Abstract
Parkinson’s disease (PD) is a chronic, progressive, neurodegenerative disease with a multifactorial etiology. Protein accumulation is speculated by some to play a prominent role in the pathogenesis of PD. The severity of neurodegeneration should correlate with cerebrospinal fluid (CSF) levels of these neurodegenerative markers (NDMs). The aims of the study were to assess the CSF levels of tau protein, beta-amyloid (1–42), cystatin C, and clusterin in patients suffering from PD and in a control group, to compare the CSF levels between the two groups and to correlate them to PD duration. NDMs in the CSF were assessed in 32 patients suffering from PD and in a control group (CG) of 30 patients. The following statistically significant differences in the CSF were found: higher tau protein (p = 0.045) and clusterin levels (p = 0.004) in PD patients versus CG; higher tau protein levels (p = 0.033), tau protein/beta-amyloid (1–42) ratio (p = 0.011), and clusterin (p = 0.044) in patients suffering from PD for <2 years versus patients suffering PD for more than 2 years. No differences between beta-amyloid (1–42) and cystatin C CSF levels were found in the CG and PD patients groups. Significantly higher tau protein and clusterin CSF levels in the group of PD patients with disease duration of <2 years probably reflect the fact that most neurodegenerative changes in PD patients occur in the initial stage of disease.
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References
Alam ZI, Jenner A, Daniel SE, Lees AJ, Cairns N, Marsden CD et al (1997) Oxidative DNA damage in the parkinsonian brain: an apparent selective increase in 8-hydroxyguanine levels in substantia nigra. J Neurochem 69:1196–1203
Arima K, Hirai S, Sunohara N, Aoto K, Izumiyama Y, Ueda K et al (1999) Cellular colocalization of phosphorylated tau- and NACP/alpha-synuclein-epitopes in Lewy bodies in sporadic Parkinson’s disease and in dementia with Lewy bodies. Brain Res 843:53–61
Bibl M, Mollenhauer B, Esselmann H, Lewczuk P, Klafki HW, Sparbier K, Smirnov A, Cepek L, Trenkwalder C, Rüther E, Kornhuber J, Otto M, Wiltfang J (2006) CSF amyloid-beta-peptides in Alzheimer’s disease, dementia with Lewy bodies and Parkinson’s disease dementia. Brain 129(Pt 5):1177–1187 c
Braak H, Del Tredici K, Rüb U et al (2003) Staging of brain pathology related to sporadic Parkinson’s disease. Neurobiol Aging 24:197–211
Cookson MR, van der Brug M (2008) Cell systems and the toxic mechanism(s) of alpha-synuclein. Exp Neurol 209:5–11
Esposito A, Dohm CP, Kermer P, Bähr M, Wouters FS (2007) alpha-Synuclein and its disease related mutants interact differentially with the microtubule protein tau and associate with the actin cytoskeleton. Neurobiol Dis 26:521–531
Fagan AM, Roe CM, Xiong C, Mintun MA, Morris JC, Holtzman DM et al (2007) Cerebrospinal fluid tau/beta-amyloid(42) ratio as a prediction of cognitive decline in nondemented older adults. Arch Neurol 64:343–349
Hughes AJ, Daniel SE, Kilford L, Lees AJ (1992) Accuracy of clinical diagnosis of idiopathic Parkinson’s disease: a clinico-pathological study of 100 cases. J Neurol Neurosurg Psychiatry 55:181–184
Jenner P, Olanow CW (2006) The pathogenesis of cell death in Parkinson’s disease. Neurology 66:S24–S36
Mareš J, Stejskal D, Vavrouškova J, Urbánek K, Herzig R, Hluštík P (2003) Use of cystatin C determination in clinical diagnostics. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 147:177–180
Marras C, Lang A (2008) Invited article: changing concepts in Parkinson disease: moving beyond the decade of the brain. Neurology 70(21):1996–2003
McNaught KS, Olanow CW (2006) Protein aggregation in the pathogenesis of familial and sporadic Parkinson’s disease. Neurobiol Aging 27:530–545
Molina JA, Benito-Leon J, Jimenez-Jimenez FJ et al (1997) Tau protein concentrations in cerebrospinal fluid of non-demented Parkinson’s disease patients. Neurosci Lett 238:139–141
Mollenhauer B, Trenkwalder C, von Ahsen N, Bibl M, Steinacker P, Brechlin P et al (2006) Beta-amyloid 1–42 and tau-protein in cerebrospinal fluid of patients with Parkinson’s disease dementia. Dement Geriatr Cogn Disord 22(3):200–208
Pucci S, Mazzarelli P, Missiroli F, Regine F, Ricci F (2008) Neuroprotection: VEGF, IL-6, and clusterin: the dark side of the moon. Prog Brain Res 173:555–573
Sasaki K, Doh-ura K, Wakisaka Y, Iwaki T (2002) Clusterin/apolipoprotein J is associated with cortical Lewy bodies: immunohistochemical study in cases with alpha-synucleinopathies. Acta Neuropathol 104(3):225–230
Schapira AH (2008) Mitochondria in the aetiology and pathogenesis of Parkinson’s disease. Lancet Neurol 7:97–109
Stejskal D, Vavroušková J, Mareš J, Urbánek K (2005) Application of new laboratory marker assays in neurological diagnosis—a pilot study. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 149(2):265–266
Vranová H, Kaňovský P, Mareš J et al (2008) Laboratory markers of neurodegeneration in cerebrospinal fluid and degree of motor involvement in Parkinson’s disease: a correlation study. Cesk Slov Neurol N 71/104(3):324–328
Vranová H, Nevrlý M, Mareš J, Nestrašil I, Stejskal D, Kaňovský P (2009) Neurodegenerative markers in cerebrospinal fluid in Parkinson’s disease. Neurology 72(11 Suppl.3):66
Weintraub D, Comella CL, Horn S (2008) Parkinson’s disease—part 1: pathophysiology, symptoms, burden, diagnosis, and assessment. Am J Manag Care 14(2 Suppl):S40–S48
Yacoubian TA, Standaert DG (2009) Targets for Neuroprotection in Parkinson’s Disease. Biochim Biophys Acta 1792(7):676–687
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Přikrylová Vranová, H., Mareš, J., Nevrlý, M. et al. CSF markers of neurodegeneration in Parkinson’s disease. J Neural Transm 117, 1177–1181 (2010). https://doi.org/10.1007/s00702-010-0462-z
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DOI: https://doi.org/10.1007/s00702-010-0462-z