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Annual Review of Pharmacology and Toxicology

Volume 64, 2024

Antiepileptic Drugs as Potential Dementia Prophylactics Following Traumatic Brain Injury

Abstract

Seizures and other forms of neurovolatility are emerging as druggable prodromal mechanisms that link traumatic brain injury (TBI) to the progression of later dementias. TBI neurotrauma has both acute and long-term impacts on health, and TBI is a leading risk factor for dementias, including chronic traumatic encephalopathy and Alzheimer's disease. Treatment of TBI already considers acute management of posttraumatic seizures and epilepsy, and impressive efforts have optimized regimens of antiepileptic drugs (AEDs) toward that goal. Here we consider that expanding these management strategies could determine which AED regimens best prevent dementia progression in TBI patients. Challenges with this prophylactic strategy include the potential consequences of prolonged AED treatment and that a large subset of patients are refractory to available AEDs. Addressing these challenges is warranted because the management of seizure activity following TBI offers a rare opportunity to prevent the onset or progression of devastating dementias.

Keyword(s): concussion, epilepsy, levetiracetam, loss of neuronal excitability homeostasis, network hyperexcitability, retigabine
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/content/journals/10.1146/annurev-pharmtox-051921-013930
2024-01-23
2024-04-29
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Literature Cited

  1. 1.
    Nguyen R, Fiest KM, McChesney J, Kwon C-S, Jette N et al. 2016. The international incidence of traumatic brain injury: a systematic review and meta-analysis. Can. J. Neurol. Sci. 43:774–85
     [Google Scholar]
  2. 2.
    Rimel RW, Giordani B, Barth JT, Boll TJ, Jane JA. 1981. Disability caused by minor head injury. Neurosurgery 9:221–28
     [Google Scholar]
  3. 3.
    Popescu C, Anghelescu A, Daia C, Onose G. 2015. Actual data on epidemiological evolution and prevention endeavours regarding traumatic brain injury. J. Med. Life 8:272–77
     [Google Scholar]
  4. 4.
    Li Y, Li X, Zhang S, Zhao J, Zhu X, Tian G. 2017. Head injury as a risk factor for dementia and Alzheimer's disease: a systematic review and meta-analysis of 32 observational studies. PLOS ONE 12:e0169650
     [Google Scholar]
  5. 5.
    McKee AC, Cantu RC, Nowinski CJ, Hedley-Whyte E, Gavett BE et al. 2009. Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury. J. Neuropathol. Exp. Neurol. 68:709–35
     [Google Scholar]
  6. 6.
    Rasmusson DX, Brandt J, Martin DB, Folstein MF. 1995. Head injury as a risk factor in Alzheimer's disease. Brain Inj. 9:213–19
     [Google Scholar]
  7. 7.
    Edwards GA III, Gamez N, Escobedo G, Calderon O, Moreno-Gonzalez I 2019. Modifiable risk factors for Alzheimer's disease. Front. Aging Neurosci. 11:146
     [Google Scholar]
  8. 8.
    McKee AC, Stein TD, Kiernan PT, Alvarez VE. 2015. The neuropathology of chronic traumatic encephalopathy. Brain Pathol. 25:350–64
     [Google Scholar]
  9. 9.
    McKee AC, Stern RA, Nowinski CJ, Stein TD, Alvarez VE et al. 2013. The spectrum of disease in chronic traumatic encephalopathy. Brain 136:43–64
     [Google Scholar]
  10. 10.
    Stein TD, Montenigro PH, Alvarez VE, Xia W, Crary JF et al. 2015. Beta-amyloid deposition in chronic traumatic encephalopathy. Acta Neuropathol. 130:21–34
     [Google Scholar]
  11. 11.
    Annegers JF, Hauser WA, Coan SP, Rocca WA. 1998. A population-based study of seizures after traumatic brain injuries. N. Engl. J. Med. 338:20–24
     [Google Scholar]
  12. 12.
    Asikainen I, Kaste M, Sarna S. 1999. Early and late posttraumatic seizures in traumatic brain injury rehabilitation patients: brain injury factors causing late seizures and influence of seizures on long-term outcome. Epilepsia 40:584–89
     [Google Scholar]
  13. 13.
    Majidi S, Makke Y, Ewida A, Sianati B, Qureshi AI, Koubeissi MZ. 2017. Prevalence and risk factors for early seizure in patients with traumatic brain injury: analysis from National Trauma Data Bank. Neurocrit. Care 27:90–95
     [Google Scholar]
  14. 14.
    Behnke JA, Ye C, Setty A, Moberg KH, Zheng JQ. 2021. Repetitive mild head trauma induces activity mediated lifelong brain deficits in a novel Drosophila model. Sci. Rep. 11:9738
     [Google Scholar]
  15. 15.
    Golub VM, Reddy DS. 2022. Post-traumatic epilepsy and comorbidities: advanced models, molecular mechanisms, biomarkers, and novel therapeutic interventions. Pharmacol. Rev. 74:387–438
     [Google Scholar]
  16. 16.
    Hunt RF, Scheff SW, Smith BN. 2009. Posttraumatic epilepsy after controlled cortical impact injury in mice. Exp. Neurol. 215:243–52
     [Google Scholar]
  17. 17.
    Bugay V, Bozdemir E, Vigil FA, Chun SH, Holstein DM et al. 2020. A mouse model of repetitive blast traumatic brain injury reveals post-trauma seizures and increased neuronal excitability. J. Neurotrauma 37:248–61
     [Google Scholar]
  18. 18.
    Alyenbaawi H, Kanyo R, Locskai LF, Kamali-Jamil R, DuVal MG et al. 2021. Seizures are a druggable mechanistic link between TBI and subsequent tauopathy. eLife 10:e58744Preclinical zebrafish model where the AED retigabine reduces dementia pathology after TBI.
     [Google Scholar]
  19. 19.
    Reith J, Jørgensen HS, Nakayama H, Raaschou HO, Olsen TS. 1997. Seizures in acute stroke: predictors and prognostic significance. The Copenhagen Stroke Study. Stroke 28:1585–89
     [Google Scholar]
  20. 20.
    Weston J, Greenhalgh J, Marson AG. 2015. Antiepileptic drugs as prophylaxis for post-craniotomy seizures. Cochrane Database Syst. Rev. 2018:CD007286
     [Google Scholar]
  21. 21.
    Lowenstein DH. 2009. Epilepsy after head injury: an overview. Epilepsia 50:Suppl. 24–9
     [Google Scholar]
  22. 22.
    Hauser WA, Beghi E. 2008. First seizure definitions and worldwide incidence and mortality. Epilepsia 49:Suppl. 18–12
     [Google Scholar]
  23. 23.
    Vespa PM, McArthur DL, Xu Y, Eliseo M, Etchepare M et al. 2010. Nonconvulsive seizures after traumatic brain injury are associated with hippocampal atrophy. Neurology 75:792–98
     [Google Scholar]
  24. 24.
    Tubi MA, Lutkenhoff E, Blanco MB, McArthur D, Villablanca P et al. 2019. Early seizures and temporal lobe trauma predict post-traumatic epilepsy: a longitudinal study. Neurobiol. Dis. 123:115–21
     [Google Scholar]
  25. 25.
    Caveness WF, Walker AE, Ascroft PB. 1962. Incidence of posttraumatic epilepsy in Korean veterans as compared with those from World War I and World War II. J. Neurosurg. 19:122–29
     [Google Scholar]
  26. 26.
    Salazar AM, Jabbari B, Vance SC, Grafman J, Amin D, Dillon JD. 1985. Epilepsy after penetrating head injury. I. Clinical correlates: a report of the Vietnam Head Injury Study. Neurology 35:1406–14
     [Google Scholar]
  27. 27.
    Gardner RC, Burke JF, Nettiksimmons J, Kaup A, Barnes DE, Yaffe K. 2014. Dementia risk after traumatic brain injury versus nonbrain trauma: the role of age and severity. JAMA Neurol. 71:1490–97
     [Google Scholar]
  28. 28.
    Kenney K, Iacono D, Edlow BL, Katz DI, Diaz-Arrastia R et al. 2018. Dementia after moderate-severe traumatic brain injury: coexistence of multiple proteinopathies. J. Neuropathol. Exp. Neurol. 77:50–63
     [Google Scholar]
  29. 29.
    Plassman BL, Havlik RJ, Steffens DC, Helms MJ, Newman TN et al. 2000. Documented head injury in early adulthood and risk of Alzheimer's disease and other dementias. Neurology 55:1158–66
     [Google Scholar]
  30. 30.
    Nordström A, Nordström P. 2018. Traumatic brain injury and the risk of dementia diagnosis: a nationwide cohort study. PLOS Med. 15:e1002496
     [Google Scholar]
  31. 31.
    Lee YK, Hou SW, Lee CC, Hsu CY, Huang YS, Su YC. 2013. Increased risk of dementia in patients with mild traumatic brain injury: a nationwide cohort study. PLOS ONE 8:e62422
     [Google Scholar]
  32. 32.
    Gavett BE, Stern RA, Cantu RC, Nowinski CJ, McKee AC. 2010. Mild traumatic brain injury: a risk factor for neurodegeneration. Alzheimers Res. Ther. 2:18
     [Google Scholar]
  33. 33.
    Vespa PM, Nuwer MR, Nenov V, Ronne-Engstrom E, Hovda DA et al. 1999. Increased incidence and impact of nonconvulsive and convulsive seizures after traumatic brain injury as detected by continuous electroencephalographic monitoring. J. Neurosurg. 91:750–60
     [Google Scholar]
  34. 34.
    Alroughani R, Javidan M, Qasem A, Alotaibi N. 2009. Non-convulsive status epilepticus: the rate of occurrence in a general hospital. Seizure 18:38–42
     [Google Scholar]
  35. 35.
    Campbell JN, Gandhi A, Singh B, Churn SB. 2014. Traumatic brain injury causes a tacrolimus-sensitive increase in non-convulsive seizures in a rat model of post-traumatic epilepsy. Int. J. Neurol. Brain Disord. 1:1–11
     [Google Scholar]
  36. 36.
    Andrade P, Banuelos-Cabrera I, Lapinlampi N, Paananen T, Ciszek R et al. 2019. Acute non-convulsive status epilepticus after experimental traumatic brain injury in rats. J. Neurotrauma 36:1890–907
     [Google Scholar]
  37. 37.
    Pooler AM, Phillips EC, Lau DH, Noble W, Hanger DP. 2013. Physiological release of endogenous tau is stimulated by neuronal activity. EMBO Rep 14:389–94
     [Google Scholar]
  38. 38.
    Yamada K, Holth JK, Liao F, Stewart FR, Mahan TE et al. 2014. Neuronal activity regulates extracellular tau in vivo. J. Exp. Med. 211:387–93
     [Google Scholar]
  39. 39.
    Wu JW, Hussaini SA, Bastille IM, Rodriguez GA, Mrejeru A et al. 2016. Neuronal activity enhances tau propagation and tau pathology in vivo. Nat. Neurosci. 19:1085–92
     [Google Scholar]
  40. 40.
    Ng SY, Lee AYW. 2019. Traumatic brain injuries: pathophysiology and potential therapeutic targets. Front. Cell Neurosci. 13:528
     [Google Scholar]
  41. 41.
    Tehse J, Taghibiglou C. 2019. The overlooked aspect of excitotoxicity: glutamate-independent excitotoxicity in traumatic brain injuries. Eur. J. Neurosci. 49:1157–70
     [Google Scholar]
  42. 42.
    Hauser WA, Morris ML, Heston LL, Anderson VE. 1986. Seizures and myoclonus in patients with Alzheimer's disease. Neurology 36:1226–30
     [Google Scholar]
  43. 43.
    Hesdorffer DC, Hauser WA, Annegers JF, Kokmen E, Rocca WA. 1996. Dementia and adult-onset unprovoked seizures. Neurology 46:727–30
     [Google Scholar]
  44. 44.
    Mendez M, Lim G. 2003. Seizures in elderly patients with dementia: epidemiology and management. Drugs Aging 20:791–803
     [Google Scholar]
  45. 45.
    Arnaldi D, Donniaquio A, Mattioli P, Massa F, Grazzini M et al. 2020. Epilepsy in neurodegenerative dementias: a clinical, epidemiological, and EEG study. J. Alzheimers Dis. 74:865–74
     [Google Scholar]
  46. 46.
    Cano A, Fonseca E, Ettcheto M, Sánchez-López E, de Rojas I et al. 2021. Epilepsy in neurodegenerative diseases: related drugs and molecular pathways. Pharmaceuticals 14:1057
     [Google Scholar]
  47. 47.
    Vossel KA, Beagle AJ, Rabinovici GD, Shu H, Lee SE et al. 2013. Seizures and epileptiform activity in the early stages of Alzheimer disease. JAMA Neurol 70:1158–66
     [Google Scholar]
  48. 48.
    Kim CK, Lee YR, Ong L, Gold M, Kalali A, Sarkar J. 2022. Alzheimer's disease: key insights from two decades of clinical trial failures. J. Alzheimers Dis. 87:83–100
     [Google Scholar]
  49. 49.
    Yiannopoulou KG, Anastasiou AI, Zachariou V, Pelidou SH. 2019. Reasons for failed trials of disease-modifying treatments for Alzheimer disease and their contribution in recent research. Biomedicines 7:97
     [Google Scholar]
  50. 50.
    Bernardi S, Scaldaferri N, Vanacore N, Trebbastoni A, Francia A et al. 2010. Seizures in Alzheimer's disease: a retrospective study of a cohort of outpatients. Epilept. Disord. 12:16–21
     [Google Scholar]
  51. 51.
    Amatniek JC, Hauser WA, DelCastillo-Castaneda C, Jacobs DM, Marder K et al. 2006. Incidence and predictors of seizures in patients with Alzheimer's disease. Epilepsia 47:867–72
     [Google Scholar]
  52. 52.
    Horváth A, Szűcs A, Hidasi Z, Csukly G, Barcs G, Kamondi A. 2018. Prevalence, semiology, and risk factors of epilepsy in Alzheimer's disease: an ambulatory EEG study. J. Alzheimers Dis. 63:1045–54
     [Google Scholar]
  53. 53.
    Lam AD, Sarkis RA, Pellerin KR, Jing J, Dworetzky BA et al. 2020. Association of epileptiform abnormalities and seizures in Alzheimer disease. Neurology 95:e2259–70
     [Google Scholar]
  54. 54.
    Vossel K, Ranasinghe KG, Beagle AJ, La A, Ah Pook K et al. 2021. Effect of levetiracetam on cognition in patients with Alzheimer disease with and without epileptiform activity: a randomized clinical trial. JAMA Neurol 78:1345–54Shows that patients with epileptic-subtype AD experience improved cognition from treatment with the AED levetiracetam.
     [Google Scholar]
  55. 55.
    Vossel KA, Ranasinghe KG, Beagle AJ, Mizuiri D, Honma SM et al. 2016. Incidence and impact of subclinical epileptiform activity in Alzheimer's disease. Ann. Neurol. 80:858–70
     [Google Scholar]
  56. 56.
    Horvath AA, Papp A, Zsuffa J, Szucs A, Luckl J et al. 2021. Subclinical epileptiform activity accelerates the progression of Alzheimer's disease: a long-term EEG study. Clin. Neurophysiol. 132:1982–89Shows AD patients with subclinical seizures experience accelerated dementia progression, linking seizures with worse disease outcomes.
     [Google Scholar]
  57. 57.
    Romoli M, Sen A, Parnetti L, Calabresi P, Costa C. 2021. Amyloid-β: a potential link between epilepsy and cognitive decline. Nat. Rev. Neurol. 17:469–85
     [Google Scholar]
  58. 58.
    Vigil FA, Belchior H, Bugay V, Bazaldua II, Stoja A, Dantas DC et al. 2023. Acute treatment with the M-channel (Kv7, KCNQ) opener retigabine reduces the long-term effects of repetitive blast traumatic brain injuries. Neurotherapeutics 20:853–69Preclinical mouse TBI model supporting retigabine's ability to reduce dementia pathology and seizures.
     [Google Scholar]
  59. 59.
    Schnier C, Duncan S, Wilkinson T, Mbizvo GK, Chin RFM. 2020. A nationwide, retrospective, data-linkage, cohort study of epilepsy and incident dementia. Neurology 95:e1686–93
     [Google Scholar]
  60. 60.
    Hauser WA, Annegers JF, Kurland LT. 1993. Incidence of epilepsy and unprovoked seizures in Rochester, Minnesota: 1935–1984. Epilepsia 34:453–68
     [Google Scholar]
  61. 61.
    Witt JA, Werhahn KJ, Krämer G, Ruckes C, Trinka E, Helmstaedter C. 2014. Cognitive-behavioral screening in elderly patients with new-onset epilepsy before treatment. Acta Neurol. Scand. 130:172–77
     [Google Scholar]
  62. 62.
    Costa C, Parnetti L, D'Amelio M, Tozzi A, Tantucci M et al. 2016. Epilepsy, amyloid-β, and D1 dopamine receptors: a possible pathogenetic link?. Neurobiol. Aging 48:161–71
     [Google Scholar]
  63. 63.
    Nardi Cesarini E, Babiloni C, Salvadori N, Farotti L, Del Percio C et al. 2020. Late-onset epilepsy with unknown etiology: a pilot study on neuropsychological profile, cerebrospinal fluid biomarkers, and quantitative EEG characteristics. Front. Neurol. 11:199
     [Google Scholar]
  64. 64.
    Costa C, Romoli M, Liguori C, Farotti L, Eusebi P et al. 2019. Alzheimer's disease and late-onset epilepsy of unknown origin: two faces of beta amyloid pathology. Neurobiol. Aging 73:61–67
     [Google Scholar]
  65. 65.
    Vigil FA, Bozdemir E, Bugay V, Chun SH, Hobbs M et al. 2020. Prevention of brain damage after traumatic brain injury by pharmacological enhancement of KCNQ (Kv7, “M-type”) K+ currents in neurons. J. Cereb. Blood Flow Metab. 40:1256–73
     [Google Scholar]
  66. 66.
    Alyenbaawi H, Allison WT, Mok SA. 2020. Prion-like propagation mechanisms in tauopathies and traumatic brain injury: challenges and prospects. Biomolecules 10:1487
     [Google Scholar]
  67. 67.
    Vigil FA, Carver CM, Shapiro MS. 2020. Pharmacological manipulation of Kv7 channels as a new therapeutic tool for multiple brain disorders. Front. Physiol. 11:688
     [Google Scholar]
  68. 68.
    Zou H, Brayer SW, Hurwitz M, Niyonkuru C, Fowler LE, Wagner AK. 2013. Neuroprotective, neuroplastic, and neurobehavioral effects of daily treatment with levetiracetam in experimental traumatic brain injury. Neurorehabil. Neural Repair 27:878–88
     [Google Scholar]
  69. 69.
    Caudle KL, Lu XC, Mountney A, Shear DA, Tortella FC. 2016. Neuroprotection and anti-seizure effects of levetiracetam in a rat model of penetrating ballistic-like brain injury. Restor. Neurol. Neurosci. 34:257–70
     [Google Scholar]
  70. 70.
    Koenig JB, Cantu D, Low C, Sommer M, Noubary F et al. 2019. Glycolytic inhibitor 2-deoxyglucose prevents cortical hyperexcitability after traumatic brain injury. JCI Insight 5:e126506
     [Google Scholar]
  71. 71.
    Gerbatin RR, Almeida Silva LF, Hoffmann MS, Della-Pace ID, do Nascimento PS et al. 2019. Delayed creatine supplementation counteracts reduction of GABAergic function and protects against seizures susceptibility after traumatic brain injury in rats. Prog. Neuropsychopharmacol. Biol. Psychiatry 92:328–38
     [Google Scholar]
  72. 72.
    Guo D, Zeng L, Brody DL, Wong M. 2013. Rapamycin attenuates the development of posttraumatic epilepsy in a mouse model of traumatic brain injury. PLOS ONE 8:e64078
     [Google Scholar]
  73. 73.
    Liu SJ, Zheng P, Wright DK, Dezsi G, Braine E et al. 2016. Sodium selenate retards epileptogenesis in acquired epilepsy models reversing changes in protein phosphatase 2A and hyperphosphorylated tau. Brain 139:1919–38
     [Google Scholar]
  74. 74.
    Shi J-Q, Wang B-R, Tian Y-Y, Xu J, Gao L et al. 2013. Antiepileptics topiramate and levetiracetam alleviate behavioral deficits and reduce neuropathology in APPswe/PS1dE9 transgenic mice. CNS Neurosci. Ther. 19:871–81
     [Google Scholar]
  75. 75.
    Zhang M-Y, Zheng C-Y, Zou M-M, Zhu J-W, Zhang Y et al. 2014. Lamotrigine attenuates deficits in synaptic plasticity and accumulation of amyloid plaques in APP/PS1 transgenic mice. Neurobiol. Aging 35:2713–25
     [Google Scholar]
  76. 76.
    Hu JP, Xie JW, Wang CY, Wang T, Wang X et al. 2011. Valproate reduces tau phosphorylation via cyclin-dependent kinase 5 and glycogen synthase kinase 3 signaling pathways. Brain Res. Bull. 85:194–200
     [Google Scholar]
  77. 77.
    Qing H, He G, Ly PT, Fox CJ, Staufenbiel M et al. 2008. Valproic acid inhibits Aβ production, neuritic plaque formation, and behavioral deficits in Alzheimer's disease mouse models. J. Exp. Med. 205:2781–89
     [Google Scholar]
  78. 78.
    Sanchez PE, Zhu L, Verret L, Vossel KA, Orr AG et al. 2012. Levetiracetam suppresses neuronal network dysfunction and reverses synaptic and cognitive deficits in an Alzheimer's disease model. PNAS 109:E2895–903
     [Google Scholar]
  79. 79.
    Zheng XY, Zhang HC, Lv YD, Jin FY, Wu XJ et al. 2022. Levetiracetam alleviates cognitive decline in Alzheimer's disease animal model by ameliorating the dysfunction of the neuronal network. Front. Aging Neurosci. 14:888784
     [Google Scholar]
  80. 80.
    Devi L, Ohno M. 2013. Effects of levetiracetam, an antiepileptic drug, on memory impairments associated with aging and Alzheimer's disease in mice. Neurobiol. Learn. Mem. 102:7–11
     [Google Scholar]
  81. 81.
    Alavi MS, Fanoudi S, Hosseini M, Sadeghnia HR. 2022. Beneficial effects of levetiracetam in streptozotocin-induced rat model of Alzheimer's disease. Metab. Brain Dis 37:689–700
     [Google Scholar]
  82. 82.
    Zhang H, Cao Y, Ma L, Wei Y, Li H. 2021. Possible mechanisms of tau spread and toxicity in Alzheimer's disease. Front. Cell Dev. Biol. 9:707268
     [Google Scholar]
  83. 83.
    Saggu S, Chen Y, Chen L, Pizarro D, Pati S et al. 2022. A peptide blocking the ADORA1-neurabin interaction is anticonvulsant and inhibits epilepsy in an Alzheimer's model. JCI Insight 7:e155002
     [Google Scholar]
  84. 84.
    Bierbower SM, Choveau FS, Lechleiter JD, Shapiro MS. 2015. Augmentation of M-type (KCNQ) potassium channels as a novel strategy to reduce stroke-induced brain injury. J. Neurosci. 35:2101–11
     [Google Scholar]
  85. 85.
    Wang L, Qiao GH, Hu HN, Gao ZB, Nan FJ. 2019. Discovery of novel retigabine derivatives as potent KCNQ4 and KCNQ5 channel agonists with improved specificity. ACS Med. Chem. Lett. 10:27–33
     [Google Scholar]
  86. 86.
    Bordey A. 2021. Treating post-traumatic seizures to limit tau accumulation in larval zebrafish. Epilepsy Curr. 21:285–86
     [Google Scholar]
  87. 87.
    Tai XY, Koepp M, Duncan JS, Fox N, Thompson P et al. 2016. Hyperphosphorylated tau in patients with refractory epilepsy correlates with cognitive decline: a study of temporal lobe resections. Brain 139:2441–55
     [Google Scholar]
  88. 88.
    Xi ZQ, Wang XF, Shu XF, Chen GJ, Xiao F et al. 2011. Is intractable epilepsy a tauopathy?. Med. Hypotheses 76:897–900
     [Google Scholar]
  89. 89.
    Bernasconi N. 2016. Is epilepsy a curable neurodegenerative disease?. Brain 139:2336–37
     [Google Scholar]
  90. 90.
    Alves M, Kenny A, de Leo G, Beamer EH, Engel T. 2019. Tau phosphorylation in a mouse model of temporal lobe epilepsy. Front. Aging Neurosci. 11:308
     [Google Scholar]
  91. 91.
    Liang Z, Liu F, Iqbal K, Grundke-Iqbal I, Gong CX. 2009. Dysregulation of tau phosphorylation in mouse brain during excitotoxic damage. J. Alzheimers Dis. 17:531–39
     [Google Scholar]
  92. 92.
    Zheng X-Y, Lv Y-D, Jin F-Y, Wu X-J, Zhu J, Ruan Y 2019. Kainic acid hyperphosphorylates tau via inflammasome activation in MAPT transgenic mice. Aging 11:10923–38
     [Google Scholar]
  93. 93.
    Hudak AM, Trivedi K, Harper CR, Booker K, Caesar RR et al. 2004. Evaluation of seizure-like episodes in survivors of moderate and severe traumatic brain injury. J. Head Trauma Rehabil. 19:290–95
     [Google Scholar]
  94. 94.
    Clavaguera F, Bolmont T, Crowther RA, Abramowski D, Frank S et al. 2009. Transmission and spreading of tauopathy in transgenic mouse brain. Nat. Cell Biol. 11:909–13
     [Google Scholar]
  95. 95.
    Dujardin S, Lécolle K, Caillierez R, Bégard S, Zommer N et al. 2014. Neuron-to-neuron wild-type tau protein transfer through a trans-synaptic mechanism: relevance to sporadic tauopathies. Acta Neuropathol. Commun. 2:14
     [Google Scholar]
  96. 96.
    Katsumoto A, Takeuchi H, Tanaka F. 2019. Tau pathology in chronic traumatic encephalopathy and Alzheimer's disease: similarities and differences. Front. Neurol. 10:980
     [Google Scholar]
  97. 97.
    Diaz-Arrastia R, Agostini MA, Frol AB, Mickey B, Fleckenstein J et al. 2000. Neurophysiologic and neuroradiologic features of intractable epilepsy after traumatic brain injury in adults. Arch. Neurol. 57:1611–16
     [Google Scholar]
  98. 98.
    Osorio I, Reed RC, Peltzer JN. 2000. Refractory idiopathic absence status epilepticus: a probable paradoxical effect of phenytoin and carbamazepine. Epilepsia 41:887–94
     [Google Scholar]
  99. 99.
    Carney N, Totten AM, O'Reilly C, Ullman JS, Hawryluk GW et al. 2017. Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery 80:6–15
     [Google Scholar]
  100. 100.
    Khan AA, Banerjee A. 2010. The role of prophylactic anticonvulsants in moderate to severe head injury. Int. J. Emerg. Med. 3:187–91
     [Google Scholar]
  101. 101.
    Walker MC. 2007. Treatment of nonconvulsive status epilepticus. Int. Rev. Neurobiol. 81:287–97
     [Google Scholar]
  102. 102.
    Laccheo I, Sonmezturk H, Bhatt AB, Tomycz L, Shi Y et al. 2015. Non-convulsive status epilepticus and non-convulsive seizures in neurological ICU patients. Neurocrit. Care 22:202–11
     [Google Scholar]
  103. 103.
    Larson EB, Zollman FS. 2010. The effect of sleep medications on cognitive recovery from traumatic brain injury. J. Head Trauma Rehabil. 25:61–67
     [Google Scholar]
  104. 104.
    Zhang XZ, Li XJ, Zhang HY. 2010. Valproic acid as a promising agent to combat Alzheimer's disease. Brain Res. Bull. 81:3–6
     [Google Scholar]
  105. 105.
    Weiner MF, Womack KB, Martin-Cook K, Svetlik DA, Hynan LS. 2005. Levetiracetam for agitated Alzheimer's disease patients. Int. Psychogeriatr. 17:327–28
     [Google Scholar]
  106. 106.
    Li C, Xue L, Liu Y, Yang Z, Chi S, Xie A. 2020. Zonisamide for the treatment of Parkinson disease: a current update. Front. Neurosci. 14:574652
     [Google Scholar]
  107. 107.
    Sharma S, Tiarks G, Haight J, Bassuk AG. 2021. Neuropathophysiological mechanisms and treatment strategies for post-traumatic epilepsy. Front. Mol. Neurosci. 14:612073
     [Google Scholar]
  108. 108.
    Abdolmohammadi B, Dupre A, Evers L, Mez J. 2020. Genetics of chronic traumatic encephalopathy. Semin. Neurol. 40:420–29
     [Google Scholar]
  109. 109.
    Atherton K, Han X, Chung J, Cherry JD, Baucom Z et al. 2022. Association of APOE genotypes and chronic traumatic encephalopathy. JAMA Neurol 79:787–96
     [Google Scholar]
  110. 110.
    Cherry JD, Mez J, Crary JF, Tripodis Y, Alvarez VE et al. 2018. Variation in TMEM106B in chronic traumatic encephalopathy. Acta Neuropathol. Commun. 6:115
     [Google Scholar]
  111. 111.
    Dardiotis E, Fountas KN, Dardioti M, Xiromerisiou G, Kapsalaki E et al. 2010. Genetic association studies in patients with traumatic brain injury. Neurosurg. Focus 28:E9
     [Google Scholar]
  112. 112.
    Chen ZP, Wang S, Zhao X, Fang W, Wang Z et al. 2023. Lipid-accumulated reactive astrocytes promote disease progression in epilepsy. Nat. Neurosci. 26:542–54
     [Google Scholar]
  113. 113.
    Solazzi R, Moscatelli M, Sebastiano DR, Canafoglia L, Pezzoli L et al. 2022. Severe epilepsy and movement disorder may be early symptoms of TMEM106B-related hypomyelinating leukodystrophy. Neurol. Genet. 8:e200022
     [Google Scholar]
  114. 114.
    Clayton EL, Isaacs AM. 2020. Progranulin and TMEM106B: when two become wan. EMBO Rep 21:e51668
     [Google Scholar]
  115. 115.
    Kuroda M, Matsuwaki T, Tanaka Y, Yamanouchi K, Nishihara M. 2020. Convulsive responses to seizure-inducible drugs are exacerbated in progranulin-deficient mice. Neuroreport 31:478–83
     [Google Scholar]
  116. 116.
    Terpollili NA, Dolp R, Waehner K, Schwarzmaier SM, Rumbler E et al. 2022. CaV2.1 channel mutations causing familial hemiplegic migraine type 1 increase the susceptibility for cortical spreading depolarizations and seizures and worsen outcome after experimental traumatic brain injury. eLife 11:e74923
     [Google Scholar]
  117. 117.
    Kang S, Gim J, Lee J, Gunasekaran TI, Choi KY et al. 2021. Potential novel genes for late-onset Alzheimer's disease in East-Asian descent identified by APOE-stratified genome-wide association study. J. Alzheimers Dis. 82:1451–60
     [Google Scholar]
  118. 118.
    Braak H, Braak E. 1995. Staging of Alzheimer's disease-related neurofibrillary changes. Neurobiol. Aging 16:271–78
     [Google Scholar]
  119. 119.
    Sanders DW, Kaufman SK, Holmes BB, Diamond MI. 2016. Prions and protein assemblies that convey biological information in health and disease. Neuron 89:433–48
     [Google Scholar]
  120. 120.
    Ayers JI, Giasson BI, Borchelt DR. 2018. Prion-like spreading in tauopathies. Biol. Psychiatry 83:337–46
     [Google Scholar]
  121. 121.
    Mudher A, Colin M, Dujardin S, Medina M, Dewachter I et al. 2017. What is the evidence that tau pathology spreads through prion-like propagation?. Acta Neuropathol. Commun. 5:99
     [Google Scholar]
  122. 122.
    Bittar A, Bhatt N, Hasan TF, Montalbano M, Puangmalai N et al. 2019. Neurotoxic tau oligomers after single versus repetitive mild traumatic brain injury. Brain Commun 1:fcz004
     [Google Scholar]
  123. 123.
    Shin MK, Vázquez-Rosa E, Koh Y, Dhar M, Chaubey K et al. 2021. Reducing acetylated tau is neuroprotective in brain injury. Cell 184:2715–32.e23
     [Google Scholar]
  124. 124.
    Baumgart M, Snyder HM, Carrillo MC, Fazio S, Kim H, Johns H. 2015. Summary of the evidence on modifiable risk factors for cognitive decline and dementia: a population-based perspective. Alzheimers Dement 11:718–26
     [Google Scholar]
  125. 125.
    Morales R, Abid K, Soto C. 2007. The prion strain phenomenon: molecular basis and unprecedented features. Biochim. Biophys. Acta 1772:681–91
     [Google Scholar]
  126. 126.
    Vaquer-Alicea J, Diamond MI, Joachimiak LA. 2021. Tau strains shape disease. Acta Neuropathol 142:57–71
     [Google Scholar]
  127. 127.
    Sanders DW, Kaufman SK, DeVos SL, Sharma AM, Mirbaha H et al. 2014. Distinct tau prion strains propagate in cells and mice and define different tauopathies. Neuron 82:1271–88
     [Google Scholar]
  128. 128.
    Kaufman SK, Sanders DW, Thomas TL, Ruchinskas AJ, Vaquer-Alicea J et al. 2016. Tau prion strains dictate patterns of cell pathology, progression rate, and regional vulnerability in vivo. Neuron 92:796–812
     [Google Scholar]
  129. 129.
    Bessen RA, Marsh RF. 1992. Identification of two biologically distinct strains of transmissible mink encephalopathy in hamsters. J. Gen. Virol. 73:Pt. 2329–34
     [Google Scholar]
/content/journals/10.1146/annurev-pharmtox-051921-013930
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Antiepileptic Drugs as Potential Dementia Prophylactics Following Traumatic Brain Injury
Annual Review of Pharmacology and Toxicology 64, 577 (2024); https://doi.org/10.1146/annurev-pharmtox-051921-013930
/content/journals/10.1146/annurev-pharmtox-051921-013930
/content/journals/10.1146/annurev-pharmtox-051921-013930
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