Fatma Şimşek, Mustafa Ceylan, Seda Aşkın, Ahmet Kızıltunç
  MNJ, pp. 93-97  


Background:  Processes such as neurodegeneration, hypoxia, blood brain barrier dysfunction and oxidative changes are effective for epileptogenesis.There is no non-invasive biomarker that can be used in the follow-up of patients with epilepsy, which is a neurodegenerative disease.

Objective: In our study, it was aimed to investigate the relationship between inflammatory, oxidative, neurodegenerative processes, and antiepileptic use in patients with epilepsy.

Methods: The groups were formed from the patients who were followed up in the epilepsy outpatient clinic between April 2019-June 2019, and the age-gender-matched control group.The study included 30 patients and 30 healthy volunteers. Venous serum samples were collected from groups to study myeloperoxidase, malondialdehyde and alpha-synuclein.

Results: The levels of myeloperoxidase and malondialdehyde were higher in the control group and this difference was statistically significant (p=0.003, p<0.001). The level of α-syn was higher in the epilepsy group and there was no statistically significant difference between the two groups (p=0.52). There was a positive correlation between the α-syn level and disease duration and as the disease duration increased, the level of α-syn increased (r=0.379, p=0.03).

Conclusion: Although the α-syn level increases with the duration of the disease in epilepsy patients, it is not a suitable parameter for use as a biomarker in the follow-up.


Epilepsy; myeloperoxidase; malondialdehyde; alpha-synuclein

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Reddy DS. Neuroendocrine aspects of catamenial epilepsy. Hormones and behavior; 2013. 63(2):254-66. DOI: 10.1016/j.yhbeh.2012.04.016

Bar-Klein G, Lublinsky S, Kamintsky L, Noyman I, Veksler R, Dalipaj H, et al. Imaging blood–brain barrier dysfunction as a biomarker for epileptogenesis. Brain; 2017. 140(6):1692-705.

DOI: 10.1093/brain/awx073

Aroniadou-Anderjaska V, Fritsch B, Qashu F, Braga MF. Pathology and pathophysiology of the amygdala in epileptogenesis and epilepsy. Epilepsy research; 2008. 78(2-3):102-16.

DOI: 10.1016/j.eplepsyres.2007.11.011

Löscher W, Brandt C. Prevention or modification of epileptogenesis after brain insults: experimental approaches and translational research. Pharmacological reviews; 2010. 62(4):668-700.

DOI: 10.1124/pr.110.003046

Ashrafi MR, Shams S, Nouri M, Mohseni M, Shabanian R, Yekaninejad MS, et al. A probable causative factor for an old problem: selenium and glutathione peroxidase appear to play important roles in epilepsy pathogenesis. Epilepsia; 2007. 48(9):1750-5. DOI: 10.1111/j.1528-1167.2007.01143.x

Vezzani A, French J, Bartfai T, Baram TZ. The role of inflammation in epilepsy. Nature reviews neurology; 2011. 7(1):31. DOI:10.1038/nrneurol.2010.178

Fabene PF, Mora GN, Martinello M, Rossi B, Merigo F, Ottoboni L, et al. A role for leukocyte-endothelial adhesion mechanisms in epilepsy. Nature medicine; 2008. 14(12):1377-83. DOI: 10.1038/nm.1878. Epub

Van der Veen BS, de Winther MP, Heeringa P. Myeloperoxidase: molecular mechanisms of action and their relevance to human health and disease. Antioxidants & redox signaling; 2009. 11(11):2899-937. DOI: 10.1089/ars.2009.2538

Pandey MK, Mittra P, Maheshwari P. The lipid peroxidation product as a marker of oxidative stress in epilepsy. J Clin Diagn Res; 2012. 6(4):590-92. Avalaible from:

Nisha Y, Bobby Z, Wadwekar V. Biochemical derangements related to metabolic syndrome in epileptic patients on treatment with valproic acid. Seizure; 2018. 60:57-60.

DOI: 10.1016/j.seizure.2018.06.003

Shichiri M. The role of lipid peroxidation in neurological disorders. Journal of clinical biochemistry and nutrition; 2014. 14-0.

DOI: 10.3164/jcbn.14-10

Andreu-Cervera A, Anselme I, Karam A, Laclef C, Catala M, Schneider-Maunoury S. The ciliopathy gene Ftm/Rpgrip1l controls mouse forebrain patterning via region-specific modulation of Hedgehog/Gli signaling. Journal of Neuroscience; 2019. 39(13):2398-415. DOI: 10.1523/JNEUROSCI.2199-18.2019

Almandoz-Gil L, Welander H, Ihse E, Khoonsari PE, Musunuri S, Lendel C, et al. Low molar excess of 4-oxo-2-nonenal and 4-hydroxy-2-nonenal promote oligomerization of alpha-synuclein through different pathways. Free Radical Biology and Medicine; 2017. 110:421-31.

DOI: 10.1016/j.freeradbiomed.2017.07.004

Liu G, Zhang C, Yin J, Li X, Cheng F, Li Y, et al. α-Synuclein is differentially expressed in mitochondria from different rat brain regions and dose-dependently down-regulates complex I activity. Neuroscience letters; 2009. 454(3):187-92.

DOI: 10.1016/j.neulet.2009.02.056

Bradley P, Da P. Christensen RD, Rothstein G: Measurement of cutaneous inflammation: Estimation of neutrophil content with an enzyme marker. J invest Dermatol; 1982. 78:206-9. DOI: 10.1111/1523-1747.ep12506462.

Ohkawa H, Ohishi N, Yagi K. Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Analytical biochemistry; 1979. 95(2):351-8. DOI: 10.1016/0003-2697(79)90738-3

Sorce S, Krause K-H. NOX enzymes in the central nervous system: from signaling to disease. Antioxidants & redox signaling; 2009. 11(10):2481-504. DOI: 10.1089/ars.2009.2578

Van Vliet E, Araujo S, Redeker S, van Schaik R, Aronica E, Gorter J. Long-lasting increased permeability of the blood-brain barrier may contribute to seizure progression in temporal lobe epilepsy: 4.110. Epilepsia; 2006. 47.

DOI: 10.1093/brain/awl318

Zhang Y, Seeburg DP, Pulli B, Wojtkiewicz GR, Bure L, Atkinson W, et al. Myeloperoxidase nuclear imaging for epileptogenesis. Radiology; 2016. 278(3):822-30. DOI: 10.1148/radiol.2015141922

Uttara B, Singh AV, Zamboni P, Mahajan R. Oxidative stress and neurodegenerative diseases: a review of upstream and downstream antioxidant therapeutic options. Current neuropharmacology; 2009. 7(1):65-74.

DOI: 10.2174/157015909787602823

Guler SK, Aytac B, Durak ZE, Cokal BG, Gunes N, Durak I, et al. Antioxidative–oxidative balance in epilepsy patients on antiepileptic therapy: A prospective case–control study. Neurological Sciences; 2016. 37(5):763-7. DOI: 10.1007/s10072-016-2494-0

Bogdanov G, Mishchenko D, Kotel'nikova R, Frog E, Faĭngol'd I, Tat'ianenko L, et al. Anticonvulsants as bioantioxidants under stress conditions. Biomeditsinskaia Khimiia; 2009. 55(4):519-24. Avalaible from:

Martinc B, Grabnar I, Vovk T. The role of reactive species in epileptogenesis and influence of antiepileptic drug therapy on oxidative stress. Current Neuropharmacology; 2012. 10(4):328-43.

DOI: 10.2174/157015912804499447

Prasad D, Satyanarayana U, Shaheen U, Prabha TS, Munshi A. Oxidative stress in the development of genetic generalised epilepsy: an observational study in southern Indian population. Journal of Clinical and Diagnostic Research: JCDR; 2017. 11(9):BC05.

DOI: 10.7860/JCDR/2017/29133.10604

Greten-Harrison B, Polydoro M, Morimoto-Tomita M, Diao L, Williams AM, Nie EH, et al. αβγ-Synuclein triple knockout mice reveal age-dependent neuronal dysfunction. Proceedings of the National Academy of Sciences; 2010. 107(45):19573-8.

DOI: 10.1073/pnas.1005005107

Li A, Choi YS, Dziema H, Cao R, Cho HY, Jung YJ, et al. Proteomic profiling of the epileptic dentate gyrus. Brain pathology; 2010. 20(6):1077-89.

DOI: 10.1111/j.1750-3639.2010.00414.x

Rong H, Jin L, Wei W, Wang X, Xi Z. Alpha-synuclein is a potential biomarker in the serum and CSF of patients with intractable epilepsy. Seizure; 2015. 27:6-9. DOI: 10.1016/j.seizure.2015.02.007

Mehrabi S, Sanadgol N, Barati M, Shahbazi A, Vahabzadeh G, Barzroudi M, et al. Evaluation of metformin effects in the chronic phase of spontaneous seizures in pilocarpine model of temporal lobe epilepsy. Metabolic Brain Disease; 2018. 33(1):107-14. DOI:10.1007/s11011-017-0132-z

Hussein AM, Eldosoky M, El-Shafey M, El-Mesery M, Ali AN, Abbas KM, et al. Effects of metformin on apoptosis and α-synuclein in a rat model of pentylenetetrazole-induced epilepsy. Canadian Journal of Physiology and Pharmacology; 2019. 97(1):37-46. DOI: 10.1139/cjpp-2018-0266


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