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A comparative study of the amount of α-synuclein in ischemic stroke and Parkinson’s disease

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Abstract

In the present study, we detected the level of oligomeric form of α-synuclein in the red blood cells of ischemic stroke, Parkinson’s disease, and normal people and compared the differences to assess the diagnosis potential of α-synuclein in ischemic stroke patients. 86 ischemic stroke, 100 PD, and 102 healthy cases were enrolled in the present study. Total protein amount in the red blood cells were quantified by BCA assay using spectrophotometer. Levels of oligomeric form of α-synuclein were characterized by a sandwich ELISA. Analysis of correlation analysis and receiver operating characteristic curve were conducted. Significant differences were detected in the levels of oligomeric forms of α-synuclein in different samples’ blood cells (P < 0.05); the levels of total protein in (188.1 ± 33.9 mmol/L) healthy people were significantly higher than that of PD (147.7 ± 45.0 mmol/L) and ischemic stroke groups (142.9 ± 43.0 mmol/L) (P < 0.05). There was no correlation between the age of patients and level of α-synuclein (R 2 = 0.216 in ischemic stroke group and −0.104 in PD group) and the receiver operating characteristic curve analysis showed a high sensitivity of α-synuclein in discriminating ischemic stroke (sensitivity was 63.7 % and specificity was 9.6 %) and PD (sensitivity was 44.1 % and specificity was 12.5 %) patients from the controls. The levels of oligomeric form of α-synuclein of red blood cells in ischemic stroke and Parkinson’s disease patients were both significant higher than normal people. And the level of oligomeric form α-synuclein showed a potential for diagnosis of ischemic stroke in clinic.

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References

  1. Morgante L, Salemi G, Meneghini F, Di Rosa AE, Epifanio A, Grigoletto F, Ragonese P, Patti F, Reggio A, Di Perri R, Savettieri G (2000) Parkinson disease survival: a population-based study. Arch Neurol 57(4):507–512

    Article  CAS  PubMed  Google Scholar 

  2. Guttman M, Slaughter PM, Theriault ME, DeBoer DP, Naylor CD (2001) Parkinsonism in Ontario: increased mortality compared with controls in a large cohort study. Neurology 57(12):2278–2282

    Article  CAS  PubMed  Google Scholar 

  3. Driver JA, Kurth T, Buring JE, Gaziano JM, Logroscino G (2008) Parkinson disease and risk of mortality: a prospective comorbidity-matched cohort study. Neurology 70(16 Pt 2):1423–1430. doi:10.1212/01.wnl.0000310414.85144.ee

    Article  CAS  PubMed  Google Scholar 

  4. Elbaz A, Bower JH, Peterson BJ, Maraganore DM, McDonnell SK, Ahlskog JE, Schaid DJ, Rocca WA (2003) Survival study of Parkinson disease in Olmsted County, Minnesota. Arch Neurol 60(1):91–96

    Article  PubMed  Google Scholar 

  5. Godwin-Austen RB, Lee PN, Marmot MG, Stern GM (1982) Smoking and Parkinson’s disease. J Neurol Neurosurg Psychiatry 45(7):577–581

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  6. Noyce AJ, Bestwick JP, Silveira-Moriyama L, Hawkes CH, Giovannoni G, Lees AJ, Schrag A (2012) Meta-analysis of early nonmotor features and risk factors for Parkinson disease. Ann Neurol 72(6):893–901. doi:10.1002/ana.23687

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  7. Spillantini MG, Schmidt ML, Lee VM, Trojanowski JQ, Jakes R, Goedert M (1997) Alpha-synuclein in Lewy bodies. Nature 388(6645):839–840. doi:10.1038/42166

    Article  CAS  PubMed  Google Scholar 

  8. Maroteaux L, Campanelli JT, Scheller RH (1988) Synuclein: a neuron-specific protein localized to the nucleus and presynaptic nerve terminal. J Neurosci 8(8):2804–2815

    CAS  PubMed  Google Scholar 

  9. Nakajo S, Omata K, Aiuchi T, Shibayama T, Okahashi I, Ochiai H, Nakai Y, Nakaya K, Nakamura Y (1990) Purification and characterization of a novel brain-specific 14-kDa protein. J Neurochem 55(6):2031–2038

    Article  CAS  PubMed  Google Scholar 

  10. Eschbach J, Danzer KM (2014) α-Synuclein in Parkinson’s disease: pathogenic function and translation into animal models. Neurodegener Dis 14(1):1–17. doi:10.1159/000354615

    Article  CAS  PubMed  Google Scholar 

  11. Barbour R, Kling K, Anderson JP, Banducci K, Cole T, Diep L, Fox M, Goldstein JM, Soriano F, Seubert P, Chilcote TJ (2008) Red blood cells are the major source of α-synuclein in blood. Neurodegener Dis 5(2):55–59. doi:10.1159/000112832

    Article  CAS  PubMed  Google Scholar 

  12. Chen YD, Li X, Yang W, Li X, Yu S (2013) Changes of α-synuclein and its oligomeric formation in plasmas of patients with stroke. J Capital Med Univ 34(6):826–829

    CAS  Google Scholar 

  13. Unal-Cevik I, Gursoy-Ozdemir Y, Yemisci M, Lule S, Gurer G, Can A, Muller V, Kahle PJ, Dalkara T (2011) Alpha-synuclein aggregation induced by brief ischemia negatively impacts neuronal survival in vivo: a study in [A30P]α-synuclein transgenic mouse. J Cereb Blood Flow Metab 31(3):913–923. doi:10.1038/jcbfm.2010.170

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  14. Huang YP, Chen LS, Yen MF, Fann CY, Chiu YH, Chen HH, Pan SL (2013) Parkinson’s disease is related to an increased risk of ischemic stroke-a population-based propensity score-matched follow-up study. PLoS ONE 8(9):e68314. doi:10.1371/journal.pone.0068314

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  15. Li FFGL, Li X, Feng T (2015) α-synuclein oligomers of red blood cell as a marker for Parkinson’s disease. Chin J Geriatric Heart Brain Vessel Dis 17(2):161–163

    CAS  Google Scholar 

  16. Chen YDYN, Li X, Yang WW, Li XR, Yu S (2013) The amount change of alpha synuclein and its oligomers in plasma of patients with stroke. J Capital Med Univ 34(6):825–829

    Google Scholar 

  17. Conway KA, Lee SJ, Rochet JC, Ding TT, Williamson RE, Lansbury PT Jr (2000) Acceleration of oligomerization, not fibrillization, is a shared property of both α-synuclein mutations linked to early-onset Parkinson’s disease: implications for pathogenesis and therapy. Proc Natl Acad Sci USA 97(2):571–576

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  18. Bucciantini M, Giannoni E, Chiti F, Baroni F, Formigli L, Zurdo J, Taddei N, Ramponi G, Dobson CM, Stefani M (2002) Inherent toxicity of aggregates implies a common mechanism for protein misfolding diseases. Nature 416(6880):507–511. doi:10.1038/416507a

    Article  CAS  PubMed  Google Scholar 

  19. Walsh DM, Klyubin I, Fadeeva JV, Cullen WK, Anwyl R, Wolfe MS, Rowan MJ, Selkoe DJ (2002) Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo. Nature 416(6880):535–539. doi:10.1038/416535a

    Article  CAS  PubMed  Google Scholar 

  20. El-Agnaf OM, Nagala S, Patel BP, Austen BM (2001) Non-fibrillar oligomeric species of the amyloid ABri peptide, implicated in familial British dementia, are more potent at inducing apoptotic cell death than protofibrils or mature fibrils. J Mol Biol 310(1):157–168. doi:10.1006/jmbi.2001.4743

    Article  CAS  PubMed  Google Scholar 

  21. Masliah E, Rockenstein E, Veinbergs I, Mallory M, Hashimoto M, Takeda A, Sagara Y, Sisk A, Mucke L (2000) Dopaminergic loss and inclusion body formation in α-synuclein mice: implications for neurodegenerative disorders. Science 287(5456):1265–1269

    Article  CAS  PubMed  Google Scholar 

  22. Kayed R, Head E, Thompson JL, McIntire TM, Milton SC, Cotman CW, Glabe CG (2003) Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis. Science 300(5618):486–489. doi:10.1126/science.1079469

    Article  CAS  PubMed  Google Scholar 

  23. Lashuel HA, Hartley D, Petre BM, Walz T, Lansbury PT Jr (2002) Neurodegenerative disease: amyloid pores from pathogenic mutations. Nature 418(6895):291. doi:10.1038/418291a

    Article  CAS  PubMed  Google Scholar 

  24. Park MJ, Cheon SM, Bae HR, Kim SH, Kim JW (2011) Elevated levels of alpha-synuclein oligomer in the cerebrospinal fluid of drug-naive patients with Parkinson’s disease. J Clin Neurol 7(4):215–222. doi:10.3988/jcn.2011.7.4.215

    Article  PubMed  PubMed Central  Google Scholar 

  25. Kim S, Jeon BS, Heo C, Im PS, Ahn TB, Seo JH, Kim HS, Park CH, Choi SH, Cho SH, Lee WJ, Suh YH (2004) Alpha-synuclein induces apoptosis by altered expression in human peripheral lymphocyte in Parkinson’s disease. FASEB J 18(13):1615–1617. doi:10.1096/fj.04-1917fje

    CAS  PubMed  Google Scholar 

  26. Tokuda T, Qureshi MM, Ardah MT, Varghese S, Shehab SA, Kasai T, Ishigami N, Tamaoka A, Nakagawa M, El-Agnaf OM (2010) Detection of elevated levels of α-synuclein oligomers in CSF from patients with Parkinson disease. Neurology 75(20):1766–1772. doi:10.1212/WNL.0b013e3181fd613b

    Article  CAS  PubMed  Google Scholar 

  27. Graeber MB (2009) Biomarkers for Parkinson’s disease. Exp Neurol 216(2):249–253. doi:10.1016/j.expneurol.2008.12.017

    Article  CAS  PubMed  Google Scholar 

  28. Withers GS, George JM, Banker GA, Clayton DF (1997) Delayed localization of synelfin (synuclein, NACP) to presynaptic terminals in cultured rat hippocampal neurons. Brain Res Dev Brain Res 99(1):87–94

    Article  CAS  PubMed  Google Scholar 

  29. Iwai A, Masliah E, Yoshimoto M, Ge N, Flanagan L, de Silva HA, Kittel A, Saitoh T (1995) The precursor protein of non-A beta component of Alzheimer’s disease amyloid is a presynaptic protein of the central nervous system. Neuron 14(2):467–475

    Article  CAS  PubMed  Google Scholar 

  30. Murphy DD, Rueter SM, Trojanowski JQ, Lee VM (2000) Synucleins are developmentally expressed, and α-synuclein regulates the size of the presynaptic vesicular pool in primary hippocampal neurons. J Neurosci 20(9):3214–3220

    CAS  PubMed  Google Scholar 

  31. Kitamura Y, Ishida Y, Takata K, Kakimura J, Mizutani H, Shimohama S, Akaike A, Taniguchi T (2001) Alpha-synuclein protein is not scavenged in neuronal loss induced by kainic acid or focal ischemia. Brain Res 898(1):181–185

    Article  CAS  PubMed  Google Scholar 

  32. Chun-song J, Xin L, Yao-hua L, Guang-wei L, Juan-juan Y, Yan-chuan W, Shun Y (2010) Change of α-synuclein level in rat brain and plasma after ischemia/reperfusion. J Capital Med Univ 31(3):368–372

    Google Scholar 

  33. Chang CY, Lai YC, Cheng TJ, Lau MT, Hu ML (1998) Plasma levels of antioxidant vitamins, selenium, total sulfhydryl groups and oxidative products in ischemic-stroke patients as compared to matched controls in Taiwan. Free Radical Res 28(1):15–24

    Article  CAS  Google Scholar 

  34. Yin N, Li X, Yang WW, Li XR, Yu S (2013) Increased formation of α-synuclein oligomers in plasma of patients with Parkinson’s disease. J Capital Med Univ 34(6):840–843. doi:10.3969/j.issn.1006-7795.2013.06.012

    CAS  Google Scholar 

  35. Ishimaru H, Ueda K, Takahashi A, Maruyama Y (1998) Changes in presynaptic protein NACP/α-synuclein in an ischemic gerbil hippocampus. Brain Res 788(1–2):311–314

    Article  CAS  PubMed  Google Scholar 

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Correspondence to Tao Feng.

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Zhao, HQ., Li, Ff., Wang, Z. et al. A comparative study of the amount of α-synuclein in ischemic stroke and Parkinson’s disease. Neurol Sci 37, 749–754 (2016). https://doi.org/10.1007/s10072-016-2485-1

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