2010/06/29 by Sigurd D. Süßmuth, Ingo Uttner, G. Bernhard Landwehrmeyer +10 · 1 citation
Medicine · #Parkinson's Disease Mechanisms and Treatments #Neurological disorders and treatments #Alzheimer's disease research and treatments
paper · doi:10.1002/mds.22895
openalex publication_date 2010/06/29 · openalex created_date 2016/06/24 · openalex updated_date 2026/08/05
To evaluate cerebrospinal fluid (CSF) proteins reflecting processes of neurodegeneration and glial activation in progressive supranuclear palsy (PSP; Richardson's syndrome, n = 20; PSP-Parkinsonism, n = 7) and multiple system atrophy (MSA, n = 25), we analyzed tau, phosphorylated tau, amyloid-beta(1-42) (Abeta1-42), Abeta1-40, glial fibrillary acidic protein (GFAP), and CSF routine variables. Individuals with PSP-Parkinsonism and MSA had elevated tau levels when compared with Richardson's syndrome, Parkinson's disease (PD), and age-matched controls (P <or= 0.001). Ratios of P-tau/T-tau were significantly different in Parkinsonian syndromes. CSF Abeta1-42 was decreased only in patients with Richardson's syndrome. In a subset of Parkinsonian syndromes, we found elevated GFAP concentrations and increased CSF/serum albumin ratios. There were no correlations between biomarker concentrations and clinical scores in any of the diseases. In conclusion, this preliminary data show that changes in CSF tau and Abeta1-42 may indicate different protein processing in PSP patients and might, therefore, be relevant in the differentiation of PSP subtypes.