Cited by 158Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchNeuroprotection in Cerebral Ischemia

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A Review of Neuroprotection Pharmacology and Therapies in Patients with Acute Traumatic Brain Injury

McConeghy, Kevin W., Hatton, Jimmi, Hughes, Lindsey, Cook, Aaron M.·2012·CNS Drugs

DOI 10.2165/11634020-000000000-00000

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Abstract

Traumatic brain injury (TBI) affects 1.6 million Americans annually. The injury severity impacts the overall outcome and likelihood for survival. Current treatment of acute TBI includes surgical intervention and supportive care therapies. Treatment of elevated intracranial pressure and optimizing cerebral perfusion are cornerstones of current therapy. These approaches do not directly address the secondary neurological sequelae that lead to continued brain injury after TBI. Depending on injury severity, a complex cascade of processes are activated and generate continued endogenous changes affecting cellular systems and overall outcome from the initial insult to the brain. Homeostatic cellular processes governing calcium influx, mitochondrial function, membrane stability, redox balance, blood flow and cytoskeletal structure often become dysfunctional after TBI. Interruption of this cascade has been the target of numerous pharmacotherapeutic agents investigated over the last two decades. Many agents such as selfotel, pegorgotein (PEG-SOD), magnesium, deltibant and dexanabinol were ineffective in clinical trials. While progesterone and ciclosporin have shown promise in phase II studies, success in larger phase III, randomized, multicentre, clinical trials is pending. Consequently, no neuroprotective treatment options currently exist that improve neurological outcome after TBI. Investigations to date have extended understanding of the injury mechanisms and sites for intervention.…

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A controlled cortical impact model of traumatic brain injury in the rat
Edward Dixon, C., Clifton, G. L., Lighthall, J. W., Yaghmai, A. A., & Hayes, R. L. (1991) · Journal of Neuroscience Methods · doi:10.1016/0165-0270(91)90104-8 · Cited by 1,141
Clinical trials in head injury
Narayan, R. K., Michel, M. E., Ansell, B., Baethmann, A., Biegon, A., Bracken, M. B., Bullock, M. R., Choi, S. C., Clifton, G. L., Contant, C. F., et al. (2002) · Journal of Neurotrauma · doi:10.1089/089771502753754037 · Cited by 913
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Hall, E. D., Vaishnav, R. A., & Mustafa, A. G. (2010) · Neurotherapeutics · doi:10.1016/j.nurt.2009.10.021 · Cited by 390 · cited 1×
“These reactive species may overwhelm endogenous antioxidant stores, such as superoxide dismutase (SOD), causing DNA damage and lipid peroxidation, which can propagate well beyond the site of origin.([38,39]) The inflammatory response to TBI, like inmany other types of critical illness, can either be harmful or helpful…”
Background
Aspects of growth hormone and insulin-like growth factor-I related to neuroprotection, regeneration, and functional plasticity in the adult brain
Åberg, N. D., Brywe, K. G., & Isgaard, J. (2006) · The Scientific World JOURNAL · doi:10.1100/tsw.2006.22 · Cited by 387
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Morales, D. M., Marklund, N., Lebold, D., Thompson, H. J., Pitkanen, A., Maxwell, W. L., Longhi, L., Laurer, H., Maegele, M., Neugebauer, E., et al. (2005) · Neuroscience · doi:10.1016/j.neuroscience.2005.08.030 · Cited by 339 · cited 1×
“However, the heterogeneity of TBI in reality is difficult to replicate.([71]) Patients often present with more than one abnormality or injury type due to neurotrauma.”
Background
Posttraumatic vasospasm: the epidemiology, severity, and time course of an underestimated phenomenon: a prospective study performed in 299 patients
Oertel, M., Boscardin, W. J., Obrist, W. D., Glenn, T. C., McArthur, D. L., Gravori, T., Lee, J. H., & Martin, N. A. (2005) · Journal of Neurosurgery · doi:10.3171/jns.2005.103.5.0812 · Cited by 227
Concussion
Ropper, A. H., & Gorson, K. C. (2007) · New England Journal of Medicine · doi:10.1056/nejmcp064645 · Cited by 215
Insulin-like Growth Factor-1 (IGF-1) Improves both Neurological Motor and Cognitive Outcome Following Experimental Brain Injury
Saatman, K. E., Contreras, P. C., Smith, D. H., Raghupathi, R., McDermott, K. L., Fernandez, S. C., Sanderson, K. L., Voddi, M., & McIntosh, T. K. (1997) · Experimental Neurology · doi:10.1006/exnr.1997.6629 · Cited by 185

Show all 0 references

Research works printed but not linked: 203

Thurman, 1999 Sep 8, JAMA, 282, 954, 10.1001/jama.282.10.954 · DOI
Thurman, 1999 Dec, J Head Trauma Rehabil, 14, 602, 10.1097/00001199-199912000-00009 · DOI
Coronado, 2011 May 6, MMWR Surveill Summ, 60, 1
Roozenbeek, 2012, J Neurotrauma, 29, 1306, 10.1089/neu.2011.1988 · DOI
Clifton, 2011 Feb, Lancet Neurol, 10, 131, 10.1016/S1474-4422(10)70300-8 · DOI
Patel, 2005 Oct 29-Nov 4, Lancet, 366, 1538, 10.1016/S0140-6736(05)67626-X · DOI
Marshall, 1991, J Neurosurg, 75, S28, 10.3171/sup.1991.75.1s.0s28 · DOI
Roberts, 2004 Oct 9-15, Lancet, 364, 1321, 10.1016/S0140-6736(04)17188-2 · DOI · Paper page
De Kruijk, 2002 Dec, J Neurol Neurosurg Psychiatr, 73, 727, 10.1136/jnnp.73.6.727 · DOI
Ryan, 2003 Nov, Int Rev Psychiatry, 15, 310, 10.1080/09540260310001606692 · DOI
Ling, 2009 Jun, J Neurotrauma, 26, 815, 10.1089/neu.2007.0484 · DOI
Sahuquillo, 2001, Curr Pharm Des, 7, 1475, 10.2174/1381612013397311 · DOI
Andriessen, 2010 Oct, J Cell Mol Med, 14, 2381, 10.1111/j.1582-4934.2010.01164.x · DOI
2007, J Neurotrauma, 24, S1, 10.1089/neu.2007.9997 · DOI
Rhoney, 2006, Nutr Clin Pract, 21, 462, 10.1177/0115426506021005462 · DOI
Clifton, 2002, Crit Care Med, 30, 739, 10.1097/00003246-200204000-00003 · DOI
Hatton, 2001, CNS Drugs, 15, 553, 10.2165/00023210-200115070-00005 · DOI
Werner, 2007 Jul, Br J Anaesth, 99, 4, 10.1093/bja/aem131 · DOI · Paper page
Enriquez, 2004, Curr Pharm Des, 10, 2131, 10.2174/1381612043384060 · DOI
Czosnyka, 2001 Nov, J Neurosurg, 95, 756, 10.3171/jns.2001.95.5.0756 · DOI
Manley, 2001 Oct, Arch Surg, 136, 1118, 10.1001/archsurg.136.10.1118 · DOI
DeWitt, 2003 Sep, J Neurotrauma, 20, 795, 10.1089/089771503322385755 · DOI · Paper page
Steiner, 2003 Oct, Stroke, 34, 2404, 10.1161/01.STR.0000089014.59668.04 · DOI
Cherian, 2004 Apr, Brain Pathol, 14, 195, 10.1111/j.1750-3639.2004.tb00053.x · DOI
Schroder, 1998, Acta Neurochir Suppl, 71, 127
Schroder, 1996 Jan, J Neurotrauma, 13, 17, 10.1089/neu.1996.13.17 · DOI
Obrist, 1984 Aug, J Neurosurg, 61, 241, 10.3171/jns.1984.61.2.0241 · DOI
Overgaard, 1974 Nov, J Neurosurg, 41, 531, 10.3171/jns.1974.41.5.0531 · DOI
Martin, 1997 Jul, J Neurosurg, 87, 9, 10.3171/jns.1997.87.1.0009 · DOI
Langham, 2003, Cochrane Database Syst Rev, 4, CD000565
Hall, 1993 Feb, J Neurochem, 60, 588, 10.1111/j.1471-4159.1993.tb03189.x · DOI
Shohami, 1997 Oct, J Cerebral Blood Flow Metab, 17, 1007, 10.1097/00004647-199710000-00002 · DOI
Lewen, 2000 Oct, J Neurotrauma, 17, 871, 10.1089/neu.2000.17.871 · DOI · Paper page
Ray, 2002 Oct, Histol Histopathol, 17, 1137
Lenzlinger, 2001 Aug-Dec, Mol Neurobiol, 24, 169, 10.1385/MN:24:1-3:169 · DOI · Paper page
Yang, 2007 Sep, Neurosci Bull, 23, 307, 10.1007/s12264-007-0046-6 · DOI
Ott, 1994, J Neurotrauma, 11, 447, 10.1089/neu.1994.11.447 · DOI
Royo, 1999 Apr 26, Neuroreport, 10, 1363, 10.1097/00001756-199904260-00038 · DOI
Stahel, 1998 Aug, Brain Res Brain Res Rev, 27, 243, 10.1016/S0165-0173(98)00015-0 · DOI
Baldwin, 1996 Sep, J Neurosurg, 85, 476, 10.3171/jns.1996.85.3.0476 · DOI
Marmarou, 2007, Neurosurg Focus, 22, 1, 10.3171/foc.2007.22.5.2 · DOI
Venero, 2004, Curr Pharm Des, 10, 2153, 10.2174/1381612043384150 · DOI
Young, 1992 Mar, J Neurotrauma, 9, S9
Kawamata, 1995 Mar 20, Brain Res, 674, 196, 10.1016/0006-8993(94)01444-M · DOI
Mazzeo, 2009 Aug, Exp Neurol, 218, 363, 10.1016/j.expneurol.2009.05.026 · DOI
Sullivan, 2005, J Neurosci Res, 79, 231, 10.1002/jnr.20292 · DOI
Kampfl, 1997 Mar, J Neurotrauma, 14, 121, 10.1089/neu.1997.14.121 · DOI
Raghupathi, 2004 Apr, Brain Pathol, 14, 215, 10.1111/j.1750-3639.2004.tb00056.x · DOI
Sarnaik, 2010 Mar, J Neurotrauma, 27, 465, 10.1089/neu.2009.1171 · DOI
Hatton, 2006 Dec, J Neurosurg, 105, 843, 10.3171/jns.2006.105.6.843 · DOI · Paper page
Neff, 1993 Dec, J Neurobiol, 24, 1578, 10.1002/neu.480241203 · DOI
Saenger, 2011 Oct, Growth Horm IGF Res, 21, 292, 10.1016/j.ghir.2011.07.006 · DOI
Taguchi, 2008, Annu Rev Physiol, 70, 191, 10.1146/annurev.physiol.70.113006.100533 · DOI
Zeger, 2007 Mar, Glia, 55, 400, 10.1002/glia.20469 · DOI
Kazanis, 2004 Apr, Exp Neurol, 186, 221, 10.1016/j.expneurol.2003.12.004 · DOI
Rockich, 1999, Pharmacotherapy, 19, 1432, 10.1592/phco.19.18.1432.30891 · DOI
Metzger, 2011 Jun 3, J Biol Chem, 286, 19501, 10.1074/jbc.M110.172189 · DOI
Xi, 2002, Neurosurg Clin N Am, 13, 371, 10.1016/S1042-3680(02)00007-4 · DOI
Schouten, 2007, Curr Opin Crit Care, 13, 134, 10.1097/MCC.0b013e3280895d5c · DOI · Paper page
Bullock, 1999, Neurosurgery, 45, 207, 10.1097/00006123-199908000-00001 · DOI
Tolias, 2004, NeuroRx, 1, 71, 10.1602/neurorx.1.1.71 · DOI
Sullivan, 2000, Neuroscience, 101, 289, 10.1016/S0306-4522(00)00380-8 · DOI
Lee, 2001, Pharmacol Rev, 53, 569, 10.1146/annurev.pharmtox.41.1.569 · DOI
Loscher, 2005, Nature Rev Neurosci, 6, 591, 10.1038/nrn1728 · DOI
Boucher, 1998, Clin Pharmacokinet, 35, 209, 10.2165/00003088-199835030-00004 · DOI
McKindley, 1997, J Clin Pharmacol, 37, 129, 10.1002/j.1552-4604.1997.tb04771.x · DOI
Baraldo, 1999, Pharmacol Res, 40, 483, 10.1006/phrs.1999.0539 · DOI
Kovarik, 1999, Drugs Aging, 15, 197, 10.2165/00002512-199915030-00003 · DOI
Ptachcinski, 1985, Clin Pharmacol Ther, 38, 296, 10.1038/clpt.1985.174 · DOI
Cook, 2009, Expert Opin Drug Saf, 8, 411, 10.1517/14740330903066742 · DOI
Empey, 2006, J Neurotrauma, 23, 109, 10.1089/neu.2006.23.109 · DOI · Paper page
Temkin, 2007, Lancet Neurol, 6, 29, 10.1016/S1474-4422(06)70630-5 · DOI
Wright, 2007, Ann Emerg Med, 49, 391, 10.1016/j.annemergmed.2006.07.932 · DOI
Guilfoyle, 2010 Dec, J Neurotrauma, 27, 2173, 10.1089/neu.2010.1353 · DOI
von Steinbuchel, 2010 Jul, J Neurotrauma, 27, 1157, 10.1089/neu.2009.1077 · DOI
Pineda, 2007 Feb, J Neurotrauma, 24, 354, 10.1089/neu.2006.003789 · DOI
Manley, 2010 Nov, Arch Phys Med Rehabil, 91, 1667, 10.1016/j.apmr.2010.05.018 · DOI
Ottens, 2010 Oct, J Neurotrauma, 27, 1837, 10.1089/neu.2010.1374 · DOI
Kochanek, 2008 Apr, Curr Opin Crit Care, 14, 135, 10.1097/MCC.0b013e3282f57564 · DOI
Maas, 2006, Lancet Neurol, 5, 38, 10.1016/S1474-4422(05)70253-2 · DOI
Marmarou, 2005 Dec, J Neurotrauma, 22, 1444, 10.1089/neu.2005.22.1444 · DOI
Hatton, 2008, J Neurosurg, 109, 699, 10.3171/JNS/2008/109/10/0699 · DOI
Marmarou, 1999 Jun, J Neurotrauma, 16, 431, 10.1089/neu.1999.16.431 · DOI
Young, 1996 Aug, JAMA, 276, 538, 10.1001/jama.1996.03540070034027 · DOI
Muizelaar, 1993, J Neurosurg, 78, 375, 10.3171/jns.1993.78.3.0375 · DOI
Xiao, 2008, Crit Care, 12, R61, 10.1186/cc6887 · DOI
Merchant, 1999, Ann N Y Acad Sci, 890, 42, 10.1111/j.1749-6632.1999.tb07979.x · DOI
Yurkewicz, 2005 Dec, J Neurotrauma, 22, 1428, 10.1089/neu.2005.22.1428 · DOI
Maas, 2006 Jan, Lancet Neurol, 5, 38, 10.1016/S1474-4422(05)70253-2 · DOI
Natale, 2007, Pediatr Crit Care Med, 8, 1, 10.1097/01.pcc.0000256620.55512.5f · DOI
Bailey, 1991, Acta Neurochir (Wien), 110, 97, 10.1007/BF01400674 · DOI
Teasdale, 1992, J Neurotruama, 9, S545
Murray, 1996, Acta Neurochir (Wien), 138, 1163, 10.1007/BF01809745 · DOI
1994, J Neurosurg, 80, 797, 10.3171/jns.1994.80.5.0797 · DOI
Pillai, 2003, Neurol India, 51, 361
Zhou, 2002, Di Yi Jun Yi Da Xue Xue Bao, 22, 527
Tapia-Perez, 2008, J Neurotrauma, 25, 1011, 10.1089/neu.2008.0554 · DOI
Morris, 1999, J Neurosurg, 91, 737, 10.3171/jns.1999.91.5.0737 · DOI
Marshall, 1998, J Neurosurg, 89, 519, 10.3171/jns.1998.89.4.0519 · DOI
LaPlaca, 2001, J Neurotrauma, 18, 369, 10.1089/089771501750170912 · DOI
Hoane, 2008, Oxid Med Cell Longev, 1, 46, 10.4161/oxim.1.1.6694 · DOI
Goffus, 2010, Oxid Med Cell Longev, 3, 145, 10.4161/oxim.3.2.11315 · DOI
Swan, 2011, J Neurotrauma, 28, 431, 10.1089/neu.2010.1519 · DOI
Hoane, 2006, J Neurotrauma, 23, 1535, 10.1089/neu.2006.23.1535 · DOI
Holland, 2008, J Neurotruama, 25, 140, 10.1089/neu.2007.0312 · DOI
Hoane, 2008, Neuroscience, 154, 861, 10.1016/j.neuroscience.2008.04.044 · DOI
Abdel Baki, 2010, PLoS ONE, 5, e12490, 10.1371/journal.pone.0012490 · DOI
Chen, 2008, Mediators Inflamm, 2008, 716458, 10.1155/2008/716458 · DOI
Khan, 2011 July 6, J Neuroinflammation, 8, 78, 10.1186/1742-2094-8-78 · DOI
Khan, 2009 Nov 4, J Neuroinflammation, 6, 32, 10.1186/1742-2094-6-32 · DOI
Qu, 2010, J Neurotrauma, 27, 1625, 10.1089/neu.2010.1359 · DOI
Arun, 2010, J Neurotruama, 27, 293, 10.1089/neu.2009.0994 · DOI
Appelberg, 2009, J Neurotrauma, 26, 497, 10.1089/neu.2008.0664 · DOI
Pike, 1995, Brain Res, 686, 37, 10.1016/0006-8993(95)00448-Y · DOI
Durmaz, 2003 Nov 15, J Neurol Sci, 215, 87, 10.1016/S0022-510X(03)00207-7 · DOI
Durmaz, 2003 May, Can J Neurol Sci, 30, 143, 10.1017/S0317167100053415 · DOI
Lu, 2009, J Neurotrauma, 26, 141, 10.1089/neu.2008.0629 · DOI
Wei, 2009 August 7, J Neuroinflammation, 6, 19, 10.1186/1742-2094-6-19 · DOI
Berman, 2000, J Neurosurg, 93, 821, 10.3171/jns.2000.93.5.0821 · DOI
Verweij, 2000, J Neurosurg, 93, 829, 10.3171/jns.2000.93.5.0829 · DOI
Faden, 2001, Exp Neurol, 167, 435, 10.1006/exnr.2000.7577 · DOI
Movsesyan, 2001, J Pharmacol Exp Ther, 296, 41
Barbre, 2006, Brain Res Bull, 69, 639, 10.1016/j.brainresbull.2006.03.009 · DOI
Hoane, 2005, J Neurotrauma, 22, 1112, 10.1089/neu.2005.22.1112 · DOI
Belayev, 2002, J Neurosurg, 96, 1077, 10.3171/jns.2002.96.6.1077 · DOI
Guluma, 1999, J Neurotrauma, 16, 311, 10.1089/neu.1999.16.311 · DOI
Dietrich, 1996, J Neurotrauma, 13, 309, 10.1089/neu.1996.13.309 · DOI
McDermott, 1997, J Neurotrauma, 14, 191, 10.1089/neu.1997.14.191 · DOI
Sun, 2009, Exp Neurol, 216, 56, 10.1016/j.expneurol.2008.11.011 · DOI
Cernak, 2002, Exp Brain Res, 147, 193, 10.1007/s00221-002-1245-z · DOI
Wahl, 2000 Nov, J Neurotrauma, 17, 1055, 10.1089/neu.2000.17.1055 · DOI
Stutzmann, 2002 Spring, CNS Drug Rev, 8, 1, 10.1111/j.1527-3458.2002.tb00213.x · DOI
Bye, 2007 Mar, Exp Neurol, 204, 220, 10.1016/j.expneurol.2006.10.013 · DOI
Crack, 2009 Jan, J Neural Transm, 116, 1, 10.1007/s00702-008-0145-1 · DOI
Homsi, 2009 Sep 29, Brain Res, 1291, 122, 10.1016/j.brainres.2009.07.031 · DOI
Homsi, 2010 May, J Neurotrauma, 27, 911, 10.1089/neu.2009.1223 · DOI
Stover, 2000, J Neurotrauma, 17, 1171, 10.1089/neu.2000.17.1171 · DOI
Zhang, 1998, J Neurosci Res, 52, 342, 10.1002/(SICI)1097-4547(19980501)52:3<342::AID-JNR10>3.0.CO;2-8 · DOI
Zhang, 2009, Brain Res, 1294, 153, 10.1016/j.brainres.2009.07.077 · DOI
Zhang, 2010, Brain Res, 1353, 249, 10.1016/j.brainres.2010.07.046 · DOI
Liao, 2008, Eur J Neurol, 15, 140, 10.1111/j.1468-1331.2007.02013.x · DOI
Zhao, 2011, Cytokine, 56, 343, 10.1016/j.cyto.2011.07.018 · DOI
Hartley, 2008, J Neurosurg, 109, 708, 10.3171/JNS/2008/109/10/0708 · DOI
Grasso, 2007, Brain Res, 1182, 99, 10.1016/j.brainres.2007.08.078 · DOI
Chen, 2007, Neurosci Lett, 425, 177, 10.1016/j.neulet.2007.08.022 · DOI
Liao, 2009, Neurol India, 57, 722, 10.4103/0028-3886.59466 · DOI
Mammis, 2009, Surg Neurol, 71, 527, 10.1016/j.surneu.2008.02.040 · DOI
Xiong, 2011, J Neurosurg, 114, 549, 10.3171/2010.10.JNS10925 · DOI
Xiong, 2010, J Neurosurg, 113, 598, 10.3171/2009.9.JNS09844 · DOI
Brines, 2000, Proc Natl Acad Sci USA, 97, 10526, 10.1073/pnas.97.19.10526 · DOI
Kuypers, 2010, J Neurotrauma, 27, 1275, 10.1089/neu.2010.1327 · DOI
Kleindienst, 2004, J Neurotrauma, 21, 541, 10.1089/089771504774129874 · DOI
Kleindienst, 2005, J Neurotruama, 22, 645, 10.1089/neu.2005.22.645 · DOI
Kline, 2002, J Neurotrauma, 19, 415, 10.1089/08977150252932370 · DOI
Mauler, 2003, Brain Res, 989, 99, 10.1016/S0006-8993(03)03376-6 · DOI
Mauler, 2003, CNS Drug Rev, 9, 343, 10.1111/j.1527-3458.2003.tb00259.x · DOI
Mesenge, 1996, J Neurotrauma, 13, 11, 10.1089/neu.1996.13.11 · DOI
Hogg, 1998, Behav Brain Res, 93, 157, 10.1016/S0166-4328(97)00145-9 · DOI
Bernert, 1996, Proc Natl Acad Sci USA, 93, 5235, 10.1073/pnas.93.11.5235 · DOI
Ikonomidou, 1996, Metab Brain Dis, 11, 125, 10.1007/BF02069500 · DOI
Pohl, 1999, Proc Natl Acad Sci USA, 96, 2508, 10.1073/pnas.96.5.2508 · DOI
McIntosh, 1999, J Neurochem, 55, 1170, 10.1111/j.1471-4159.1990.tb03122.x · DOI
Okiyama, 1998, Brain Res, 792, 291, 10.1016/S0006-8993(98)00158-9 · DOI
Kroppenstedt, 1998, J Neurotrauma, 15, 191, 10.1089/neu.1998.15.191 · DOI
Toulmond, 1993, Brain Res, 620, 32, 10.1016/0006-8993(93)90267-Q · DOI
Hogg, 1998, J Neurotrauma, 15, 545, 10.1089/neu.1998.15.545 · DOI
Mueller, 2000, Amino Acids, 19, 177, 10.1007/s007260070047 · DOI
Dohi, 2006, J Neurotrauma, 23, 1591, 10.1089/neu.2006.23.1591 · DOI
Itoh, 2010, Neurochem Res, 35, 348, 10.1007/s11064-009-0061-2 · DOI
Wang, 2011, J Neurotrauma, 28, 2123, 10.1089/neu.2011.1939 · DOI
Belayev, 2001, J Neurotrauma, 18, 1031, 10.1089/08977150152693728 · DOI
Kline, 2001, Neuroscience, 106, 547, 10.1016/S0306-4522(01)00300-1 · DOI
Mauler, 2005, J Cereb Blood Flow Metab, 25, 451, 10.1038/sj.jcbfm.9600038 · DOI
Cheng, 2007, Neurosci Lett, 416, 165, 10.1016/j.neulet.2007.02.006 · DOI
Cheng, 2008, Behav Brain Res, 194, 79, 10.1016/j.bbr.2008.06.025 · DOI
Kline, 2007, Behav Brain Res, 177, 186, 10.1016/j.bbr.2006.11.036 · DOI
Kline, 2004, J Neurotrauma, 21, 175, 10.1089/089771504322778631 · DOI
Kline, 2010, J Neurotruama, 27, 2021, 10.1089/neu.2010.1535 · DOI
Kline, 2002, Neurosci Lett, 333, 179, 10.1016/S0304-3940(02)01101-1 · DOI
Ma, 2011, Mol Med Rep, 4, 849
Wallenquist, 2009, Restor Neurol Neurosci, 2009, 323
Harting, 2009, J Surg Res, 153, 188, 10.1016/j.jss.2008.03.037 · DOI
Shohami, 1996, J Cereb Blood Flow Metab, 16, 378, 10.1097/00004647-199605000-00004 · DOI
Chio, 2010, J Neurochem, 115, 921, 10.1111/j.1471-4159.2010.06969.x · DOI
Kinoshita, 2002, J Neurotrauma, 19, 681, 10.1089/08977150260139075 · DOI
Liu-DeRyke, 2009, Neurocrit Care, 11, 151, 10.1007/s12028-009-9228-6 · DOI
Rovlias, 2000, Neurosurgery, 46, 342, 10.1097/00006123-200002000-00015 · DOI
Salim, 2009, Am Surg, 75, 25, 10.1177/000313480907500105 · DOI
Diaz-Parejo, 2003, Intensive Care Med, 29, 544, 10.1007/s00134-003-1669-3 · DOI
Alderson, 2005 Jan 25, Cochrane Database Syst Rev, 1, CD000196
Mazzeo, 2008, Acta Neurochir (Wien), 150, 1019, 10.1007/s00701-008-0021-7 · DOI
Mazzeo, 2009 Dec, J Neurotrauma, 26, 2195, 10.1089/neu.2009.1012 · DOI
Knoller, 2002, Crit Care Med, 30, 548, 10.1097/00003246-200203000-00009 · DOI
McIntosh, 1988, J Neurotrauma, 5, 17, 10.1089/neu.1988.5.17 · DOI
Lee, 2004, J Neurotrauma, 21, 549, 10.1089/089771504774129883 · DOI
Hoane, 2005, Restor Neurol Neurosci, 23, 67
Wagstaff, 1995 Sep 15, Ann N Y Acad Sci, 15, 332, 10.1111/j.1749-6632.1995.tb16607.x · DOI
Bullock, 1999, Ann N Y Acad Sci, 51-, 8
Stein, 2008, Brain Res Rev, 57, 386, 10.1016/j.brainresrev.2007.06.012 · DOI
Weant, 2007, Pharmacotherapy, 27, 1279, 10.1592/phco.27.9.1279 · DOI

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Jassam, Y. N., Izzy, S., Whalen, M., McGavern, D. B., & El Khoury, J. (2017) · Neuron · doi:10.1016/j.neuron.2017.07.010 · Cited by 799
Effect of exosomes derived from multipluripotent mesenchymal stromal cells on functional recovery and neurovascular plasticity in rats after traumatic brain injury
Zhang, Y., Chopp, M., Meng, Y., Katakowski, M., Xin, H., Mahmood, A., & Xiong, Y. (2015) · Journal of neurosurgery · doi:10.3171/2014.11.jns14770 · Cited by 737
Transcranial amelioration of inflammation and cell death after brain injury.
Roth, T. L., Nayak, D., Atanasijevic, T., Koretsky, A. P., Latour, L. L., & McGavern, D. B. (2014) · Nature · doi:10.1038/nature12808 · Cited by 574
“moderate, and severe forms of injury 5 , but therapeutic research in these models has not yet translated successfully into the clinic 4, 13 .”
Long-Term Consequences of Traumatic Brain Injury: Current Status of Potential Mechanisms of Injury and Neurological Outcomes
Bramlett, H. M., & Dietrich, W. D. (2014) · Journal of Neurotrauma · doi:10.1089/neu.2014.3352 · Cited by 590
“258 However, lessons have been learned and strategies proposed on how best to approach the translation of pre-clinical data to the clinic.”
Systemic administration of cell-free exosomes generated by human bone marrow derived mesenchymal stem cells cultured under 2D and 3D conditions improves functional recovery in rats after traumatic brain injury
Zhang, Y., Chopp, M., Zhang, Z. G., Katakowski, M., Xin, H., Qu, C., Ali, M. M., Mahmood, A., & Xiong, Y. (2016) · Neurochemistry International · doi:10.1016/j.neuint.2016.08.003 · Cited by 400
Traumatic Brain Injury: Oxidative Stress and Neuroprotection
Cornelius, C., Crupi, R., Calabrese, V., Graziano, A., Milone, P., Pennisi, G., Radak, Z. O., Calabrese, E. J., & Cuzzocrea, S. (2013) · Antioxidants and Redox Signaling · doi:10.1089/ars.2012.4981 · Cited by 355
“Transgenic mice that overexpress Cu/Zn SOD are signiﬁcantly protected against post-TBI pathophysiology and neurodegeneration (112).”
Glutamate neurotransmission in rodent models of traumatic brain injury
Dorsett, C. R., McGuire, J. L., DePasquale, E. A. K., Gardner, A. E., Floyd, C. L., & McCullumsmith, R. E. (2017) · Journal of Neurotrauma · doi:10.1089/neu.2015.4373 · Cited by 163
“competitive NMDA receptor antagonists, cannabinoid agonists, nitric oxide synthase inhibitors, AMPA antagonists, serotonin agonists, and magnesium sulfates.(114,115) While initially promising in phase II clinical trials, the synthetic cannabinoid receptor agonist”
Background
Transplantation of human mesenchymal stem cells loaded on collagen scaffolds for the treatment of traumatic brain injury in rats
Guan, J., Zhu, Z., Zhao, R. C., Xiao, Z., Wu, C., Han, Q., Chen, L., Tong, W., Zhang, J. C., Han, Q., et al. (2013) · Biomaterials · doi:10.1016/j.biomaterials.2013.04.047 · Cited by 152
“Traumatic brain injury (TBI) is a common clinical disease with few effective treatments [2].”
Background
Long noncoding RNA MALAT1 in exosomes drives regenerative function and modulates inflammation-linked networks following traumatic brain injury
Patel, N. A., Moss, L. D., Lee, J.-Y., Tajiri, N., Acosta, S., Hudson, C., Parag, S., Cooper, D. R., Borlongan, C. V., & Bickford, P. C. (2018) · Journal of Neuroinflammation · doi:10.1186/s12974-018-1240-3 · Cited by 178
Neurorestoration after traumatic brain injury through angiotensin II receptor blockage
Villapol, S., Balarezo, M. G., Affram, K. O., Saavedra, J. M., & Symes, A. J. (2015) · Brain · doi:10.1093/brain/awv172 · Cited by 153
“offer significant improvement over current symptomatic treatment of TBI (Andriessen et al., 2010; McConeghy et al., 2012).”
Background
Predictors of outcome in civilian gunshot wounds to the head.
Aarabi, B., Tofighi, B., Kufera, J. A., Hadley, J. A., Ahn, E. S., Cooper, C., Malik, J. M., Naff, N., Chang, L., Radley, M. G., et al. (2014) · Journal of Neurosurgery · doi:10.3171/2014.1.jns131869 · Cited by 133
The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease
Kokiko-Cochran, O. N., & Godbout, J. P. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.00672 · Cited by 128
A State-of-the-Science Overview of Randomized Controlled Trials Evaluating Acute Management of Moderate-to-Severe Traumatic Brain Injury
Bragge, P., Synnot, A., Maas, A. I. R., Menon, D. K., Cooper, D. J., Rosenfeld, J. V., & Gruen, R. L. (2015) · Journal of Neurotrauma · doi:10.1089/neu.2015.4233 · Cited by 126
Perspectives on Molecular Biomarkers of Oxidative Stress and Antioxidant Strategies in Traumatic Brain Injury
Arent, A. M., de Souza, L. F., Walz, R., & Dafré, A. L. (2014) · BioMed Research International · doi:10.1155/2014/723060 · Cited by 106
“In a phase II study, progesterone showed significant reduction in mortality and improvement in the Glasgow outcome scale at 3 and 6 months after TBI; however, results from a phase III multicentre, randomized clinical trial are pending [207].”
BackgroundMethod
Pre-Clinical Traumatic Brain Injury Common Data Elements: Toward a Common Language Across Laboratories
Smith, D. H., Hicks, R. R., Johnson, V. E., Bergstrom, D. A., Cummings, D. M., Noble‐Haeusslein, L. J., Hovda, D. A., Whalen, M. J., Ahlers, S. T., LaPlaca, M. C., et al. (2015) · Journal of Neurotrauma · doi:10.1089/neu.2014.3861 · Cited by 105
Berberine Protects against Neuronal Damage via Suppression of Glia-Mediated Inflammation in Traumatic Brain Injury
Chen, C.-C., Hung, T., Lee, C. Y., Wang, L.-F., Wu, C., Ke, C., & Chen, S. (2014) · PLoS ONE · doi:10.1371/journal.pone.0115694 · Cited by 114
“Although a number of drugs targeting inflammatory pathways following TBI have been tested in clinical trials, none has conferred a significant benefit [5].”
BackgroundInfluential
Core-Cross-Linked Nanoparticles Reduce Neuroinflammation and Improve Outcome in a Mouse Model of Traumatic Brain Injury
Yoo, D., Magsam, A. W., Kelly, A. M., Stayton, P. S., Kievit, F. M., & Convertine, A. J. (2017) · ACS Nano · doi:10.1021/acsnano.7b03426 · Cited by 121
Fisetin alleviates oxidative stress after traumatic brain injury via the Nrf2-ARE pathway
Zhang, L., Wang, H., Zhou, Y., Zhu, Y., & Fei, M. (2018) · Neurochemistry International · doi:10.1016/j.neuint.2018.05.011 · Cited by 104
“Despite the development in diagnosis, neuroradiology and neurosurgical treatment of TBI in the recent years, no effective pharmacological therapy is currently available (McConeghy et al., 2012).”
ATP Induces Disruption of Tight Junction Proteins via IL-1 Beta-Dependent MMP-9 Activation of Human Blood-Brain Barrier In Vitro
Yang, F.-X., Zhao, K., Zhang, X., Zhang, J., & Xu, B.-N. (2016) · Journal of Neural Transplantation and Plasticity · doi:10.1155/2016/8928530 · Cited by 89
“Currently, there is no effective neuroprotective agent that is available clinically, to prevent the damage to BBB following CNS trauma/stress injury [4, 5].”
Background
Pharmacologic neuroprotection for functional outcomes after traumatic brain injury: a systematic review of the clinical literature
Gruenbaum, S. E., Zlotnik, A., Gruenbaum, B. F., Hersey, D., & Bilotta, F. (2016) · CNS Drugs · doi:10.1007/s40263-016-0355-2 · Cited by 86
“In 2012, McConeghy and colleagues reviewed the findings of studies published to 2012 in which pharmacological therapies were used to treat TBI [12].”
Background
Investigational agents for treatment of traumatic brain injury
Xiong, Y., Zhang, Y.-L., Mahmood, A., & Chopp, M. (2015) · Expert Opinion on Investigational Drugs · doi:10.1517/13543784.2015.1021919 · Cited by 82
“Over the past 40 years, > 100 RCTs in TBI were conducted [11,23,34-41].”
Background
IonStar enables high-precision, low-missing-data proteomics quantification in large biological cohorts
Shen, X., Shen, S., Li, J., Hu, Q., Nie, L., Tu, C., Wang, X., Poulsen, D. J., Orsburn, B. C., Wang, J., et al. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1800541115 · Cited by 76
“To develop an effective therapy for treating severe TBI, it is essential to understand the highly complex and heterogeneous mechanisms of the disease (49).”
Background
Humble beginnings with big goals: Small molecule soluble epoxide hydrolase inhibitors for treating CNS disorders
Zarriello, S., Tuazon, J. P., Corey, S., Schimmel, S. J., Rajani, M., Gorsky, A., Abraham, D. I., Hammock, B. D., & Borlongan, C. V. (2018) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2018.11.001 · Cited by 92
“TBI, characterized by a blow or penetration to the head, induces primary damage to the brain tissue, followed by cerebral inflammation representing a major secondary cell death pathway (McConeghy et al., 2012).”
Background
Pharmacological Sequestration of Mitochondrial Calcium Uptake Protects Neurons Against Glutamate Excitotoxicity
Angelova, P. R., Vinogradova, D., Neganova, M., Serkova, T., Sokolov, V. V., Bachurin, S., Shevtsova, E., & Abramov, A. (2018) · Molecular Neurobiology · doi:10.1007/s12035-018-1204-8 · Cited by 74
Neuroprotective effect of allicin against traumatic brain injury via Akt/endothelial nitric oxide synthase pathway-mediated anti-inflammatory and anti-oxidative activities.
Chen, W., Qi, J., Feng, F., Wang, M.-D., Bao, G., Wang, T., Xiang, M., & Xie, W.-F. (2014) · Neurochemistry International · doi:10.1016/j.neuint.2014.01.015 · Cited by 73
“Several endogenous antioxidant enzymes, such as CAT, SOD and GST, work together to provide a line of defense against oxidative damage, but this important defense mechanism is incapable of scavenging the over-generated free radicals under secondary brain injury conditions (McConeghy et al., 2012; Slemmer et al., 2008).”
Early posttraumatic CSF1R inhibition via PLX3397 leads to time- and sex-dependent effects on inflammation and neuronal maintenance after traumatic brain injury in mice
Wang, Y., Wernersbach, I., Strehle, J., Li, S., Appel, D., Klein, M., Ritter, K., Hummel, R., Tegeder, I., & Schäfer, M. K. E. (2022) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2022.07.164 · Cited by 69
“50 Despite the identification of neuroprotective drugs in animal models of TBI and decades of clinical research, therapeutic options are limited to surgical interventions and symptomatic relief (McConeghy et al., 2012), owing to the complexity of pathophysiological processes comprising cerebral ischemia, impaired cere…”
Background
Valproic Acid: A New Candidate of Therapeutic Application for the Acute Central Nervous System Injuries
Chen, S., Wu, H., Klebe, D. W., Hong, Y., & Zhang, J. (2014) · Neurochemical Research · doi:10.1007/s11064-014-1241-2 · Cited by 66
Ablation of Type-1 IFN Signaling in Hematopoietic Cells Confers Protection Following Traumatic Brain Injury
Karve, I. P., Zhang, M., Habgood, M. D., Frugier, T., Brody, K. M., Sashindranath, M., Ek, C. J., Chappaz, S., Kile, B. T., Wright, D. K., et al. (2016) · eNeuro · doi:10.1523/eneuro.0128-15.2016 · Cited by 64
Strategies for CNS repair following TBI
Aertker, B. M., Bedi, S. S., & Cox, C. S. (2015) · Experimental Neurology · doi:10.1016/j.expneurol.2015.01.008 · Cited by 65
Posttraumatic administration of luteolin protects mice from traumatic brain injury: implication of autophagy and inflammation.
Xu, J., Wang, H.-D., Lu, X.-Y., Ding, K., Zhang, L. D., He, J., Wei, W.-T., & Wu, Y. (2014) · Brain Research · doi:10.1016/j.brainres.2014.07.042 · Cited by 59
“…development in understanding the pathological process after TBI, a formidable problem facing us is, effective pharmacological therapy remains limited (McConeghy et al., 2012); therefore, searching for neuroprotective agents still represents a promising therapeutic strategy for the treatment of TBI.”
Sigma-1 receptor: a potential therapeutic target for traumatic brain injury
Shi, M., Chen, F., Chen, Z., Yang, W., Yue, S., Zhang, J., & Chen, X. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2021.685201 · Cited by 58
Glutamate Neurotoxicity and Destruction of the Blood–Brain Barrier: Key Pathways for the Development of Neuropsychiatric Consequences of TBI and Their Potential Treatment Strategies
Gruenbaum, B. F., Zlotnik, A. A., Fleidervish, I. A., Frenkel, A., & Boyko, M. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23179628 · Cited by 63
Protective Effects of Chinese Herbal Medicine Rhizoma drynariae in Rats After Traumatic Brain Injury and Identification of Active Compound
Wang, W., Li, H., Yu, J., Hong, M., Zhou, J., Zhu, L., Wang, Y., Luo, M., Xia, Z., Yang, Z.-J., et al. (2015) · Molecular Neurobiology · doi:10.1007/s12035-015-9385-x · Cited by 59
“than 40 phase II and phase III clinical trials have failed to show efficacy of monotherapy for TBI [6, 7], including two”
Chronic Cognitive Dysfunction after Traumatic Brain Injury Is Improved with a Phosphodiesterase 4B Inhibitor
Titus, D. J., Wilson, N., Freund, J. E., Carballosa, M., Sikah, K. E., Furones, C., Dietrich, W., Gurney, M., & Atkins, C. M. (2016) · Journal of Neuroscience · doi:10.1523/jneurosci.3212-15.2016 · Cited by 56
“Although a significant amount of experimental work has clarified the pathophysiology of TBI, limited success has been obtained in translating therapies to the patient (McConeghy et al., 2012).”
Background
Low-Molecular-Weight Fucoidan Attenuates Mitochondrial Dysfunction and Improves Neurological Outcome After Traumatic Brain Injury in Aged Mice: Involvement of Sirt3
Wang, T., Zhu, M., & He, Z.-Z. (2016) · Cellular and molecular neurobiology · doi:10.1007/s10571-015-0323-2 · Cited by 56
“…antioxidant enzymes, such as CAT, SOD, and GPx, work together to provide a line of defense against oxidative damage, but this important defense mechanism is incapable of scavenging the overgenerated free radicals under secondary brain injury conditions (McConeghy et al. 2012; Chen et al. 2014).”
Background
Clinical implications of leukocyte infiltration at the choroid plexus in (neuro)inflammatory disorders
Demeestere, D., Libert, C., & Vandenbroucke, R. E. (2015) · Drug Discovery Today · doi:10.1016/j.drudis.2015.05.003 · Cited by 63
Neuroprotective pentapeptide CN-105 is associated with reduced sterile inflammation and improved functional outcomes in a traumatic brain injury murine model
Laskowitz, D. T., Wang, H., Chen, T., Lubkin, D. T., Cantillana, V., Tu, T. M., Kernagis, D., Zhou, G., Macy, G., Kolls, B. J., et al. (2017) · Scientific Reports · doi:10.1038/srep46461 · Cited by 55
Deletion or inhibition of soluble epoxide hydrolase protects against brain damage and reduces microglia-mediated neuroinflammation in traumatic brain injury
Hung, T., Shyue, S., Wu, C., Chen, C.-C., Lin, C.-C., Chang, C.-F., & Chen, S. (2017) · Oncotarget · doi:10.18632/oncotarget.21139 · Cited by 53
“TBI induces brain damage due to initial physical disruption of tissue (primary injury) and subsequent development of excitotoxicity, oxidative damage, and inflammation (secondary injury) [2].”
Neuroprotection Trials in Traumatic Brain Injury
Chakraborty, S., Skolnick, B. E., & Narayan, R. K. (2016) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-016-0625-x · Cited by 50
“Fhe mGluR5 agonist, (RS)-2-chloro-5hydroxyphenylglycine (CHPG), is neuroprotective and has anti-apoptotic properties in neuronal cell culture and microglial culture models. Loane et al. have also shown good in vivo neuroprotection results in animal models, and current clinical trials are underway [37]. The NMDA partia…”
Background
A dual-enzymatically cross-linked injectable gelatin hydrogel loaded with BMSC improves neurological function recovery of traumatic brain injury in rats.
Yao, M.-H., Gao, F., Xu, R., Zhang, J., Chen, Y., & Guan, F. (2019) · Biomaterials Science · doi:10.1039/c9bm00749k · Cited by 48
Sex hormones modulate pathogenic processes in experimental traumatic brain injury
Gölz, C., Kirchhoff, F. P., Westerhorstmann, J., Schmidt, M., Hirnet, T., Rune, G. M., Bender, R. A., & Schäfer, M. K. E. (2019) · Journal of Neurochemistry · doi:10.1111/jnc.14678 · Cited by 58
TLR4 inhibitor resatorvid provides neuroprotection in experimental traumatic brain injury: implication in the treatment of human brain injury.
Zhang, D., Li, H., Li, T., Zhou, M.-L., Hao, S., Yan, H., Yu, Z., Li, W., Li, K.-Y., & Hang, C. (2014) · Neurochemistry International · doi:10.1016/j.neuint.2014.05.003 · Cited by 48
Tailored Reconstituted Lipoprotein for Site-Specific and Mitochondria-Targeted Cyclosporine A Delivery to Treat Traumatic Brain Injury
Chen, L., Song, Q., Chen, Y., Meng, S., Zheng, M., Huang, J., Zhang, Q., Jiang, J., Feng, J., Chen, H., et al. (2020) · ACS Nano · doi:10.1021/acsnano.9b09186 · Cited by 59
Intravenous Immunomodulatory Nanoparticle Treatment for Traumatic Brain Injury
Sharma, S., Ifergan, I., Kurz, J., Linsenmeier, R., Xu, D.-L., Cooper, J. G., Miller, S. D., & Kessler, J. (2020) · Annals of Neurology · doi:10.1002/ana.25675 · Cited by 47
“clinical and clinical trials designed to limit such secondary damage, no successful therapies have emerged.(5,6) Here, we”
Background
Should losartan be administered following brain injury?
Friedman, A., Bar-Klein, G., Serlin, Y., Parmet, Y., Heinemann, U., & Kaufer, D. (2014) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2014.972945 · Cited by 47
“Despite a large number of clinical trials testing different potential neuroprotective strategies, to date, no available agents or strategies have been shown to produce improved outcome (for review see [30,31]).”
Background
Targeted delivery of PARP inhibitors to neuronal mitochondria via biomimetic engineered nanosystems in a mouse model of traumatic brain injury.
Sun, J.-J., Liu, J., Gao, C.-H., Zheng, J.-P., Zhang, J., Ding, Y., Gong, W., Yang, M.-Y., Li, Z.-P., Wang, Y.-L., et al. (2021) · Acta Biomaterialia · doi:10.1016/j.actbio.2021.12.023 · Cited by 45
A Role for Nanoparticles in Treating Traumatic Brain Injury
Bony, B. A., & Kievit, F. M. (2019) · Pharmaceutics · doi:10.3390/pharmaceutics11090473 · Cited by 55
“Indeed, many strategies that inhibit the effects of these biomolecules have shown promise in preclinical models and have been tested clinically, yet none have shown efficacy in the Phase III trial [18].”
Background
Theranostic Oxygen Reactive Polymers for Treatment of Traumatic Brain Injury
Xu, J. M., Ypma, M., Chiarelli, P. A., Park, J. C., Ellenbogen, R. G., Stayton, P. S., Mourad, P. D., Lee, D., Convertine, A. J., & Kievit, F. M. (2016) · Advanced Functional Materials · doi:10.1002/adfm.201504416 · Cited by 54
Fecal Microbiota Transplantation Derived from Alzheimer’s Disease Mice Worsens Brain Trauma Outcomes in Wild-Type Controls
Soriano, S., Curry, K. D., Wang, Q., Chow, E., Treangen, T. J., & Villapol, S. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23094476 · Cited by 42
“TBI has a devastating effect on the brain, causing both short- and long-term damage that is not effectively alleviated by traditional pharmacological treatments [16,17].”
Background
Metalloporphyrins as Therapeutic Catalytic Oxidoreductants in Central Nervous System Disorders
Sheng, H., Chaparro, R., Sasaki, T., Izutsu, M., Pearlstein, R. D., Tovmasyan, A. G., & Warner, D. S. (2013) · Antioxidants and Redox Signaling · doi:10.1089/ars.2013.5413 · Cited by 40
“It is unlikely that bioavailability can explain lack of effect, because behavioral responses to intravenous MnTE-2-PyP treatment were similar to those observed with intracerebroventricular injection, and closed cranial impact is associated with major BBB disruption (127).”
The Role of Estradiol in Traumatic Brain Injury: Mechanism and Treatment Potential
Kövesdi, E., Szabó‐Meleg, E., & Ábrahám, I. M. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms22010011 · Cited by 52
“Therefore, to date, there is still no approved therapy for TBI [8,9].”
Background
Using functional and molecular MRI techniques to detect neuroinflammation and neuroprotection after traumatic brain injury
Wang, W., Zhang, H., Lee, D.-H., Yu, J.-T., Cheng, T., Hong, M., Jiang, S.-S., Fan, H., Huang, X., Zhou, J.-Y., et al. (2017) · Brain, behavior, and immunity · doi:10.1016/j.bbi.2017.04.019 · Cited by 40
“Currently, no drug is effective for treatment of TBI, and clinical trials of neuroprotective drugs have not shown clear benefit in reducing or preventing secondary brain damage (McConeghy et al., 2012).”
Background
Chaperone-Mediated Autophagy in Neurodegenerative Diseases and Acute Neurological Insults in the Central Nervous System
Kanno, H., Handa, K., Murakami, T., Aizawa, T., & Ozawa, H. (2022) · Cells · doi:10.3390/cells11071205 · Cited by 47
Fine Tuning of Traumatic Brain Injury Management in Neurointensive Care—Indicative Observations and Future Perspectives
Wettervik, T. S., Lewén, A., & Enblad, P. (2021) · Frontiers in Neurology · doi:10.3389/fneur.2021.638132 · Cited by 47
“Many neuroprotective agents have been developed to counteract these pathomechanisms, but there has so far been limited success in translation from animal to clinical studies (113).”
Background
Effects of early rolipram treatment on histopathological outcome after controlled cortical impact injury in mice
Atkins, C. M., Cepero, M. L., Kang, Y., Liebl, D. J., & Dietrich, W. D. (2012) · Neuroscience Letters · doi:10.1016/j.neulet.2012.10.019 · Cited by 39
Traumatic brain injury causes long-term behavioral changes related to region-specific increases of cerebral blood flow
Pöttker, B., Stöber, F., Hummel, R., Angenstein, F., Radyushkin, K., Goldschmidt, J., & Schäfer, M. K. E. (2017) · Brain Structure and Function · doi:10.1007/s00429-017-1452-9 · Cited by 35
“Due to its complex pathophysiology, treatment options are restricted to surgical intervention and supportive care and do not directly address the secondary neurological sequelae (McConeghy et al. 2012; Corps et al. 2015).”
Background
Can Microbiota Research Change Our Understanding of Neurodegenerative diseases?
Scheperjans, F. (2016) · Neurodegenerative Disease Management · doi:10.2217/nmt-2015-0012 · Cited by 31
The cysteine-rich whey protein supplement, Immunocal®, preserves brain glutathione and improves cognitive, motor, and histopathological indices of traumatic brain injury in a mouse model of controlled cortical impact
Ignowski, E., Winter, A. N., Duval, N., Fleming, H., Wallace, T., Manning, E., Koza, L. A., Huber, K. M., Serkova, N. J., & Linseman, D. A. (2018) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2018.06.026 · Cited by 38
“Given the multi-factorial nature of secondary injury, many different therapeutic approaches have been investigated in an attempt to mitigate the post-acute neuronal damage caused by TBI including antioxidants, neurorestorative therapies, neuroprotective pharmacological agents, and drugs that modulate neuroinflammation…”
Effect of Telenursing on Levels of Depression and Anxiety in Caregivers of Patients with Stroke: A Randomized Clinical Trial
Goudarzian, M., Fallahi-Khoshknab, M., Dalvandi, A., Delbari, A., & Biglarian, A. (2018) · Iranian Journal of Nursing and Midwifery Research · doi:10.4103/ijnmr.ijnmr_242_16 · Cited by 34
“[1,2] The incidence rate of first‐time stroke in Iran is 139 per 100,000 people that today we see an increasing number of these individuals due to the advancement of science in the field of diagnosis and treatment of diseases.[3,4] According to the World Health Organization, after discharge from hospital, about 80% of…”
Background
Reactive Oxygen Species-Induced Aggregation of Nanozymes for Neuron Injury
He, H., Shi, X., Wang, J., Wang, X., Wang, Q., Yu, D., Ge, B., Zhang, X., & Huang, F. L. (2019) · ACS Applied Materials & Interfaces · doi:10.1021/acsami.9b17509 · Cited by 41
Xuefu zhuyu decoction improves cognitive impairment in experimental traumatic brain injury via synaptic regulation
Zhou, J.-H., Liu, T., Cui, H.-J., Fan, R., Zhang, C., Peng, W.-J., Yang, A., Zhu, L., Wang, Y., & Tang, T. (2017) · OncoTarget · doi:10.18632/oncotarget.18895 · Cited by 31
Curcumin alleviates brain edema by lowering AQP4 expression levels in a rat model of hypoxia-hypercapnia-induced brain damage
Yu, L., Fan, Y., Ye, G.-H., Li, J., Feng, X., Lin, K., Dong, M.-W., & Wang, Z. (2016) · Experimental and Therapeutic Medicine · doi:10.3892/etm.2016.3022 · Cited by 32
“These drugs, which typically have a single therapeutic target and defined underlying pharmacological mechanisms, have demonstrated effectiveness in various experimental studies; however, they have shown mixed effectiveness and, in some cases serious side-effects, in human clinical trials (6-8).”
Downregulation of Homer1b/c improves neuronal survival after traumatic neuronal injury.
Fei, F., Rao, W., Zhang, L., Chen, B.-G., Li, J., Fei, Z., & Chen, Z. (2014) · Neuroscience · doi:10.1016/j.neuroscience.2014.02.037 · Cited by 29
“However, none of them has shown favorable efficacy on severe brain injuries in the recent clinical trials (Loane and Faden, 2010; McConeghy et al., 2012).”
Fluid biomarkers of chronic traumatic brain injury
Friberg, S., Lindblad, C., Zeiler, F. A., Zetterberg, H., Granberg, T., Svenningsson, P., Piehl, F., & Thelin, E. P. (2024) · Nature Reviews Neurology · doi:10.1038/s41582-024-01024-z · Cited by 36
Downregulation of miR-491-5p promotes neovascularization after traumatic brain injury
Tang, W., Guo, Z.-D., Chai, W., Du, D., Yang, X., Cao, L., Chen, H., Zhou, C., Cheng, C.-J., Sun, X.-C., et al. (2021) · Neural Regeneration Research · doi:10.4103/1673-5374.314326 · Cited by 28
“Secondary ischemic injury exacerbates secondary brain injury, resulting in excessive inflammation and oxidative stress, which eventually aggravates neuronal apoptosis (McConeghy et al., 2012; Gyoneva and Ransohoff, 2015).”
Background
The potential for immune checkpoint modulators in cerebrovascular injury and inflammation
Kim, J. E., Patel, K. K., & Jackson, C. M. (2020) · Expert Opinion on Therapeutic Targets · doi:10.1080/14728222.2021.1869213 · Cited by 30
“Despite promising preclinical studies, most clinical trials of therapeutic immunomodulators for the treatment of TBI have had disappointing results [53,54].”
Background
Guanosine Attenuates Behavioral Deficits After Traumatic Brain Injury by Modulation of Adenosinergic Receptors
Dobrachinski, F., Gerbatin, R. R., Sartori, G., Golombieski, R. M., Antoniazzi, A. Q., Nogueira, C. W., Royes, L. F. F., Fighera, M. R., Porciúncula, L. O., Cunha, R. A., et al. (2018) · Molecular Neurobiology · doi:10.1007/s12035-018-1296-1 · Cited by 33
Protective Effects of Hinokitiol on Neuronal Ferroptosis by Activating the Keap1/Nrf2/HO-1 Pathway in Traumatic Brain Injury
Tang, H., He, K., Zhao, K., Chen, Z., Wu, W., Jin, W., Yang, L., & Xie, B. (2023) · Journal of Neurotrauma · doi:10.1089/neu.2023.0150 · Cited by 31
“26,27 Unfortunately, none of the compounds have been moved into clinical trials.”
Evaluating differential nanoparticle accumulation and retention kinetics in a mouse model of traumatic brain injury via Ktrans mapping with MRI
Miller, H. A., Magsam, A. W., Tarudji, A. W., Romanova, S., Weber, L., Gee, C. C., Madsen, G. L., Bronich, T. K., & Kievit, F. M. (2019) · Scientific Reports · doi:10.1038/s41598-019-52622-7 · Cited by 31
Adjudin Attenuates Cerebral Edema and Improves Neurological Function in Mice with Experimental Traumatic Brain Injury
Liu, Y., Yuan, F., Yang, D., Xu, Z., Yao, J., Yang, G., Geng, Z., Xia, W., & Tian, H. (2018) · Journal of Neurotrauma · doi:10.1089/neu.2017.5397 · Cited by 24
“3 Cerebral edema, which is a fatal pathological phenomenon following TBI, elevates intracranial pressure (ICP) due to an increase in brain volume within the enclosed skull.”
Maturation-dependent response of neurogenesis after traumatic brain injury in children
Taylor, S. R., Smith, C. M., Harris, B. T., Costine, B. A., & Duhaime, A. (2013) · Journal of Neurosurgery Pediatrics · doi:10.3171/2013.8.peds13154 · Cited by 22
Bexarotene promotes microglia/macrophages - Specific brain - Derived Neurotrophic factor expression and axon sprouting after traumatic brain injury
He, J., Huang, Y., Liu, H., Sun, X., Wu, J., Zhang, Z., Liu, L., Zhou, C., Jiang, S., Huang, Z., et al. (2020) · Experimental Neurology · doi:10.1016/j.expneurol.2020.113462 · Cited by 36
Effects of estrogen receptor GPR30 agonist G1 on neuronal apoptosis and microglia polarization in traumatic brain injury rats
Pan, M., Tang, J.-C., Liu, R., Feng, Y.-G., & Wan, Q. (2018) · Chinese journal of traumatology = Zhonghua chuang shang za zhi · doi:10.1016/j.cjtee.2018.04.003 · Cited by 24
Blood glutamate scavenging as a novel glutamate-based therapeutic approach for post-traumatic brain injury anxiety and social impairment
Frank, D., Gruenbaum, B., Shelef, I., Zvenigorodsky, V., Severynovska, O., Fleidervish, I., Knyazer, B., Frenkel, A., Zlotnik, A., Kofman, O., et al. (2023) · Translational Psychiatry · doi:10.1038/s41398-023-02329-1 · Cited by 23
“Neurological motor symptoms of TBI were attenuated by limiting excess glutamate with dextorphan [28], n-methyl-D-aspartate (NMDA) antagonists [29], stimulation of Na+ -dependent excitatory amino acid transporters [30], or antibiotics and other drugs that block calcium channels or glutamate release [31].”
Background
The migration and differentiation of hUC-MSCsCXCR4/GFP encapsulated in BDNF/chitosan scaffolds for brain tissue engineering
Huang, C.-J., Zhao, L., Gu, J., Nie, D.-K., Chen, Y.-N., Zuo, H., Huan, W., Shi, J.-L., Chen, J., & Shi, W. (2016) · Biomedical Materials · doi:10.1088/1748-6041/11/3/035004 · Cited by 23
“Traumatic brain injury (TBI) often results in mortality or long-term disabilities such as dysphasia or cognitive deficits [1].”
Background
Hypocalcaemia as a prognostic factor of early mortality in moderate and severe traumatic brain injury
Viñas-Ríos, J. M., Sánchez-Aguilar, M., Sánchez-Rodríguez, J., González-Aguirre, D., Heinen, C., Meyer, F., & Kretschmer, T. (2014) · Neurological Research · doi:10.1179/1743132813y.0000000272 · Cited by 23
Early increase of cannabinoid receptor density after experimental traumatic brain injury in the newborn piglet
Donat, C. K., Fischer, F., Walter, B. L., Deuther‐Conrad, W., Brodhun, M., Bauer, R., & Brust, P. (2014) · Acta Neurobiologiae Experimentalis · doi:10.55782/ane-2014-1985 · Cited by 24
“However, while some trials are still ongoing, many failed (Tolias and Bullock 2004, McConeghy et al. 2012).”
Background
Comparison of the Effect of Minocycline and Simvastatin on Functional Recovery and Gene Expression in a Rat Traumatic Brain Injury Model
Haar, C. V., Anderson, G., Elmore, B. E., Moore, L. H., Wright, A. M., Kantor, E., Farin, F., Bammler, T., MacDonald, J. W., & Hoane, M. (2014) · Journal of Neurotrauma · doi:10.1089/neu.2013.3119 · Cited by 22
Pharmacological inhibition of STING reduces neuroinflammation‐mediated damage post‐traumatic brain injury
Fryer, A. L., Abdullah, A., Mobilio, F., Jobling, A., Moore, Z., de Veer, M., Zheng, G., Wong, B., Taylor, J. M., & Crack, P. (2024) · British Journal of Pharmacology · doi:10.1111/bph.16347 · Cited by 21
“Secondary injury in TBI is a complex array of interrelated molecular processes, such as excitotoxicity, necrosis and neuroinflammation, which all contribute to chronic neurodegeneration (Dixon, 2017; McConeghy et al., 2012).”
Argon gas: a potential neuroprotectant and promising medical therapy
Nowrangi, D., Tang, J., & Zhang, J. H. (2014) · Medical Gas Research · doi:10.1186/2045-9912-4-3 · Cited by 19
“physical trauma [33,34].”
The Role of Magnesium in Depression, Migraine, Alzheimer’s Disease, and Cognitive Health: A Comprehensive Review
Varga, P., Lehoczki, A., Fekete, M., Jarecsny, T., Kryczyk‐Poprawa, A., Zábó, V., Major, D., Fazekas‐Pongor, V., Csípő, T., & Varga, J. T. (2025) · Nutrients · doi:10.3390/nu17132216 · Cited by 21
“Patients with acute neurological conditions (e.g., stroke, traumatic brain injury) may not benefit substantially from magnesium therapy due to its slow cellular uptake and the narrow therapeutic window in such emergencies [176,177].”
Proteomics: in pursuit of effective traumatic brain injury therapeutics
Lizhnyak, P. N., & Ottens, A. K. (2015) · Espert Review of Proteomics · doi:10.1586/14789450.2015.1000869 · Cited by 19
“On reflection, we have been ineffective matching drug pharmacology within the heterogeneous human TBI population [13].”
Method
Neuroprotection strategies in traumatic brain injury: Studying the effectiveness of different clinical approaches
Buccilli, B., Alan, A., Aljeradat, B., Shahzad, A., Almealawy, Y. F., Chisvo, N. S., Ennabe, M., & Weinand, M. E. (2024) · Surgical Neurology International · doi:10.25259/sni_773_2023 · Cited by 22
“[49,53] Immune system modulation e immunosuppressant Cyclosporine-A reduces T-cell-mediated immunity and is used in organ transplant recipients.”
Background
The lncRNA-AK046375 Upregulates Metallothionein-2 by Sequestering miR-491-5p to Relieve the Brain Oxidative Stress Burden after Traumatic Brain Injury
Tang, W., Chai, W., Du, D., Xia, Y.-Z., Wu, Y.-F., Jiang, L., Cheng, C.-J., Guo, Z.-D., Sun, X.-C., Huang, Z., et al. (2022) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2022/8188404 · Cited by 18
“The secondary injury, such as oxidative stress, mitochondrial dysfunction, calcium over-loading, and neuroin ﬂ ammation, strongly in ﬂ uences the outcomes of TBI, which to some degree are reversible and can be mitigated by therapeutics [3 – 5].”
Design and Synthesis of Brain Penetrant Glycopeptide Analogues of PACAP With Neuroprotective Potential for Traumatic Brain Injury and Parkinsonism
Apostol, C. R., Bernard, K., Tanguturi, P., Molnar, G., Bartlett, M. J., Szabó, L., Liu, C., Ortiz, J. B., Saber, M., Giordano, K. R., et al. (2022) · Frontiers in Drug Discovery · doi:10.3389/fddsv.2021.818003 · Cited by 21
“None of the available treatments have been clinically successful for TBI to date (Hall et al., 2010; Xiong et al., 2010; McConeghy et al., 2012; Tsang and Whitfield, 2012; Algattas and Huang, 2013).”
Background
C-terminal binding proteins 1 and 2 in traumatic brain injury-induced inflammation and their inhibition as an approach for anti-inflammatory treatment
Li, H., Zhang, C., Yang, C., Blevins, M. A., Norris, D. A., Zhao, R., & Huang, M. (2020) · International Journal of Biological Sciences · doi:10.7150/ijbs.42109 · Cited by 20
“There is a compelling need for effective neuroprotective interventions that improve functional outcomes in TBI patients [22, 23].”
Background
Post‐injury administration of a combination of memantine and 17&bgr;‐estradiol is protective in a rat model of traumatic brain injury
Day, N. L., Carle, M. S., & Floyd, C. L. (2017) · Neurochemistry International · doi:10.1016/j.neuint.2017.04.018 · Cited by 18
“L. Day), Msc4705@uab.edu du (C.L. Floyd). pharmacotherapeutics available that effectively attenuate the secondary biochemical damage (Loane and Faden, 2010; McConeghy et al., 2012).”
Protection against Blast-Induced Traumatic Brain Injury by Increase in Brain Volume
Gu, M., Kawoos, U., Mccarron, R., & Chavko, M. (2017) · BioMed Research International · doi:10.1155/2017/2075463 · Cited by 18
“Several attempts to minimize secondary brain injury after TBI by pharmacological intervention or hypothermia were ineffective in clinical trials [14].”
Why Does Brain Trauma Research Fail?
Alves, J. L., Rato, J. R., & da Silva, V. M. M. (2019) · World Neurosurgery · doi:10.1016/j.wneu.2019.06.212 · Cited by 26
Diltiazem Promotes Regenerative Axon Growth
Huebner, E. A., Budel, S., Jiang, Z.-X., Omura, T., Ho, T., Barrett, L. B., Merkel, J., Pereira, L. M., Andrews, N., Wang, X.-X., et al. (2018) · Molecular Neurobiology · doi:10.1007/s12035-018-1349-5 · Cited by 17
A Pulsed Electromagnetic Field Protects against Glutamate-Induced Excitotoxicity by Modulating the Endocannabinoid System in HT22 Cells
Li, X., Xu, H., Lei, T., Yang, Y.-F., Jing, D., Dai, S.-H., Luo, P., & Xu, Q. (2017) · Frontiers in Neuroscience · doi:10.3389/fnins.2017.00042 · Cited by 17
“However, clinical trials have reported unsatisfactory results for drugs designed to treat excitotoxicity (McConeghy et al., 2012).”
Background
The neuroprotective potential of arginine-rich peptides for the acute treatment of traumatic brain injury
Chiu, L.-S., Anderton, R., Knuckey, N., & Meloni, B. (2016) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2016.1150180 · Cited by 17
“However, it appears that these agents may be of limited benefit following TBI [5,7].”
Background
Therapeutic Development of Apolipoprotein E Mimetics for Acute Brain Injury: Augmenting Endogenous Responses to Reduce Secondary Injury
James, M. L., Komisarow, J. M., Wang, H., & Laskowitz, D. T. (2020) · Neurotherapeutics · doi:10.1007/s13311-020-00858-x · Cited by 24
Peptide Pharmacological Approaches to Treating Traumatic Brain Injury: a Case for Arginine-Rich Peptides
Chiu, L. S., Anderton, R. S., Knuckey, N. W., & Meloni, B. P. (2016) · Molecular Neurobiology · doi:10.1007/s12035-016-0287-3 · Cited by 14
Effect of Traumatic Brain Injury, Erythropoietin, and Anakinra on Hepatic Metabolizing Enzymes and Transporters in an Experimental Rat Model
Anderson, G. D., Peterson, T. C., Haar, C. V., Farin, F. M., Bammler, T. K., MacDonald, J. W., Kantor, E. D., & Hoane, M. R. (2015) · The AAPS Journal · doi:10.1208/s12248-015-9792-y · Cited by 21
Blood Glutamate Scavenging With Pyruvate as a Novel Preventative and Therapeutic Approach for Depressive-Like Behavior Following Traumatic Brain Injury in a Rat Model
Frank, D., Gruenbaum, B., Shelef, I., Zvenigorodsky, V., Severynovska, O., Gal, R., Dubilet, M., Zlotnik, A., Kofman, O., & Boyko, M. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.832478 · Cited by 15
Effects of nicotinamide on spatial memory and inflammation after juvenile traumatic brain injury
Smith, A. C., Holden, R., Rasmussen, S. M., Hoane, M. R., & Hylin, M. J. (2019) · Behavioural Brain Research · doi:10.1016/j.bbr.2019.02.024 · Cited by 16
“Preclinical trials of neuroprotective compounds have been numerous over the years, but many of these treatments have failed to show consistent neuroprotection in Phase II/III trials [13].”
Endogenous Neuroprotective Molecules and Their Mechanisms in the Central Nervous System.
Hayashi, H., & Takagi, N. (2015) · Biological and Pharmaceutical Bulletin · doi:10.1248/bpb.b15-00361 · Cited by 15
Brain Metabolic Crisis in Traumatic Brain Injury: What Does It Mean?
Oliveira, M. D. L., Paiva, W., Teixeira, M., & Bor-Seng-Shu, E. (2014) · Journal of Neurotrauma · doi:10.1089/neu.2014.3386 · Cited by 15
“Some studies have found favorable effects of cyclosporin A on mitochondrial dysfunction, 10,12,14 which is linked to LPR1.”

Authors: McConeghy, K. W., Hatton, J., Hughes, L., & Cook, A. M.
Affiliations: University of Kentucky HealthCare (US)
University of Kentucky (US)
Corresponding author: Cook, Aaron M.
ORCID: McConeghy, Kevin W.
Hatton, Jimmi
Cook, Aaron M.
Venue: CNS Drugs
Publisher: Springer Science and Business Media LLC
Published: 2012-07
Volume: 26
Issue: 7
Pages: 613-636
ISSN: 1172-7047 (ISSN-L)
DOI: 10.2165/11634020-000000000-00000
OpenAlex: W2006925820
Cited by: 158
References: 0
Citations by year: 2025: 4 · 2024: 8 · 2023: 3 · 2022: 10 · 2021: 8 · 2020: 10 · 2019: 11 · 2018: 16 · 2017: 20 · 2016: 17 · 2015: 18 · 2014: 17 · 2013: 13 · 2012: 3
FWCI: 2.29
Type: journal article
Language: en
Open access: closed
Locations: CNS Drugs (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
Keywords: traumatic brain injury, neuroprotection, secondary brain injury, intracranial pressure, cerebral perfusion, calcium influx, mitochondrial dysfunction, redox homeostasis, blood flow, cytoskeleton, magnesium, progesterone, cyclosporine, biomarkers, clinical trial design
MeSH terms: Animals, Brain Injuries, Clinical Trials as Topic, Humans, Prognosis, Multicenter Studies as Topic, Randomized Controlled Trials as Topic, Neuroprotective Agents

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A Review of Neuroprotection Pharmacology and Therapies in Patients with Acute Traumatic Brain Injury

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