Display options
Cite
Toral-Rios D, Pichardo-Rojas PS, Alonso-Vanegas M, et al. GSK3β and Tau Protein in Alzheimer's Disease and Epilepsy. Front Cell Neurosci. 2020;14:19doi: 10.3389/fncel.2020.00019.
Toral-Rios, D., Pichardo-Rojas, P. S., Alonso-Vanegas, M., & Campos-Peña, V. (2020). GSK3β and Tau Protein in Alzheimer's Disease and Epilepsy. Frontiers in cellular neuroscience, 1419. https://doi.org/10.3389/fncel.2020.00019
Toral-Rios, Danira, et al. "GSK3β and Tau Protein in Alzheimer's Disease and Epilepsy." Frontiers in cellular neuroscience vol. 14 (2020): 19. doi: https://doi.org/10.3389/fncel.2020.00019
Toral-Rios D, Pichardo-Rojas PS, Alonso-Vanegas M, Campos-Peña V. GSK3β and Tau Protein in Alzheimer's Disease and Epilepsy. Front Cell Neurosci. 2020 Mar 17;14:19. doi: 10.3389/fncel.2020.00019. eCollection 2020. PMID: 32256316; PMCID: PMC7089874.
Copy Download .nbib Format: NLM
Share it on

Front Cell Neurosci. 2020 Mar 17;14:19. doi: 10.3389/fncel.2020.00019. eCollection 2020.

GSK3β and Tau Protein in Alzheimer's Disease and Epilepsy.

Frontiers in cellular neuroscience

Danira Toral-Rios, Pavel S Pichardo-Rojas, Mario Alonso-Vanegas, Victoria Campos-Peña

Affiliations

  1. Departamento de Fisiología Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del IPN, Mexico City, Mexico.
  2. Facultad de Ciencias de la Salud, Universidad Autónoma de Baja California, Ensenada, Mexico.
  3. Centro Internacional de Cirug#x000ED;a de Epilepsia, Instituto Nacional de Neurología y Neurocirugía, HMG, Hospital Coyoacán, Mexico City, Mexico.
  4. Laboratorio Experimental de Enfermedades Neurodegenerativas, Instituto Nacional de Neurología y Neurocirugía, Mexico City, Mexico.

PMID: 32256316 PMCID: PMC7089874 DOI: 10.3389/fncel.2020.00019

Abstract

Alzheimer's disease (AD) is the most common form of dementia present in older adults; its etiology involves genetic and environmental factors. In recent years, epidemiological studies have shown a correlation between AD and chronic epilepsy since a considerable number of patients with AD may present seizures later on. Although the pathophysiology of seizures in AD is not completely understood, it could represent the result of several molecular mechanisms linked to amyloid beta-peptide (Aβ) accumulation and the hyperphosphorylation of tau protein, which may induce an imbalance in the release and recapture of excitatory and inhibitory neurotransmitters, structural alterations of the neuronal cytoskeleton, synaptic loss, and neuroinflammation. These changes could favor the recurrent development of hypersynchronous discharges and epileptogenesis, which, in a chronic state, favor the neurodegenerative process and influence the cognitive decline observed in AD. Supporting this correlation, histopathological studies in the brain tissue of temporal lobe epilepsy (TLE) patients have revealed the presence of Aβ deposits and the accumulation of tau protein in the neurofibrillary tangles (NFTs), accompanied by an increase of glycogen synthase kinase-3 beta (GSK3β) activity that may lead to an imminent alteration in posttranslational modifications of some microtubule-associated proteins (MAPs), mainly tau. The present review is focused on understanding the pathological aspects of GSK3β and tau in the development of TLE and AD.

Copyright © 2020 Toral-Rios, Pichardo-Rojas, Alonso-Vanegas and Campos-Peña.

Keywords: GSK3β; epilepsy; hippocampal sclerosis; neurodegeneration; tau protein

References

  1. J Biol Chem. 2003 Aug 29;278(35):33067-77 - PubMed
  2. J Neurochem. 2008 Mar;104(6):1433-9 - PubMed
  3. Trends Mol Med. 2009 Mar;15(3):112-9 - PubMed
  4. Sci Rep. 2017 Oct 27;7(1):14189 - PubMed
  5. Philos Trans R Soc Lond B Biol Sci. 1999 Jun 29;354(1386):1101-18 - PubMed
  6. Epilepsia. 2007 Aug;48(8):1447-54 - PubMed
  7. FEBS Lett. 1998 Oct 23;437(3):207-10 - PubMed
  8. Hum Mol Genet. 2005 Sep 15;14(18):2727-36 - PubMed
  9. Epileptic Disord. 2015 Jun;17(2):101-16 - PubMed
  10. Molecules. 2018 Sep 12;23(9): - PubMed
  11. Neurobiol Dis. 2007 Mar;25(3):561-70 - PubMed
  12. J Neural Transm (Vienna). 1998;105(2-3):295-303 - PubMed
  13. Drugs Aging. 2005;22(7):615-26 - PubMed
  14. Epilepsia. 2002 May;43(5):482-90 - PubMed
  15. Proc Natl Acad Sci U S A. 2008 Jun 10;105(23):8050-4 - PubMed
  16. J Neurosci. 2011 Jan 12;31(2):700-11 - PubMed
  17. Discov Med. 2017 Apr;23(127):221-234 - PubMed
  18. Proc Natl Acad Sci U S A. 1986 Jun;83(11):4040-3 - PubMed
  19. Front Integr Neurosci. 2013 Aug 13;7:59 - PubMed
  20. Neurochem Res. 2015 Jul;40(7):1319-32 - PubMed
  21. EBioMedicine. 2019 Jan;39:377-387 - PubMed
  22. Neurochem Int. 2011 Mar;58(4):458-71 - PubMed
  23. Neurobiol Aging. 2014 Nov;35(11):2474-2478 - PubMed
  24. J Med Chem. 2013 Jun 13;56(11):4135-55 - PubMed
  25. J Biol Chem. 2000 Aug 11;275(32):24977-83 - PubMed
  26. Philos Trans R Soc Lond B Biol Sci. 2013 Dec 02;369(1633):20130144 - PubMed
  27. Clin Exp Pharmacol Physiol. 2010 Oct;37(10):1010-5 - PubMed
  28. Epilepsia. 1999 Sep;40(9):1279-85 - PubMed
  29. Neurotoxicology. 2015 Jan;46:44-52 - PubMed
  30. Neuroreport. 2010 Aug 23;21(12):846-50 - PubMed
  31. Brain Res. 1990 May 14;516(1):15-9 - PubMed
  32. Int J Alzheimers Dis. 2011;2011:861072 - PubMed
  33. Ageing Res Rev. 2013 Jan;12(1):289-309 - PubMed
  34. Biochim Biophys Acta. 2005 Jan 3;1739(2-3):91-103 - PubMed
  35. Epilepsia. 2001 Jun;42(6):764-71 - PubMed
  36. Nat Rev Neurol. 2010 Oct;6(10):532-3 - PubMed
  37. Curr Drug Targets. 2006 Nov;7(11):1421-34 - PubMed
  38. Neuron. 2007 Mar 1;53(5):703-17 - PubMed
  39. Neuron. 2011 May 12;70(3):410-26 - PubMed
  40. J Biol Chem. 2012 Sep 14;287(38):32040-53 - PubMed
  41. PLoS One. 2012;7(6):e38789 - PubMed
  42. ACS Chem Neurosci. 2019 Apr 17;10(4):1992-2003 - PubMed
  43. Brain Res Brain Res Rev. 2000 Aug;33(1):95-130 - PubMed
  44. J Neurosci. 2015 Apr 15;35(15):6221-30 - PubMed
  45. Mol Neurodegener. 2008 Jul 24;3:9 - PubMed
  46. Neurosci Lett. 1996 Jan 12;203(1):33-6 - PubMed
  47. Int J Mol Sci. 2018 Apr 05;19(4): - PubMed
  48. Epilepsy Behav. 2005 May;6(3):373-81 - PubMed
  49. Front Neurosci. 2018 Nov 02;12:798 - PubMed
  50. J Neurosci. 2013 Jan 23;33(4):1651-9 - PubMed
  51. Neurobiol Dis. 2009 Sep;35(3):359-67 - PubMed
  52. Epilepsia. 1994 Mar-Apr;35(2):381-90 - PubMed
  53. Neurobiol Aging. 1995 May-Jun;16(3):355-62; discussion 362-3 - PubMed
  54. Brain. 2016 Sep;139(Pt 9):2441-55 - PubMed
  55. NPJ Vaccines. 2018 Feb 27;3:9 - PubMed
  56. Neuroscience. 2015 Dec 17;311:474-83 - PubMed
  57. J Neurosci. 2015 Mar 25;35(12):4804-12 - PubMed
  58. Neuron. 2013 Apr 24;78(2):256-68 - PubMed
  59. Genes Brain Behav. 2008 Feb;7 Suppl 1:57-66 - PubMed
  60. Acta Neuropathol. 2002 Feb;103(2):91-9 - PubMed
  61. J Neurosci. 2004 Nov 3;24(44):9993-10002 - PubMed
  62. Int J Alzheimers Dis. 2011;2011:189728 - PubMed
  63. Oncotarget. 2017 Mar 14;8(11):18118-18128 - PubMed
  64. Neurobiol Dis. 2010 Mar;37(3):622-9 - PubMed
  65. Eur J Clin Pharmacol. 1993;44(6):529-33 - PubMed
  66. Biomolecules. 2016 Apr 19;6(2): - PubMed
  67. J Biol Chem. 1986 May 5;261(13):6084-9 - PubMed
  68. Neurochem Int. 2007 Jan;50(2):435-42 - PubMed
  69. J Neurosci. 2013 Jul 31;33(31):12887-97 - PubMed
  70. Science. 2008 Feb 22;319(5866):1086-9 - PubMed
  71. Science. 2007 May 4;316(5825):750-4 - PubMed
  72. Nat Med. 1996 Jul;2(7):783-7 - PubMed
  73. Brain. 2011 Oct;134(Pt 10):2969-81 - PubMed
  74. J Biomed Biotechnol. 2006;2006(3):74539 - PubMed
  75. Nat Med. 2015 Oct;21(10):1154-62 - PubMed
  76. Epilepsy Curr. 2012 Sep;12(5):184-7 - PubMed
  77. Stroke. 2004 Jul;35(7):1769-75 - PubMed
  78. Int J Mol Sci. 2018 Apr 11;19(4): - PubMed
  79. Epilepsia. 2007 Apr;48(4):694-705 - PubMed
  80. Epilepsy Behav. 2010 Apr;17(4):461-6 - PubMed
  81. Cell Death Dis. 2018 Sep 20;9(10):969 - PubMed
  82. Biochemistry. 1992 Nov 3;31(43):10626-33 - PubMed
  83. Front Neurosci. 2017 Oct 17;11:572 - PubMed
  84. Neurology. 1995 Aug;45(8):1494-9 - PubMed
  85. Lancet. 2001 Jan 20;357(9251):216-22 - PubMed

Publication Types