Tau protein, beta-amyloid1–42 and clusterin CSF levels in the differential diagnosis of Parkinsonian syndrome with dementia

• Published in: Journal of the neurological sciences 2014-08, Vol.343 (1), p.120-124
• Main Authors: Vranová, Hana Přikrylová, Hényková, Eva, Kaiserová, Michaela, Menšíková, Kateřina, Vaštík, Miroslav, Mareš, Jan, Hluštík, Petr, Zapletalová, Jana, Strnad, Miroslav, Stejskal, David, Kaňovský, Petr
• Format: Article
• Language: English
• Subjects: Adult; Aged; Aged, 80 and over; Alzheimer disease; Amyloid beta-Peptides - cerebrospinal fluid; Biomarkers; Cerebrospinal fluid; Clusterin; Dementia - cerebrospinal fluid; Dementia - complications; Dementia - diagnosis; Diagnosis, Differential; Enzyme-Linked Immunosorbent Assay; Female; Humans; Lewy body dementia; Male; Mental Status Schedule; Middle Aged; Neurology; Parkinson Disease - cerebrospinal fluid; Parkinson Disease - complications; Parkinson Disease - diagnosis; Parkinson's disease; Peptide Fragments - cerebrospinal fluid; Reproducibility of Results; Sensitivity and Specificity; Severity of Illness Index; tau Proteins - cerebrospinal fluid
• ISSN: 0022-510X; 1878-5883
• DOI: 10.1016/j.jns.2014.05.052

Abstract Background Parkinson's disease (PD), PD with dementia (PDD) and Lewy body dementia (DLB) are synucleinopathies. PDD and DLB are sometimes considered a transition between PD and Alzheimer dementia (AD). Finding in vivo markers or their combination could help in the differential diagnosis of these neurodegenerative (ND) diseases. Objective The aim of this study was to assess cerebrospinal fluid (CSF) levels of tau protein, betaamyloid1–42 and clusterin and to compare these levels among patients with probable PD, PDD, DLB and AD. Methods CSF levels of ND markers were assessed in 96 patients (27 patients with PD, 14 with PDD, 14 with DLB, 17 with AD and 24 subjects as a control group). Results In all of the groups of patients, beta-amyloid1–42 levels were decreasing in the order PD > PDD > DLB > AD, whereas tau protein and the tau protein/beta-amyloid1–42 index were increasing in the same order (PD < PDD < AD), except for DLB. In paired group comparisons, higher levels of clusterin in PD patients ( p = 0.005) and PDD patients ( p = 0.052) compared to the CG were found. Conclusion The results of the present study support the role of clusterin in PD pathogenesis. The decreasing CSF beta-amyloid1–42 levels in the order PDD, DLB and AD may relate to the increasing presence of AD pathology in these disorders.