficits after traumatic brain injury, Exp. Neurol., 290, 115, 10.1016/j.expneurol.2017.01.005 · DOI
  86. Wallisch, 2017, Cerebrospinal Fluid NLRP3 is Increased After Severe Traumatic Brain Injury in Infants and Children, Neurocrit. Care, 27, 44, 10.1007/s12028-017-0378-7 · DOI
  87. Pop, 2013, Early brain injury alters the blood-brain barrier phenotype in parallel with β-amyloid and cognitive changes in adulthood, J. Cereb. Blood Flow Metab., 33, 205, 10.1038/jcbfm.2012.154 · DOI
  88. Fann, 2018, Long-term risk of dementia among people with traumatic brain injury in Denmark: A population-based observational cohort study, Lancet. Psychiatry, 5, 424, 10.1016/S2215-0366(18)30065-8 · DOI · Paper page
  89. Wenger, 2017, Contribution of neuroinflammation and immunity to brain aging and the mitigating effects of physical and cognitive interventions, Neurosci. Biobehav. Rev., 75, 114, 10.1016/j.neubiorev.2017.01.044 · DOI · Paper page
  90. Rosado, 2016, Monocyte Phenotype and Polyfunctionality Are Associated With Elevated Soluble Inflammatory Markers, Cytomegalovirus Infection, and Functional and Cognitive Decline in Elderly Adults, J. Gerontol. A Biol. Sci. Med. Sci., 71, 610, 10.1093/gerona/glv121 · DOI
  91. Hearps, 2012, Aging is associated with chronic innate immune activation and dysregulation of monocyte phenotype and function, Aging Cell, 11, 867, 10.1111/j.1474-9726.2012.00851.x · DOI · Paper page
  92. Schnydrig, 2007, Peripheral lipopolysaccharide administration transiently affects expression of brain-derived neurotrophic factor, corticotropin and proopiomelanocortin in mouse brain, Neurosci. Lett., 429, 69, 10.1016/j.neulet.2007.09.067 · DOI
  93. Guan, 2006, Peripheral immune activation by lipopolysaccharide decreases neurotrophins in the cortex and hippocampus in rats, Brain Behav. Immun., 20, 64, 10.1016/j.bbi.2005.04.005 · DOI · Paper page
  94. Tumati, S., Burger, H., Martens, S., van der Schouw, Y.T., and Aleman, A. (2016). Association between Cognition and Serum Insulin-Like Growth Factor-1 in Middle-Aged & Older Men: An 8 Year Follow-Up Study. PLoS ONE, 11. · DOI
  95. Ubukata, 2020, Spatial Patterns of Amyloid Deposition in Patients with Chronic Focal or Diffuse Traumatic Brain Injury Using 18F-FPYBF-2 PET, Neuropsychiatr. Dis. Treat., 16, 2719, 10.2147/NDT.S268504 · DOI
  96. Hay, 2015, Blood-Brain Barrier Disruption Is an Early Event That May Persist for Many Years After Traumatic Brain Injury in Humans, J. Neuropathol. Exp. Neurol., 74, 1147
  97. Jullienne, 2014, Juvenile traumatic brain injury induces long-term perivascular matrix changes alongside amyloid-beta accumulation, J. Cereb. Blood Flow Metab., 34, 1637, 10.1038/jcbfm.2014.124 · DOI
  98. Roberts, 1991, beta A4 amyloid protein deposition in brain after head trauma, Lancet, 338, 1422, 10.1016/0140-6736(91)92724-G · DOI · Paper page
  99. Blasko, 2004, Experimental traumatic brain injury in rats stimulates the expression, production and activity of Alzheimer’s disease beta-secretase (BACE-1), J. Neural. Transm., 111, 523, 10.1007/s00702-003-0095-6 · DOI
  100. Nadler, 2008, Increased expression of the gamma-secretase components presenilin-1 and nicastrin in activated astrocytes and microglia following traumatic brain injury, Glia, 56, 552, 10.1002/glia.20638 · DOI
  101. Lepelletier, 2017, Early changes in extracellular matrix in Alzheimer’s disease, Neuropathol. Appl. Neurobiol., 43, 167, 10.1111/nan.12295 · DOI
  102. Crehan, 2012, Complement receptor 1 (CR1) and Alzheimer’s disease, Immunobiology, 217, 244, 10.1016/j.imbio.2011.07.017 · DOI · Paper page
  103. Lashkari, K., Teague, G., Chen, H., Lin, Y.Q., Kumar, S., McLaughlin, M.M., and López, F.J. (2018). A monoclonal antibody targeting amyloid β (Aβ) restores complement factor I bioactivity: Potential implications in age-related macular degeneration and Alzheimer’s disease. PLoS ONE, 13. · DOI
  104. Bradt, 1998, Complement-dependent proinflammatory properties of the Alzheimer’s disease beta-peptide, J. Exp. Med., 188, 431, 10.1084/jem.188.3.431 · DOI · Paper page
  105. Stevens, 2007, The classical complement cascade mediates CNS synapse elimination, Cell, 131, 1164, 10.1016/j.cell.2007.10.036 · DOI · Paper page
  106. Alawieh, 2018, Identifying the Role of Complement in Triggering Neuroinflammation after Traumatic Brain Injury, J. Neurosci., 38, 2519, 10.1523/JNEUROSCI.2197-17.2018 · DOI
  107. Cryan, 1918, Pituitary demage due to skull base fracture, Dtsch. Med. Wochenschr., 44, 1261
  108. Prodam, F., Caputo, M., Mele, C., Marzullo, P., and Aimaretti, G. (2020). Insights into non-classic and emerging causes of hypopituitarism. Nat. Rev. Endocrinol., Online ahead of print. · DOI
  109. Agha, 2005, The natural history of post-traumatic hypopituitarism: Implications for assessment and treatment, Am. J. Med., 118, 1416, 10.1016/j.amjmed.2005.02.042 · DOI · Paper page
  110. Glynn, 2019, The frequency and the diagnosis of pituitary dysfunction after traumatic brain injury, Pituitary, 22, 249, 10.1007/s11102-019-00938-y · DOI · Paper page
  111. Agha, 2004, Posterior pituitary dysfunction after traumatic brain injury, J. Clin. Endocrinol. Metab., 89, 5987, 10.1210/jc.2004-1058 · DOI · Paper page
  112. Tritos, 2015, American Association of Clinical Endocrinologists and American College of Endocrinology disease state clinical review: A neuroendocrine approach to patients with traumatic brain injury, Endocr. Pract., 21, 823, 10.4158/EP14567.DSCR · DOI · Paper page
  113. Fenske, 2012, Clinical review: Current state and future perspectives in the diagnosis of diabetes insipidus: A clinical review, J. Clin. Endocrinol. Metab., 97, 3426, 10.1210/jc.2012-1981 · DOI
  114. Aimaretti, 2005, Residual pituitary function after brain injury-induced hypopituitarism: A prospective 12-month study, J. Clin. Endocrinol. Metab., 90, 6085, 10.1210/jc.2005-0504 · DOI · Paper page
  115. Krewer, 2016, Neuroendocrine Disturbances One to Five or More Years after Traumatic Brain Injury and Aneurysmal Subarachnoid Hemorrhage: Data from the German Database on Hypopituitarism, J. Neurotrauma, 33, 1544, 10.1089/neu.2015.4109 · DOI · Paper page
  116. Jonasdottir, 2018, Hypopituitarism 3 and 12 months after traumatic brain injury and subarachnoid haemorrhage, Brain Inj., 32, 310, 10.1080/02699052.2017.1418906 · DOI · Paper page
  117. Klose, 2007, Posttraumatic hypopituitarism s associated with an unfavorable body composition and lipid profile, and decreased quality of life 12 months after injury, J. Clin. Endocrinol. Metab., 92, 3861, 10.1210/jc.2007-0901 · DOI · Paper page
  118. Prodam, 2012, Quality of life, mood disturbances and psychological parameters in adult patients with GH deficiency, Panminerva. Med., 54, 323
  119. Kelly, 2006, Neurobehavioral and quality of life changes associated with growth hormone insufficiency after complicated mild, moderate, or severe traumatic brain injury, J. Neurotrauma, 23, 928, 10.1089/neu.2006.23.928 · DOI · Paper page
  120. Ozdemir, 2012, Relationship between circulating IGF-1 levels and traumatic brain injury-induced hippocampal damage and cognitive dysfunction in immature rats, Neurosci. Lett., 507, 84, 10.1016/j.neulet.2011.11.059 · DOI · Paper page
  121. Chesnut, 1993, The role of secondary brain injury in determining outcome from severe head injury, J. Trauma, 34, 216, 10.1097/00005373-199302000-00006 · DOI · Paper page
  122. Ceballos, 1966, Pituitary changes in head trauma (analysis of 102 consecutive cases of head injury), Ala. J. Med. Sci., 3, 185
  123. Kornblum, 1969, Pituitary lesions in craniocerebral injuries, Arch. Pathol., 88, 242
  124. Dubourg, 2011, Sports-related chronic repetitive head trauma as a cause of pituitary dysfunction, Neurosurg. Focus, 31, E2, 10.3171/2011.8.FOCUS11182 · DOI
  125. Sheehan, 1971, The recognition of chronic hypopituitarism resulting from postpartum pituitary necrosis, Am. J. Obstet. Gynecol., 111, 852, 10.1016/0002-9378(71)90500-X · DOI · Paper page
  126. Laskowitz, 1997, Apolipoprotein E suppresses glial cell secretion of TNF alpha, J. Neuroimmunol., 76, 70, 10.1016/S0165-5728(97)00021-0 · DOI · Paper page
  127. Lynch, 2005, A novel therapeutic derived from apolipoprotein E reduces brain inflammation and improves outcome after closed head injury, Exp. Neurol., 192, 109, 10.1016/j.expneurol.2004.11.014 · DOI
  128. Laskowitz, 2001, Downregulation of microglial activation by apolipoprotein E and apoE-mimetic peptides, Exp. Neurol., 167, 74, 10.1006/exnr.2001.7541 · DOI · Paper page
  129. Rudehill, 2006, Autoreactive antibodies against neurons and basal lamina found in serum following experimental brain contusion in rats, Acta Neurochir., 148, 199, 10.1007/s00701-005-0673-5 · DOI
  130. Stahr, 2017, Tanycytes control the hormonal output of the hypothalamic-pituitary-thyroid axis, Nat. Commun., 8, 484, 10.1038/s41467-017-00604-6 · DOI
  131. Prevot, 2010, Function-related structural plasticity of the GnRH system: A role for neuronal-glial-endothelial interactions, Front. Neuroendocrinol., 31, 241, 10.1016/j.yfrne.2010.05.003 · DOI
  132. Vennekens, 2019, Traumatic brain injury and resultant pituitary dysfunction: Insights from experimental animal models, Pituitary, 22, 212, 10.1007/s11102-019-00961-z · DOI
  133. Lozano, 2015, Neuroinflammatory responses to traumatic brain injury: Etiology, clinical consequences, and therapeutic opportunities, Neuropsychiatr. Dis. Treat., 11, 97
  134. Schmidt, 2005, Closed head injury--an inflammatory disease?, Brain Res. Brain Res. Rev., 48, 388, 10.1016/j.brainresrev.2004.12.028 · DOI · Paper page
  135. Riggio, 2009, Neurobehavioral sequelae of traumatic brain injury, Mt. Sinai. J. Med., 76, 163, 10.1002/msj.20097 · DOI
  136. Rabinowitz, 2014, Cognitive sequelae of traumatic brain injury, Psychiatr. Clin. N. Am., 37, 1, 10.1016/j.psc.2013.11.004 · DOI · Paper page
  137. Wang, 2016, Cognitive impairment after traumatic brain injury: The role of MRI and possible pathological basis, J. Neurol. Sci., 370, 244, 10.1016/j.jns.2016.09.049 · DOI
  138. Deijen, 1996, Cognitive impairments and mood disturbances in growth hormone deficient men, Psychoneuroendocrinology, 21, 313, 10.1016/0306-4530(95)00050-X · DOI
  139. Hagmar, 2002, High incidence of mental disorders, reduced mental well-being and cognitive function in hypopituitary women with GH deficiency treated for pituitary disease, Clin. Endocrinol., 56, 183, 10.1046/j.0300-0664.2001.01461.x · DOI
  140. Burman, 1995, Quality of life in adults with growth hormone (GH) deficiency: Response to treatment with recombinant human GH in a placebo-controlled 21-month trial, J. Clin. Endocrinol. Metab., 80, 3585, 10.1210/jcem.80.12.8530603 · doi:10.1210/jcem.80.12.8530603 · Paper page
  141. Devesa, 2015, Brain Recovery after a Plane Crash: Treatment with Growth Hormone (GH) and Neurorehabilitation: A Case Report, Int. J. Mol. Sci., 16, 30470, 10.3390/ijms161226244 · DOI
  142. Dubiel, 2018, Phase 2 Randomized, Placebo-Controlled Clinical Trial of Recombinant Human Growth Hormone (rhGH) During Rehabilitation From Traumatic Brain Injury, Front. Endocrinol., 9, 520, 10.3389/fendo.2018.00520 · DOI

Cited by

See all 53

Metadata

Authors
Mele, C., Pingue, V., Caputo, M., Zavattaro, M., Pagano, L., Prodam, F., Nardone, A., Aimaretti, G., & Marzullo, P.
Affiliations
  • Department of Clinical-Surgical, Diagnostic and Pediatric Sciences, University of Pavia, 27100 Pavia, Italy
  • Neurorehabilitation and Spinal Unit, Istituti Clinici Scientifici Maugeri SPA SB, Institute of Pavia, IRCCS, 27100 Pavia, Italy
  • Department of Health Sciences, University of Piemonte Orientale, 28100 Novara, Italy
  • Division of Endocrinology, University Hospital “Maggiore della Carità”, 28100 Novara, Italy
  • Division of Endocrinology, Diabetology and Metabolism, Department of Medical Sciences, University of Turin, 10124 Turin, Italy
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2021-03-07
Volume
22
Issue
5
Pages
2686
ISSN
1422-0067
Cited by
53
References
64
Language
en

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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.

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Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.