Serum inflammatory biomarkers in Parkinson's disease

被引:77
作者
Dufek, M. [1 ]
Hamanova, M. [2 ]
Lokaj, J. [2 ]
Goldemund, D. [1 ]
Rektorova, I. [1 ]
Michalkova, Z. [1 ]
Sheardova, K. [1 ]
Rektor, I. [1 ]
机构
[1] Masaryk Univ, St Annes Univ Hosp, Dept Neurol 1, Brno 65691, Czech Republic
[2] Masaryk Univ, St Annes Univ Hosp, Dept Clin Immunol & Allergol, Brno 65691, Czech Republic
关键词
Parkinson's disease; Inflammation; Tumor necrosis factor-alpha; Mannan-binding lectin; Microglial activation; MICROGLIAL ACTIVATION; COMPLEMENT; NEUROINFLAMMATION; NEURODEGENERATION; MODELS;
D O I
10.1016/j.parkreldis.2008.05.014
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Numerous recent findings indicate the involvement of a neuroinflammatory reaction in the neurodegeneration in idiopathic Parkinson's disease (PD). We examined 29 consecutive patients with PD, ages 54-84 years, most of whom were moderately impaired (median UPDRS 19; Hoehn-Yahr 3; MMSE 28). A series of serum biomarkers were investigated, and their levels were correlated with the degree of the motor and cognitive impairment. There were no abnormalities of IL-6, acute phase proteins (C-reactive protein, serum amyloid A, alpha 1-antitrypsin, orosomucoid, ceruloplasmin, alpha 2-macroglobulin, transferrin, prealbumin) and factors of the complement system (C1q, C1-INH, C3, C4). A decrease in Mannan-binding lectin (MBL) levels was observed in six patients; an elevation of tumor necrosis factor-alpha (TNF-alpha) was found in 12 patients. No statistically significant correlation was found between the patient's clinical state (neuropsychologic and motor, as expressed by UPDRS III, Hoehn-Yahr, and MMSE) and the immunomarker changes. Our results indicate that the inflammatory process may be reflected in the serum; nevertheless, further research is needed to elucidate the possible clinical implications. (C) 2008 Elsevier Ltd. All rights reserved.
引用
收藏
页码:318 / 320
页数:3
相关论文
共 12 条
[1]   Neuroinflammation in the pathophysiology of Parkinson's disease:: Evidence from animal models to human in vivo studies with [11C]-PKI1195 PET [J].
Bartels, Anna L. ;
Leenders, Klaus L. .
MOVEMENT DISORDERS, 2007, 22 (13) :1852-1856
[2]   Interleukin-1 beta and interleukin-6 are elevated in the cerebrospinal fluid of Alzheimer's and de novo Parkinson's disease patients [J].
BlumDegen, D ;
Muller, T ;
Kuhn, W ;
Gerlach, M ;
Przuntek, H ;
Riederer, P .
NEUROSCIENCE LETTERS, 1995, 202 (1-2) :17-20
[3]   Role of complement in neurodegeneration and neuroinflammation [J].
Bonifati, Domenico Marco ;
Kishore, Uday .
MOLECULAR IMMUNOLOGY, 2007, 44 (05) :999-1010
[4]   Nonsteroidal antiinflammatory drug use and the risk for Parkinson's disease [J].
Chen, HL ;
Jacobs, E ;
Schwarzschild, MA ;
McCullough, ML ;
Calle, EE ;
Thun, MJ ;
Ascherio, A .
ANNALS OF NEUROLOGY, 2005, 58 (06) :963-967
[5]   Microglial activation with atypical proinflammatory cytokine expression in a rat model of Parkinson's disease [J].
Depino, AM ;
Earl, C ;
Kaczmarczyk, E ;
Ferrari, C ;
Besedovsky, H ;
del Rey, A ;
Pitossi, FJ ;
Oertel, WH .
EUROPEAN JOURNAL OF NEUROSCIENCE, 2003, 18 (10) :2731-2742
[6]   Complement protein isoforms in CSF as possible biomarkers for neurodegenerative disease [J].
Finehout, EJ ;
Franck, Z ;
Lee, KH .
DISEASE MARKERS, 2005, 21 (02) :93-101
[7]  
Hirsch EC, 2003, ANN NY ACAD SCI, V991, P214
[8]   Blocking soluble tumor necrosis factor signaling with dominant-negative tumor necrosis factor inhibitor attenuates loss of dopaminergic neurons in models of Parkinson's disease [J].
McCoy, Melissa K. ;
Martinez, Terina N. ;
Ruhn, Kelly A. ;
Szymkowski, David E. ;
Smith, Christine G. ;
Botterman, Barry R. ;
Tansey, Keith E. ;
Tansey, Malu G. .
JOURNAL OF NEUROSCIENCE, 2006, 26 (37) :9365-9375
[9]   Inflammation and neurodegeneration in Parkinson's disease [J].
McGeer, PL ;
McGeer, EG .
PARKINSONISM & RELATED DISORDERS, 2004, 10 :S3-S7
[10]   Inflammatory process in Parkinson's disease: Role for cytokines [J].
Nagatsu, T ;
Sawada, M .
CURRENT PHARMACEUTICAL DESIGN, 2005, 11 (08) :999-1016