Tau protein and beta-amyloid^sub 1-42^ CSF levels in different phenotypes of Parkinson's disease

• Published in: Journal of neural transmission Vol. 119; no. 3; p. 353
• Main Authors: Prikrylová Vranová, Hana, Mares, Jan, Hlustík, Petr, Nevrlý, Martin, Stejskal, David, Zapletalová, Jana, Obereigneru, Radko, Kaovský, Petr
• Format: Journal Article
• Language: English
• Published: Wien Springer Nature B.V 01-03-2012
• ISSN: 0300-9564; 1435-1463
• DOI: 10.1007/s00702-011-0708-4

Parkinson's disease (PD) is a neurodegenerative disorder with highly heterogeneous clinical manifestations. This fact has prompted many attempts to divide PD patients into clinical subgroups. This could lead to a better recognition of pathogenesis, improving targeted treatment and the prognosis of PD patients. The aim of the present study was to obtain cerebrospinal fluid (CSF) samples in PD patients and to search for a relationship between neurodegenerative CSF markers (tau protein, beta-amyloid^sub 1-42^ and index tau protein/beta-amyloid^sub 1-42^) and the clinical subtypes. PD patients were divided into three subgroups: early disease onset (EDO), tremor-dominant PD (TD-PD), and non-tremor dominant PD (NT-PD) according to the previously published classification. Neurodegenerative markers in the CSF were assessed in these three groups of patients suffering from PD (EDO-17, TD-15, NT-16 patients) and in a control group (CG) of 19 patients suffering from non-degenerative neurological diseases and 18 patients with Alzheimer's disease (AD). The NT-PD patients were found to have significantly higher levels of CSF tau protein and index tau/beta than the control subjects and other Parkinsonian subgroups, but no significant differences in these markers were found between AD and NT-PD patients. In the context of more rapid clinical progression and more pronounced neuropathological changes in the NT-PD patient group, our results corroborate the opinion that CSF level of tau protein may be regarded as a potential laboratory marker of the presence and severity of neurodegeneration.[PUBLICATION ABSTRACT]