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Recent Patents on Food, Nutrition & Agriculture

Editor-in-Chief

ISSN (Print): 2212-7984
ISSN (Online): 1876-1429

General Review Article

Impact of Curcumin on Traumatic Brain Injury and Involved Molecular Signaling Pathways

Author(s): Tahereh Farkhondeh, Saeed Samarghandian*, Babak Roshanravan and Leila Peivasteh-roudsari

Volume 11, Issue 2, 2020

Page: [137 - 144] Pages: 8

DOI: 10.2174/2212798410666190617161523

Abstract

Traumatic Brain Injury (TBI) is one of the main causes of mortality and morbidity worldwide with no suitable treatment. The present study was designed to review the present literature about the protective effects of curcumin and the underlying mechanism against TBI. All published English language papers from beginning to 2019 were selected in this study. The findings indicate that curcumin may be effective against TBI outcomes by modulating the molecular signaling pathways involved in oxidative stress, inflammation, apoptosis, and autophagy. However, more experimental studies should be done to identify all mechanisms involved in the pathogenesis of TBI. Patents for Curcumin and chronic inflammation and traumatic brain injury management (WO2017097805A1 and US9101580B2) were published. In conclusion, the present study confirmed the potential therapeutic impact of curcumin for treating TBI.

Keywords: Curcumin, traumatic brain injury, inflammation, oxidative stress, apoptosis, autophagy.

Graphical Abstract

[1]
Pearn ML, Niesman IR, Egawa J, et al. Pathophysiology associated with traumatic brain injury: current treatments and potential novel therapeutics. Cell Mol Neurobiol 2017; 37(4): 571-85.
[http://dx.doi.org/10.1007/s10571-016-0400-1] [PMID: 27383839]
[2]
Paterno R, Folweiler KA, Cohen AS. Pathophysiology and treatment of memory dysfunction after traumatic brain injury. Curr Neurol Neurosci Rep 2017; 17(7): 52.
[http://dx.doi.org/10.1007/s11910-017-0762-x] [PMID: 28500417]
[3]
Williams AL. Traumatic brain injury. In: Physical Management for Neurological Conditions E-Book . 2018; p. 153.
[4]
Dewan MC, et al. Epidemiology of global pediatric traumatic brain injury: qualitative review. In: World neurosurgery 497-509. 2016; p. 91.
[5]
Weiner MW, Harvey D, Hayes J, et al. Effects of traumatic brain injury and posttraumatic stress disorder on development of Alzheimer’s disease in Vietnam Veterans using the Alzheimer’s Disease Neuroimaging Initiative: Preliminary Report. Alzheimers Dement (N Y) 2017; 3(2): 177-88.
[http://dx.doi.org/10.1016/j.trci.2017.02.005] [PMID: 28758146]
[6]
Wolf JA, Koch PF. Disruption of network synchrony and cognitive dysfunction after traumatic brain injury. Front Syst Neurosci 2016; 10: 43.
[http://dx.doi.org/10.3389/fnsys .2016.00043] [PMID: 27242454]
[7]
Brandel MG, Hirshman BR, McCutcheon BA, et al. The association between psychiatric comorbidities and outcomes for inpatients with traumatic brain injury. J Neurotrauma 2017; 34(5): 1005-16.
[http://dx.doi.org/10.1089/neu.2016.4504] [PMID: 27573722]
[8]
Peeters W, van den Brande R, Polinder S, et al. Epidemiology of traumatic brain injury in Europe. Acta Neurochir (Wien) 2015; 157(10): 1683-96.
[http://dx.doi.org/10.1007/s00701-015-2512-7] [PMID: 26269030]
[9]
Neumann K, et al. Targeting Translocator Protein (TSPO) with GE-180: Imaging brain inflammation and reactive gliosis. J Nucl Med 2016; 57(Suppl. 2): 1032-2.
[10]
Gerbatin RDR, Cassol G, Dobrachinski F, et al. Guanosine protects against traumatic brain injury-induced functional impairments and neuronal loss by modulating excitotoxicity, mitochondrial dysfunction, and inflammation. Mol Neurobiol 2017; 54(10): 7585-96.
[http://dx.doi.org/10.1007/s12035-016-0238-z] [PMID: 27830534]
[11]
Failla MD, Kumar RG, Peitzman AB, Conley YP, Ferrell RE, Wagner AK. Variation in the BDNF gene interacts with age to predict mortality in a prospective, longitudinal cohort with severe TBI. Neurorehabil Neural Repair 2015; 29(3): 234-46.
[http://dx.doi.org/10.1177/1545968314542617] [PMID: 25063686]
[12]
Di Paola M, Phillips O, Costa A, et al. Selective cognitive dysfunction is related to a specific pattern of cerebral damage in persons with severe traumatic brain injury. J Head Trauma Rehabil 2015; 30(6): 402-10.
[http://dx.doi.org/10.1097/HTR.0000000000000063] [PMID: 24901328]
[13]
Barnes DE, et al. Traumatic Brain Injury (TBI) severity and age of dementia diagnosis among veterans. Alzheimers Dement 2017; 13(7): 853-4.
[http://dx.doi.org/10.1016/j.jalz.2017.06.1205]
[14]
Gardner RC, et al. The national alzheimer’s coordinating center uniform data set Traumatic Brain Injury (TBI) exposure screen misses more than half of TBI exposures identified using a comprehensive TBI interview. Alzheimers Dement 2018; 14(7): 1337.
[http://dx.doi.org/10.1016/j.jalz.2018.06.1924]
[15]
Hayes JP, Logue MW, Sadeh N, et al. Mild traumatic brain injury is associated with reduced cortical thickness in those at risk for Alzheimer’s disease. Brain 2017; 140(3): 813-25.
[http://dx.doi.org/10.1093/brain/aww344] [PMID: 28077398]
[16]
Lou D, Du Y, Huang D, et al. Traumatic Brain Injury Alters the Metabolism and Facilitates Alzheimer’s Disease in a Murine Model. Mol Neurobiol 2018; 55(6): 4928-39.
[http://dx.doi.org/10.1007/s12035-017-0687-z] [PMID: 28776265]
[17]
Faden AI, Loane DJ. Chronic neurodegeneration after traumatic brain injury: Alzheimer disease, chronic traumatic encephalopathy, or persistent neuroinflammation? Neurotherapeutics 2015; 12(1): 143-50.
[http://dx.doi.org/10.1007/s13311-014-0319-5] [PMID: 25421001]
[18]
Hay J, Johnson VE, Smith DH, Stewart W. Chronic traumatic encephalopathy: the neuropathological legacy of traumatic brain injury. Annu Rev Pathol 2016; 11: 21-45.
[http://dx.doi.org/10.1146/annurev-pathol-012615-044116] [PMID: 26772317]
[19]
Abdul-Muneer PM, Chandra N, Haorah J. Interactions of oxidative stress and neurovascular inflammation in the pathogenesis of traumatic brain injury. Mol Neurobiol 2015; 51(3): 966-79.
[http://dx.doi.org/10.1007/s12035-014-8752-3] [PMID: 24865512]
[20]
Fu C, Wang Q, Zhai X, Gao J. Sinomenine reduces neuronal cell apoptosis in mice after traumatic brain injury via its effect on mitochondrial pathway. Drug Des Devel Ther 2018; 12: 77-84.
[http://dx.doi.org/10.2147/DDDT.S154391] [PMID: 29379271]
[21]
Samarghandian S, Ohata H, Yamauchi N, Shibasaki T. Corticotropin-releasing factor as well as opioid and dopamine are involved in tail-pinch-induced food intake of rats. Neuroscience 2003; 116(2): 519-24.
[22]
Shehadeh M, Ben-Shabat M, Livshits J, Palzur E. Involvement of epigenetic regulation in cerebral cell death following traumatic brain injury in a rat model. Harefuah 2017; 156(5): 280-4.
[PMID: 28551908]
[23]
Dobrachinski F, da Rosa Gerbatin R, Sartori G, et al. Regulation of mitochondrial function and glutamatergic system are the target of guanosine effect in traumatic brain injury. J Neurotrauma 2017; 34(7): 1318-28.
[http://dx.doi.org/10.1089/neu.2016.4563] [PMID: 27931151]
[24]
Mehrpour O, Karrari P, Abdollahi M. Chronic lead poisoning in Iran; a silent diseaseDaru. 2012; 20(1): 8.
[25]
Scheff SW, Ansari MA. Natural compounds as a therapeutic intervention following traumatic brain injury: the role of phytochemicals. J Neurotrauma 2017; 34(8): 1491-510.
[http://dx.doi.org/10.1089/neu.2016.4718] [PMID: 27846772]
[26]
Lucke-Wold BP, Logsdon AF, Nguyen L, et al. Supplements, nutrition, and alternative therapies for the treatment of traumatic brain injury. Nutr Neurosci 2018; 21(2): 79-91.
[http://dx.doi.org/10.1080/1028415X.2016.1236174] [PMID: 27705610]
[27]
Samarghandian S, Azimi-Nezhad M, Borji A, Samini M, Farkhondeh T. Protective effects of carnosol against oxidative stress induced brain damage by chronic stress in rats. BMC Complement Altern Med 2017; 17(1): 249.
[28]
Samarghandian S, Azimi-Nezhad M, Farkhondeh T. Preventive effect of carvacrol against oxidative damage in aged rat liver. Int J Vitam Nutr Res 2017; 87(1-2): 59-65.
[29]
Motterlini R, Foresti R, Bassi R, Green CJ. Curcumin, an antioxidant and anti-inflammatory agent, induces heme oxygenase-1 and protects endothelial cells against oxidative stress. Free Radic Biol Med 2000; 28(8): 1303-12.
[http://dx.doi.org/10.1016/S0891-5849(00)00294-X] [PMID: 10889462]
[30]
Sanmukhani J, Satodia V, Trivedi J, et al. Efficacy and safety of curcumin in major depressive disorder: a randomized controlled trial. Phytother Res 2014; 28(4): 579-85.
[http://dx.doi.org/10.1002/ptr.5025] [PMID: 23832433]
[31]
Chandran B, Goel A. A randomized, pilot study to assess the efficacy and safety of curcumin in patients with active rheumatoid arthritis. Phytother Res 2012; 26(11): 1719-25.
[http://dx.doi.org/10.1002/ptr.4639] [PMID: 22407780]
[32]
Begum AN, Jones MR, Lim GP, et al. Curcumin structure-function, bioavailability, and efficacy in models of neuroinflammation and Alzheimer’s disease. J Pharmacol Exp Ther 2008; 326(1): 196-208.
[http://dx.doi.org/10.1124/jpet.108.137455] [PMID: 18417733]
[33]
Sundaram JR, Poore CP, Sulaimee NHB, et al. Curcumin ameliorates neuroinflammation, neurodegeneration, and memory deficits in p25 transgenic mouse model that bears hallmarks of Alzheimer’s disease. J Alzheimers Dis 2017; 60(4): 1429-42.
[http://dx.doi.org/10.3233/JAD-170093] [PMID: 29036814]
[34]
van der Merwe C, van Dyk HC, Engelbrecht L, et al. Curcumin rescues a PINK1 knock down SH-SY5Y cellular model of Parkinson’s disease from mitochondrial dysfunction and cell death. Mol Neurobiol 2017; 54(4): 2752-62.
[http://dx.doi.org/10.1007/s12035-016-9843-0] [PMID: 27003823]
[35]
Liu Z, Ran Y, Huang S, et al. Curcumin protects against ischemic stroke by Titrating microglia/macrophage polarization. Front Aging Neurosci 2017; 9: 233.
[http://dx.doi.org/10.3389/fnagi.2017.00233] [PMID: 28785217]
[36]
Dai W, Wang H, Fang J, et al. Curcumin provides neuroprotection in model of traumatic brain injury via the Nrf2-ARE signaling pathway. Brain Res Bull 2018; 140: 65-71.
[http://dx.doi.org/10.1016/j.brainresbull.2018.03.020] [PMID: 29626606]
[37]
Hinzman JM, Wilson JA, Mazzeo AT, Bullock MR, Hartings JA. Excitotoxicity and metabolic crisis are associated with spreading depolarizations in severe traumatic brain injury patients. J Neurotrauma 2016; 33(19): 1775-83.
[http://dx.doi.org/10.1089/neu.2015.4226] [PMID: 26586606]
[38]
Lozano D, Gonzales-Portillo GS, Acosta S, et al. Neuroinflammatory responses to traumatic brain injury: etiology, clinical consequences, and therapeutic opportunities. Neuropsychiatr Dis Treat 2015; 11: 97-106.
[PMID: 25657582]
[39]
Hubbard WB, Harwood CL, Geisler JG, Vekaria HJ, Sullivan PG. Mitochondrial uncoupling prodrug improves tissue sparing, cognitive outcome, and mitochondrial bioenergetics after traumatic brain injury in male mice. J Neurosci Res 2018; 96(10): 1677-88.
[http://dx.doi.org/10.1002/jnr.24271] [PMID: 30063076]
[40]
Magi S, et al. Intracellular calcium dysregulation: Implications for Alzheimer’s disease. BioMed Res Int 2016.
[41]
Wang C, Liu F, Patterson TA, Paule MG, Slikker W Jr. Relationship between ketamine-induced developmental neurotoxicity and NMDA receptor-mediated calcium influx in neural stem cell-derived neurons. Neurotoxicology 2017; 60: 254-9.
[http://dx.doi.org/10.1016/j.neuro.2016.04.015] [PMID: 27132109]
[42]
Song JH, Shin MS, Hwang GS, Oh ST, Hwang JJ, Kang KS. Chebulinic acid attenuates glutamate-induced HT22 cell death by inhibiting oxidative stress, calcium influx and MAPKs phosphorylation. Bioorg Med Chem Lett 2018; 28(3): 249-53.
[http://dx.doi.org/10.1016/j.bmcl.2017.12.062] [PMID: 29317168]
[43]
Guerriero RM, Giza CC, Rotenberg A. Glutamate and GABA imbalance following traumatic brain injury. Curr Neurol Neurosci Rep 2015; 15(5): 27.
[http://dx.doi.org/10.1007/s11910-015-0545-1] [PMID: 25796572]
[44]
Jakaria M, Park SY, Haque ME, et al. Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors. Front Mol Neurosci 2018; 11: 307.
[http://dx.doi.org/10.3389/fnmol.2018.00307] [PMID: 30210294]
[45]
Nagata K, Kumasaka K, Browne KD, et al. Unfractionated heparin after TBI reduces in vivo cerebrovascular inflammation, brain edema and accelerates cognitive recovery. J Trauma Acute Care Surg 2016; 81(6): 1088-94.
[http://dx.doi.org/10.1097/TA.0000000000001215] [PMID: 27533909]
[46]
Russo MV, McGavern DB. Inflammatory neuroprotection following traumatic brain injury. Science 2016; 353(6301): 783-5.
[http://dx.doi.org/10.1126/science.aaf6260] [PMID: 27540166]
[47]
Loane DJ, Kumar A. Microglia in the TBI brain: The good, the bad, and the dysregulated. Exp Neurol 2016; 275(Pt 3): 316-27.
[http://dx.doi.org/10.1016/j.expneurol.2015.08.018] [PMID: 26342753]
[48]
Chen Z, Trapp BD. Microglia and neuroprotection. J Neurochem 2016; 136(Suppl. 1): 10-7.
[http://dx.doi.org/10.1111/jnc.13062] [PMID: 25693054]
[49]
Burda JE, Bernstein AM, Sofroniew MV. Astrocyte roles in traumatic brain injury. Exp Neurol 2016; 275(Pt 3): 305-15.
[http://dx.doi.org/10.1016/j.expneurol.2015.03.020] [PMID: 25828533]
[50]
Lin CJ, Chen TH, Yang LY, Shih CM. Resveratrol protects astrocytes against traumatic brain injury through inhibiting apoptotic and autophagic cell death. Cell Death Dis 2014; 5(3)e1147
[http://dx.doi.org/10.1038/cddis.2014.123]] [PMID: 24675465]
[51]
Bellaver B, Dos Santos JP, Leffa DT, et al. Systemic inflammation as a driver of brain injury: the astrocyte as an emerging player. Mol Neurobiol 2018; 55(3): 2685-95.
[http://dx.doi.org/10.1007/s12035-017-0526-2] [PMID: 28421541]
[52]
Setiadi A, May CN, Yao ST. Ablation of astrocytes in the paraventricular nucleus disrupts the blood-brain barrier and increases blood pressure in rats. The FASEB Journal 31(1) 1010.5. 2017
[53]
Begum G, Song S, Wang S, et al. Selective knockout of astrocytic Na+/H+ exchanger isoform 1 reduces astrogliosis, BBB damage, infarction, and improves neurological function after ischemic stroke. Glia 2018; 66(1): 126-44.
[http://dx.doi.org/10.1002/glia.23232] [PMID: 28925083]
[54]
Quintana FJ. Astrocytes to the rescue! Glia limitans astrocytic endfeet control CNS inflammation. J Clin Invest 2017; 127(8): 2897-9.
[http://dx.doi.org/10.1172/JCI95769] [PMID: 28737511]
[55]
Jing B, Zhang C, Liu X, et al. Glycosylation of dentin matrix protein 1 is a novel key element for astrocyte maturation and BBB integrity. Protein Cell 2018; 9(3): 298-309.
[http://dx.doi.org/10.1007/s13238-017-0449-8] [PMID: 28822114]
[56]
Perez EJ, Tapanes SA, Loris ZB, et al. Enhanced astrocytic d-serine underlies synaptic damage after traumatic brain injury. J Clin Invest 2017; 127(8): 3114-25.
[http://dx.doi.org/10.1172/JCI92300] [PMID: 28714867]
[57]
Bylicky MA, Mueller GP, Day RM. Mechanisms of Endogenous Neuroprotective Effects of Astrocytes in Brain Injury. Oxid Med Cell Longev 2018.
[http://dx.doi.org/10.1155/2018/6501031]
[58]
Wang Z-R, Li YX, Lei HY, Yang DQ, Wang LQ, Luo MY. Regulating effect of activated NF-κB on edema induced by traumatic brain injury of rats. Asian Pac J Trop Med 2016; 9(3): 274-7.
[http://dx.doi.org/10.1016/j.apjtm.2016.01.027] [PMID: 26972401]
[59]
Bergold PJ. Treatment of traumatic brain injury with anti-inflammatory drugs. Exp Neurol 2016; 275(Pt 3): 367-80.
[http://dx.doi.org/10.1016/j.expneurol.2015.05.024] [PMID: 26112314]
[60]
Dugue R, et al. Roles of Pro-and Anti-inflammatory Cytokines in Traumatic Brain Injury and Acute Ischemic Stroke. In:Mechanisms of Neuroinflammation. InTech 2017.
[http://dx.doi.org/10.5772/intechopen.70099]
[61]
Hill RL, Kulbe JR, Singh IN, Wang JA, Hall ED. Synaptic mitochondria are more susceptible to traumatic brain injury-induced oxidative damage and respiratory dysfunction than non-synaptic mitochondria. Neuroscience 2018; 386: 265-83.
[http://dx.doi.org/10.1016/j.neuroscience.2018.06.028] [PMID: 29960045]
[62]
Hirase H, Koizumi S. Astrocytes as therapeutic targets in brain diseases In: . Elsevier 2018.
[http://dx.doi.org/10.1016/j.neures.2017.12.003]
[63]
Furman JL, Sompol P, Kraner SD, et al. Blockade of astrocytic calcineurin/NFAT signaling helps to normalize hippocampal synaptic function and plasticity in a rat model of traumatic brain injury. J Neurosci 2016; 36(5): 1502-15.
[http://dx.doi.org/10.1523/JNEUROSCI.1930-15.2016] [PMID: 26843634]
[64]
Plummer S, Van den Heuvel C, Thornton E, Corrigan F, Cappai R. The neuroprotective properties of the amyloid precursor protein following traumatic brain injury. Aging Dis 2016; 7(2): 163-79.
[http://dx.doi.org/10.14336/AD.2015.0907] [PMID: 27114849]
[65]
Acosta SA, Tajiri N, Sanberg PR, Kaneko Y, Borlongan CV. Increased amyloid precursor protein and tau expression manifests as key secondary cell death in chronic traumatic brain injury. J Cell Physiol 2017; 232(3): 665-77.
[http://dx.doi.org/10.1002/jcp.25629] [PMID: 27699791]
[66]
Makinde HM, Just TB, Cuda CM, Perlman H, Schwulst SJ. The Role of Microglia in the Etiology and Evolution of Chronic Traumatic Encephalopathy. Shock 2017; 48(3): 276-83.
[http://dx.doi.org/10.1097/SHK.0000000000000859] [PMID: 28234788]
[67]
Washington PM, Villapol S, Burns MP. Polypathology and dementia after brain trauma: Does brain injury trigger distinct neurodegenerative diseases, or should they be classified together as traumatic encephalopathy? Exp Neurol 2016; 275(Pt 3): 381-8.
[http://dx.doi.org/10.1016/j.expneurol.2015.06.015] [PMID: 26091850]
[68]
Veenith TV, Carter EL, Geeraerts T, et al. Pathophysiologic mechanisms of cerebral ischemia and diffusion hypoxia in traumatic brain injury. JAMA Neurol 2016; 73(5): 542-50.
[http://dx.doi.org/10.1001/jamaneurol.2016.0091] [PMID: 27019039]
[69]
McKee AC, Daneshvar DH. The neuropathology of traumatic brain injury. In: Handbook of clinical neurology. Elsevier 2015; pp. 45-66.
[70]
Lucke-Wold BP, Logsdon AF, Smith KE, et al. Bryostatin-1 restores blood brain barrier integrity following blast-induced traumatic brain injury. Mol Neurobiol 2015; 52(3): 1119-34.
[http://dx.doi.org/10.1007/s12035-014-8902-7] [PMID: 25301233]
[71]
Rubenstein R, Chang B, Grinkina N, et al. Tau phosphorylation induced by severe closed head traumatic brain injury is linked to the cellular prion protein. Acta Neuropathol Commun 2017; 5(1): 30.
[http://dx.doi.org/10.1186/s40478-017-0435-7] [PMID: 28420443]
[72]
Grant DA, Serpa R, Moattari CR, et al. Repeat Mild Traumatic Brain Injury in Adolescent Rats Increases Subsequent β-Amyloid Pathogenesis. J Neurotrauma 2018; 35(1): 94-104.
[http://dx.doi.org/10.1089/neu.2017.5042] [PMID: 28728464]
[73]
Hay JR, Johnson VE, Young AM, Smith DH, Stewart W. Blood-brain barrier disruption is an early event that may persist for many years after traumatic brain injury in humans. J Neuropathol Exp Neurol 2015; 74(12): 1147-57.
[PMID: 26574669]
[74]
Bird SM, Sohrabi HR, Sutton TA, et al. Cerebral amyloid-β accumulation and deposition following traumatic brain injury--A narrative review and meta-analysis of animal studies. Neurosci Biobehav Rev 2016; 64: 215-28.
[http://dx.doi.org/10.1016/j.neubiorev.2016.01.004] [PMID: 26899257]
[75]
Tarasoff-Conway JM, Carare RO, Osorio RS, et al. Clearance systems in the brain-implications for Alzheimer disease. Nat Rev Neurol 2015; 11(8): 457-70.
[http://dx.doi.org/10.1038/nrneurol.2015.119] [PMID: 26195256]
[76]
Nelson A, Sagare A, Zlokovic B. Blood–Brain Barrier Transport of Alzheimer’s Amyloid β-Peptide. In: Developing Therapeutics for Alzheimer’s Disease. Elsevier 2016; pp. 251-70.
[http://dx.doi.org/10.1016/B978-0-12-802173-6.00009-5]
[77]
Ramos-Cejudo J, Wisniewski T, Marmar C, et al. Traumatic Brain Injury and Alzheimer’s Disease: The Cerebrovascular Link. EBioMedicine 2018; 28: 21-30.
[http://dx.doi.org/10.1016/j.ebiom.2018.01.021] [PMID: 29396300]
[78]
Hill C. Experimental Modelling and Molecular Mechanisms of Wallerian Degeneration in Traumatic Axonal Injury In: . University of Cambridge 2018.
[79]
Maxwell WL, Bartlett E, Morgan H. Wallerian degeneration in the optic nerve stretch-injury model of traumatic brain injury: a stereological analysis. J Neurotrauma 2015; 32(11): 780-90.
[http://dx.doi.org/10.1089/neu.2014.3369] [PMID: 25333317]
[80]
Lauterbach MD, Notarangelo PL, Nichols SJ, Lane KS, Koliatsos VE. Diagnostic and treatment challenges in traumatic brain injury patients with severe neuropsychiatric symptoms: insights into psychiatric practice. Neuropsychiatr Dis Treat 2015; 11: 1601-7.
[http://dx.doi.org/10.2147/NDT.S80457] [PMID: 26170672]
[81]
Stewart W, McNamara PH, Lawlor B, Hutchinson S, Farrell M. Chronic traumatic encephalopathy: a potential late and under recognized consequence of rugby union? QJM 2016; 109(1): 11-5.
[http://dx.doi.org/10.1093/qjmed/hcv070] [PMID: 25998165]
[82]
Katsumoto A, Miranda AS, Butovsky O, Teixeira AL, Ransohoff RM, Lamb BT. Laquinimod attenuates inflammation by modulating macrophage functions in traumatic brain injury mouse model. J Neuroinflammation 2018; 15(1): 26.
[http://dx.doi.org/10.1186/s12974-018-1075-y] [PMID: 29382353]
[83]
Wilde EA, Taylor BA, Jorge RE. Brain Morphometric Techniques Applied to the Study of Traumatic Brain Injury, in Brain Morphometry. In: Springer . 469-530. 2018; pp.
[84]
Ruet A, Joyeux F, Segobin S, et al. Severe Traumatic Brain Injury Patients without Focal Lesion but with Behavioral Disorders: Shrinkage of Gray Matter Nuclei and Thalamus Revealed in a Pilot Voxel-Based MRI Study. J Neurotrauma 2018; 35(13): 1552-6.
[http://dx.doi.org/10.1089/neu.2017.5242] [PMID: 29648977]
[85]
Cummins T. Tau and beta-amyloid deposition, structural integrity, and cognitive function following traumatic brain injury in Australian war veterans 2018.
[86]
Edwards GA, et al. THE EFFECT OF REPETITIVE MILD TRAUMATIC BRAIN INJURY ON TAU PATHOLOGY. Alzheimers Dement 2018; 14(7): 370.
[http://dx.doi.org/10.1016/j.jalz.2018.06.243]
[87]
Chen ST, et al. FDDNP-PET Tau Brain Protein Binding Patterns in Military Personnel with Suspected Chronic Traumatic Encephalopathy. Journal of Alzheimer's Disease 1-10.2018; Preprint
[88]
Becker RE, Kapogiannis D, Greig NH. Does traumatic brain injury hold the key to the Alzheimer’s disease puzzle? Alzheimers Dement 2018; 14(4): 431-43.
[http://dx.doi.org/10.1016/j.jalz.2017.11.007] [PMID: 29245000]
[89]
Guedes JR, Lao T, Cardoso AL, El Khoury J. Roles of Microglial and Monocyte Chemokines and Their Receptors in Regulating Alzheimer’s Disease-Associated Amyloid-β and Tau Pathologies. Front Neurol 2018; 9: 549.
[http://dx.doi.org/10.3389/fneur.2018.00549] [PMID: 30158892]
[90]
He Z, Guo JL, McBride JD, et al. Amyloid-β plaques enhance Alzheimer’s brain tau-seeded pathologies by facilitating neuritic plaque tau aggregation. Nat Med 2018; 24(1): 29-38.
[http://dx.doi.org/10.1038/nm.4443] [PMID: 29200205]
[91]
Peng W, Ren M. Correlation of serum Tau and 8-iso-PGF2α levels with nerve injury and oxidative stress in patients with traumatic brain injury. Hainan Yixueyuan Xuebao 2017; 23(16): 126-9.
[92]
Kulbe JR, Hall ED. Chronic traumatic encephalopathy-integration of canonical traumatic brain injury secondary injury mechanisms with tau pathology. Prog Neurobiol 2017; 158: 15-44.
[http://dx.doi.org/10.1016/j.pneurobio.2017.08.003] [PMID: 28851546]
[93]
Hiebert JB, Shen Q, Thimmesch AR, Pierce JD. Traumatic brain injury and mitochondrial dysfunction. Am J Med Sci 2015; 350(2): 132-8.
[http://dx.doi.org/10.1097/MAJ.0000000000000506] [PMID: 26083647]
[94]
Ding K, Wang H, Xu J, et al. Melatonin stimulates antioxidant enzymes and reduces oxidative stress in experimental traumatic brain injury: the Nrf2-ARE signaling pathway as a potential mechanism. Free Radic Biol Med 2014; 73: 1-11.
[http://dx.doi.org/10.1016/j.freeradbiomed.2014.04.031] [PMID: 24810171]
[95]
Chandran R, Kim T, Mehta SL, et al. 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 2018; 38(10): 1818-27.
[http://dx.doi.org/10.1177/0271678X17738701] [PMID: 29083257]
[96]
Ma MW, Wang J, Dhandapani KM, Brann DW. Deletion of NADPH oxidase 4 reduces severity of traumatic brain injury. Free Radic Biol Med 2018; 117: 66-75.
[http://dx.doi.org/10.1016/j.freeradbiomed.2018.01.031] [PMID: 29391196]
[97]
Zhang H-B, Cheng SX, Tu Y, Zhang S, Hou SK, Yang Z. Protective effect of mild-induced hypothermia against moderate traumatic brain injury in rats involved in necroptotic and apoptotic pathways. Brain Inj 2017; 31(3): 406-15.
[http://dx.doi.org/10.1080/02699052.2016.1225984] [PMID: 28140659]
[98]
McGinn MJ, Povlishock JT. Pathophysiology of traumatic brain injury. Neurosurg Clin N Am 2016; 27(4): 397-407.
[http://dx.doi.org/10.1016/j.nec.2016.06.002] [PMID: 27637392]
[99]
Lorente L, Martín MM, Argueso M, et al. Serum caspase-3 levels and mortality are associated in patients with severe traumatic brain injury. BMC Neurol 2015; 15(1): 228.
[http://dx.doi.org/10.1186/s12883-015-0485-z] [PMID: 26545730]
[100]
Flygt J, et al. Neutralization of Interleukin-1β following Diffuse Traumatic Brain Injury in the Mouse attenuates the loss of Mature Oligodendrocytes. J Neurotrauma 2018.
[http://dx.doi.org/10.1089/neu.2018.5660]
[101]
Takase H, Washida K, Hayakawa K, et al. Oligodendrogenesis after traumatic brain injury. Behav Brain Res 2018; 340: 205-11.
[http://dx.doi.org/10.1016/j.bbr.2016.10.042] [PMID: 27829126]
[102]
Igarashi Y, et al. Relation between extracellular Chemistry and Patient Outcome for Severe Traumatic Brain Injury within the First 24 hours: A Microdialysis Study. Indian Journal of Neurotrauma 14(02/03): 122-8. 2017
[http://dx.doi.org/10.1055/s-0038-1649283]
[103]
Kozlov AV, Bahrami S, Redl H, Szabo C. Alterations in nitric oxide homeostasis during traumatic brain injury. Biochim Biophys Acta Mol Basis Dis 2017; 1863(10 Pt B): 2627-32.
[http://dx.doi.org/10.1016/j.bbadis.2016.12.020] [PMID: 28064018]
[104]
Bramlett HM, Dietrich WD. Long-term consequences of traumatic brain injury: current status of potential mechanisms of injury and neurological outcomes. J Neurotrauma 2015; 32(23): 1834-48.
[http://dx.doi.org/10.1089/neu.2014.3352] [PMID: 25158206]
[105]
Wang G, Shi Y, Jiang X, et al. HDAC inhibition prevents white matter injury by modulating microglia/macrophage polarization through the GSK3β/PTEN/Akt axis. Proc Natl Acad Sci USA 2015; 112(9): 2853-8.
[http://dx.doi.org/10.1073/pnas.1501441112] [PMID: 25691750]
[106]
Gao T, Chen Z, Chen H, et al. Inhibition of HMGB1 mediates neuroprotection of traumatic brain injury by modulating the microglia/macrophage polarization. Biochem Biophys Res Commun 2018; 497(1): 430-6.
[http://dx.doi.org/10.1016/j.bbrc.2018.02.102] [PMID: 29448108]
[107]
Li C, Götz J. Tau-based therapies in neurodegeneration: opportunities and challenges. Nat Rev Drug Discov 2017; 16(12): 863-83.
[http://dx.doi.org/10.1038/nrd.2017.155] [PMID: 28983098]
[108]
Fidler IJ. Methods for treatment and prevention of tauopathies by inhibiting endothelin receptors.In: Google Patents . 2015.
[109]
Drake DF, Hudak AM, Robbins W. Integrative medicine in traumatic brain injury. Phys Med Rehabil Clin N Am 2017; 28(2): 363-78.
[http://dx.doi.org/10.1016/j.pmr.2016.12.011] [PMID: 28390519]
[110]
Sadighara P, Godarzi S, Bahmani M, Asadi-Samani M. Antioxidant activity and properties of walnut brown seed coat extract. J Glob Pharma Technol 2016; 11(8): 26-30.
[111]
Wu A, Molteni R, Ying Z, Gomez-Pinilla F. A saturated-fat diet aggravates the outcome of traumatic brain injury on hippocampal plasticity and cognitive function by reducing brain-derived neurotrophic factor. Neuroscience 2003; 119(2): 365-75.
[http://dx.doi.org/10.1016/S0306-4522(03)00154-4] [PMID: 12770552]
[112]
Wu A, Ying Z, Gomez-Pinilla F. Dietary curcumin counteracts the outcome of traumatic brain injury on oxidative stress, synaptic plasticity, and cognition. Exp Neurol 2006; 197(2): 309-17.
[http://dx.doi.org/10.1016/j.expneurol.2005.09.004] [PMID: 16364299]
[113]
Bronner M, Hertz R, Bar-Tana J. Kinase-independent transcriptional co-activation of peroxisome proliferator-activated receptor α by AMP-activated protein kinase. Biochem J 2004; 384(Pt 2): 295-305.
[http://dx.doi.org/10.1042/BJ20040955] [PMID: 15312046]
[114]
Jones RG, Plas DR, Kubek S, et al. AMP-activated protein kinase induces a p53-dependent metabolic checkpoint. Mol Cell 2005; 18(3): 283-93.
[http://dx.doi.org/10.1016/j.molcel.2005.03.027] [PMID: 15866171]
[115]
Dagon Y, Avraham Y, Magen I, Gertler A, Ben-Hur T, Berry EM. Nutritional status, cognition, and survival: a new role for leptin and AMP kinase. J Biol Chem 2005; 280(51): 42142-8.
[http://dx.doi.org/10.1074/jbc.M507607200] [PMID: 16203737]
[116]
Sharma S, Zhuang Y, Ying Z, Wu A, Gomez-Pinilla F. Dietary curcumin supplementation counteracts reduction in levels of molecules involved in energy homeostasis after brain trauma. Neuroscience 2009; 161(4): 1037-44.
[http://dx.doi.org/10.1016/j.neuroscience.2009.04.042] [PMID: 19393301]
[117]
Laird MD, Sukumari-Ramesh S, Swift AE, Meiler SE, Vender JR, Dhandapani KM. Curcumin attenuates cerebral edema following traumatic brain injury in mice: a possible role for aquaporin-4? J Neurochem 2010; 113(3): 637-48.
[http://dx.doi.org/10.1111/j.1471-4159.2010.06630.x] [PMID: 20132469]
[118]
Samini F, Samarghandian S, Borji A, Mohammadi G. bakaian M. Curcumin pretreatment attenuates brain lesion size and improves neurological function following traumatic brain injury in the rat. Pharmacol Biochem Behav 2013; 110: 238-44.
[http://dx.doi.org/10.1016/j.pbb.2013.07.019] [PMID: 23932920]
[119]
Zhu HT, Bian C, Yuan JC, et al. Curcumin attenuates acute inflammatory injury by inhibiting the TLR4/MyD88/NF-κB signaling pathway in experimental traumatic brain injury. J Neuroinflammation 2014; 11(1): 59.
[http://dx.doi.org/10.1186/1742-2094-11-59] [PMID: 24669820]
[120]
Gao Y, Li J, Wu L, et al. Tetrahydrocurcumin provides neuroprotection in rats after traumatic brain injury: autophagy and the PI3K/AKT pathways as a potential mechanism. J Surg Res 2016; 206(1): 67-76.
[http://dx.doi.org/10.1016/j.jss.2016.07.014] [PMID: 27916377]
[121]
Shintani T, Klionsky DJ. Autophagy in health and disease: a double-edged sword. Science 2004; 306(5698): 990-5.
[http://dx.doi.org/10.1126/science.1099993] [PMID: 15528435]
[122]
Dong W, Yang B, Wang L, et al. Curcumin plays neuroprotective roles against traumatic brain injury partly via Nrf2 signaling. Toxicol Appl Pharmacol 2018; 346: 28-36.
[http://dx.doi.org/10.1016/j.taap.2018.03.020] [PMID: 29571711]
[123]
Wu A, Ying Z, Schubert D, Gomez-Pinilla F. Brain and spinal cord interaction: a dietary curcumin derivative counteracts locomotor and cognitive deficits after brain trauma. Neurorehabil Neural Repair 2011; 25(4): 332-42.
[http://dx.doi.org/10.1177/1545968310397706] [PMID: 21343524]

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