Browsing by Author "Petzold, Axel"

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) (A beta 1-42), A beta 1-40, 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 <= 0.001). Ratios of P-tau/T-tau were significantly different in Parkinsonian syndromes. CSF A beta 1-42 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 A beta 1-42 may indicate different protein processing in PSP patients and might, therefore, be relevant in the differentiation of PSP subtypes. (C) 2010 Movement Disorder Society

Despite major advances in deciphering the neuropathological hallmarks of amyotrophic lateral sclerosis (ALS), validated neurochemical biomarkers for monitoring disease activity, earlier diagnosis, defining prognosis and unlocking key pathophysiological pathways are lacking. Although several candidate biomarkers exist, translation into clinical application is hindered by small sample numbers, especially longitudinal, for independent verification. This review considers the potential routes to the discovery of neurochemical markers in ALS, and provides a consensus statement on standard operating procedures that will facilitate multicenter collaboration, validation and ultimately clinical translation.