Alpha-synuclein in the Cerebrospinal Fluid Differentiates Synucleinopathies (Parkinson Disease, Dementia With Lewy Bodies, Multiple System Atrophy) From Alzheimer Disease

被引:98
作者
Tateno, Fuyuki [1 ]
Sakakibara, Ryuji [1 ]
Kawai, Takayuki [2 ]
Kishi, Masahiko [1 ]
Murano, Takeyoshi [2 ]
机构
[1] Toho Univ, Sakura Med Ctr, Dept Internal Med, Div Neurol, Sakura 2858741, Japan
[2] Toho Univ, Sakura Med Ctr, Res Adv Unit, Sakura, Japan
关键词
alpha-synuclein; Alzheimer disease; dementia with lewy bodies; Parkinson disease; multiple system atrophy; CLINICAL-DIAGNOSIS; A-BETA; TAU; PROTEIN; CSF; BIOMARKERS; DISORDERS; DJ-1;
D O I
10.1097/WAD.0b013e31823899cc
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background: We examined the utility of quantification of alpha-synuclein (SNCA) in the cerebrospinal fluid (CSF) to differentiate patients with Alzheimer disease (AD), dementia with Lewy bodies (DLB), Parkinson disease (PD), and multiple system atrophy (MSA). Methods: Thirty-seven patients were divided into 4 age-matched and sex-matched clinical groups: AD (n = 9), DLB (n = 6), PD (n = 11), and MSA (n = 11). Eleven subjects served as neurological disease controls. The total of 48 subjects included 27 men and 21 women, aged 66.5 +/- 11.4 years. We performed a solid-phase sandwich enzyme-linked immunosorbent assay, which enables the sensitive quantification of CSF SNCA. Results: In comparison with controls, CSF SNCA levels in AD were significantly higher (P < 0.05). CSF SNCA levels in PD (P < 0.001), DLB (P < 0.01), and MSA (P < 0.05) were all significantly lower than those in AD. However, CSF SNCA levels did not differ significantly among the 3 synucleinopathies. Conclusions: The results of the present study suggest that quantification of CSF SNCA helps in the differentiation of synucleinopathies (PD, DLB, and MSA) from AD. However, CSF SNCA levels did not differ significantly among the 3 synucleinopathies.
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页码:213 / 216
页数:4
相关论文
共 30 条
[1]   Full length α-synuclein is present in cerebrospinal fluid from Parkinson's disease and normal subjects [J].
Borghi, R ;
Marchese, R ;
Negro, A ;
Marinelli, L ;
Forloni, G ;
Zaccheo, D ;
Abbruzzese, G ;
Tabaton, M .
NEUROSCIENCE LETTERS, 2000, 287 (01) :65-67
[2]   Fine epitope mapping of monoclonal antibodies specific to human α-synuclein [J].
Choi, JY ;
Park, HJ ;
Seong, YM ;
Choi, EY ;
Min, BR ;
Rhim, H .
NEUROSCIENCE LETTERS, 2006, 397 (1-2) :53-58
[3]   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 [J].
Conway, KA ;
Lee, SJ ;
Rochet, JC ;
Ding, TT ;
Williamson, RE ;
Lansbury, PT .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (02) :571-576
[4]   Role of Synucleins in Alzheimer's Disease [J].
Crews, Leslie ;
Tsigelny, Igor ;
Hashimoto, Makoto ;
Masliah, Eliezer .
NEUROTOXICITY RESEARCH, 2009, 16 (03) :306-317
[5]   Non-Aβ component of Alzheimer's disease amyloid (NAC) revisited -: NAC and α-synuclein are not associated with Aβ amyloid [J].
Culvenor, JG ;
McLean, CA ;
Cutt, S ;
Campbell, BCV ;
Maher, F ;
Jäkälä, P ;
Hartmann, T ;
Beyreuther, K ;
Masters, CL ;
Li, QX .
AMERICAN JOURNAL OF PATHOLOGY, 1999, 155 (04) :1173-1181
[6]   Mitochondrial trafficking of APP and alpha synuclein: Relevance to mitochondrial dysfunction in Alzheimer's and Parkinson's diseases [J].
Devi, Latha ;
Anandatheerthavarada, Hindupur K. .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 2010, 1802 (01) :11-19
[7]   α-synuclein and its disease-related mutants interact differentially with the microtubule protein tau and associate with the actin cytoskeleton [J].
Esposito, Alessandro ;
Dohm, Christoph P. ;
Kermer, Pawel ;
Baehr, Mathias ;
Wouters, Fred S. .
NEUROBIOLOGY OF DISEASE, 2007, 26 (03) :521-531
[8]   Cerebrospinal fluid tau, Aβ, and phosphorylated tau protein for the diagnosis of Alzheimer's disease [J].
Formichi, Patrizia ;
Battisti, Carla ;
Radi, Elena ;
Federico, Antonio .
JOURNAL OF CELLULAR PHYSIOLOGY, 2006, 208 (01) :39-46
[9]   Tau phosphorylation increases in symptomatic mice overexpressing A30P α-synuclein [J].
Frasier, M ;
Walzer, M ;
McCarthy, L ;
Magnuson, D ;
Lee, JM ;
Haas, C ;
Kahle, P ;
Wolozin, B .
EXPERIMENTAL NEUROLOGY, 2005, 192 (02) :274-287
[10]  
Giasson BI, 2000, J NEUROSCI RES, V59, P528, DOI 10.1002/(SICI)1097-4547(20000215)59:4<528::AID-JNR8>3.0.CO